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	<title>Pet Health Library - Marin Pet Hospital, San Rafael, CA</title>
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		<title>2010 Summer Reading List</title>
		<link>http://marinpethospital.com/library/uncategorized/2010-summer-reading-list/</link>
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		<pubDate>Fri, 14 May 2010 20:38:29 +0000</pubDate>
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		<description><![CDATA[For all you avid readers out there, we compiled a book list of staff favorites for your summer reading pleasure.
1. A Dog&#8217;s Life by Peter Mayle
2. If Wishes Were Horses  by Anne McCaffrey
3. Simon&#8217;s Cat by Simon Tofield
4. How to be YOur Dog&#8217;s Best Friend by the Monks of Newskeet
5. The Art of Racing in [...]]]></description>
			<content:encoded><![CDATA[<p>For all you avid readers out there, we compiled a book list of staff favorites for your summer reading pleasure.</p>
<p>1.<span style="text-decoration: underline;"> A Dog&#8217;s Life</span> by Peter Mayle</p>
<p>2. <span style="text-decoration: underline;">If Wishes Were Horses</span>  by Anne McCaffrey</p>
<p>3. <span style="text-decoration: underline;">Simon&#8217;s Cat</span> by Simon Tofield</p>
<p>4. <span style="text-decoration: underline;">How to be YOur Dog&#8217;s Best Friend</span> by the Monks of Newskeet</p>
<p>5. <span style="text-decoration: underline;">The Art of Racing in the Rain</span> by Garth Stein</p>
<p>6.<span style="text-decoration: underline;"> All Creatures Great and Small</span> by James Herriot</p>
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		<title>Lyme Borreliosis</title>
		<link>http://marinpethospital.com/library/cats/lyme-borreliosis/</link>
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		<pubDate>Thu, 13 May 2010 19:58:00 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
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Lyme Borreliosis
 Kathi Smith, RVT




submitted 4/2003
Definition: A polysystemic tick transmitted spirochete disease found in the northeastern coastal states, southeast, Midwest, and western states.
Etiologic Agent involved with Lyme Borreliosis is the spirochete, Borrelia burgdorferi 
Vector: The vector is the deer tick (Ixodes sammini in the Northeast, Ixodes scapularis in the southeast and Ixodes pacificus in the western [...]]]></description>
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<td valign="top"><em><strong>Lyme Borreliosis</strong><br />
<strong> </strong></em>Kathi Smith, RVT</td>
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<p>submitted 4/2003</p>
<p><strong>Definition:</strong> A polysystemic tick transmitted spirochete disease found in the northeastern coastal states, southeast, Midwest, and western states.</p>
<p><strong>Etiologic Agent</strong> involved with Lyme Borreliosis is the spirochete, <em>Borrelia burgdorferi </em></p>
<p><strong>Vector: </strong>The vector is the deer tick (<em>Ixodes sammini</em> in the Northeast, <em>Ixodes scapularis</em> in the southeast and <em>Ixodes pacificus</em> in the western states and California). Other species of ticks (including the dog tick) and insects such as horseflies, deerflies, and mosquitoes can carry <em>B. burgdorferi</em>; however, only ticks have been linked with disease transmission. The route of infection is through the bite of an infected tick and requires 48 hours of attachment to the host. Mice are the main reservoirs due to the fact that they maintain the larval and nymph stages. Deer support the adult population but it is thought that they do not become infected by the spirochete. Birds however, may also be important reservoirs because they can transmit ticks and spirochetes over long distances.</p>
<p><strong>Clinical Signs </strong>associated with Lyme Borreliosis infection are typically subclinical, but may be septic or immune mediated. These include:</p>
<blockquote><p>· Sudden joint lameness (usually bilateral and involves the carpus) and evidence of severe pain, depression, fever, inappetence, lethargy, lymphadenopathy, limb shifting due to polyarthritis, acute progressive renal failure and protein losing glomerulonephropathy (especially in Labradors, and Golden Retrievers.), rheumatoid arthritis, meningitis, and myocarditis</p></blockquote>
<p><strong>Hematological and Biochemical Abnormalities are not usually seen with Lyme Borreliosis. </strong></p>
<blockquote><p>· Azotemia, protenuria, hematuria, pyuria, and tubular casts have been associated with dogs that have renal involvement of the infection.<br />
· Synovial fluid analyses are consistent for supportive polyarthritis with increased leukocyte numbers seen. Borrelia organisms are rarely isolated from joint fluid</p></blockquote>
<p><strong>Diagnosis of Lyme Borreliosis</strong>, like other tick borne diseases, can be difficult. There can be many other causes for the clinical signs seen with the disease and more than 50% of seropositive dogs remain asymptomatic while dogs with acute disease may be seronegative. To document seroconversion, retesting should be done in 3 to 4 weeks. Diagnosis should then be made on a combination of criteria:</p>
<blockquote><p>· Recent exposure to an endemic area<br />
· Detection of ticks on dog<br />
· Serologic test results, Enzyme-linked immunosorbent assay (ELISA) is considered more sensitive and specific than the indirect fluorescent antibody (IFA) test</p>
<blockquote><p>serum titers<br />
&lt; 1:28 = NEG<br />
1:128-1:256 = low +<br />
1:512 or &gt; = high +</p></blockquote>
<p>· Prompt response to antibiotic therapy<br />
· Immune-mediated diseases should be ruled<br />
· Radiographs and joint taps to rule out other causes of lameness</p></blockquote>
<p><strong>Treatment </strong>for Lyme Borreliosis consists of antibiotics and supportive care.</p>
<blockquote><p>· <strong>Doxycycline</strong> 10 mg/kg PO q 12 hours for 14-30 days<br />
· <strong>Cephalexin and Amoxicillin</strong> 22 mg/kg PO q 12 hours for 14-30 days<br />
· <strong>Azithromycin or Ceftriaxone</strong> should be used for refractory infection 5mg/kg PO q 12 hours<br />
· <strong>Anti-inflammatory drugs</strong> to reduce joint pain and swelling is debatable</p></blockquote>
<p><strong>Prognosis</strong> is good with proper treatment therapy. If the patient does not respond to antibiotic therapy in 7-10 days, the antibiotic should be changed.</p>
<p><strong>Prevention</strong> is through avoidance of tick-infested areas, control with the use of sprays, spot-ons, collars and vaccination (reserve vaccines for high risk dogs-outdoor, hunting, field trial)</p>
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<td colspan="2"><em>Date Published: April 29, 2003</em></td>
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		<title>Canine Pancreatitis</title>
		<link>http://marinpethospital.com/library/cats/canine-pancreatitis/</link>
		<comments>http://marinpethospital.com/library/cats/canine-pancreatitis/#comments</comments>
		<pubDate>Thu, 13 May 2010 19:39:55 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
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<td valign="bottom"><a href="http://www.veterinarypartner.com/Content.plx?P=SRC&amp;S=4&amp;SourceID=42&amp;EVetID=0">THE PET HEALTH LIBRARY</a><br />
By Wendy C. Brooks, DVM, DipABVP<br />
Educational Director, VeterinaryPartner.com</td>
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<p>Canine Pancreatitis<br />
 </p>
<p><strong>The Normal Pancreas and What It Does</strong></p>
<p>We eat food, chew it up into a slurry, and swallow it. It travels down the esophagus to the stomach where it is ground up further and enzymes are added to begin protein break-down (digestion). When the food particles are small enough, they are propelled into the small intestine for further digestive treatment and ultimately nutrient absorption. The small intestine has three portions: the duodenum that connects to the stomach, and the jejunum and ileum below. The jejunum and ileum are mostly involved in absorption but the duodenum, being so close to the stomach, is the site of further digestion.</p>
<p>There are two ducts that enter the duodenum near where the stomach contents enter. One duct is for bile, squirted in directly from the liver’s gall bladder. The bile serves to neutralize the acid that the stomach had added, to emulsify (or dissolve) dietary fats for absorption later in the tract, and also to excrete some toxins. The other duct is the pancreatic duct, which squirts in more digestive enzymes so as to break down starches and more protein.</p>
<p>The pancreas is a pale pink glandular organ that nestles cozily just under the stomach and along the duodenum. As a glandular organ, the pancreas is all about secretion, and it has two main jobs: the first job is the secretion of digestive enzymes to help us break down the food we eat, the second job being secretion of insulin and glucagon (to regulate sugar metabolism). The digestive enzymes are the part of the story that concerns us in pancreatitis.</p>
<p><strong>Pancreatitis Is Inflammation of the Pancreas</strong></p>
<p>In pancreatitis, inflammation disrupts the normal integrity of the pancreas. Digestive enzymes that are normally safely stored in granules are released prematurely where they digest the body itself. The result can be a metabolic catastrophe. The living tissue becomes further inflamed and the tissue damage quickly involves the adjacent liver. Toxins released from this orgy of tissue destruction are released into the circulation and can cause a body-wide inflammatory response. If the pancreas is affected so as to disrupt its ability to produce insulin, diabetes mellitus can result; this diabetes can be either temporary or permanent.</p>
<p>Special disasters include the disruption of “surfactants” in the lung tissue that normally keep the tiny air-filled alveoli from collapsing after each exhaled breath. Without surfactants, the alveoli close up and respiratory failure results.</p>
<p>Also, there is a syndrome called Weber-Christian syndrome in which fats throughout the body are destroyed.</p>
<p>Pancreatitis is one of the chief risk factors for the development of what is called disseminated intravascular coagulation, or DIC, which is basically a massive uncoupling of normal blood clotting and clot dissolving mechanisms. This leads to abnormal simultaneous bleeding and clotting of blood throughout the body.</p>
<p>Pancreatic encephalopathy (brain damage) can occur if the fats protecting the central nervous system become digested.</p>
<p><strong><em>The good news is that most commonly the inflammation is confined to the area of the liver and pancreas but even with this limitation, pancreatitis can be painful and life-threatening.</em></strong></p>
<p><strong><em>Pancreatitis can be acute or chronic, mild or severe</em></strong>.</p>
<p><strong>What Causes Pancreatitis</strong></p>
<p>In most cases we never find out but we do know some events that can cause pancreatitis:</p>
<p>• Reflux of duodenal contents into the pancreatic duct. The pancreas has numerous safety mechanisms to prevent self-digestion. One of these mechanisms is the fact that the enzymes it creates are stored in an inactive form. They are harmless until they are mixed with activating enzymes. The strongest activating enzymes are made by duodenal cells, which means that the digestive enzymes do not actually activate until they are out of the pancreas and mixing with food in the duodenum. If duodenal fluids backwash up the pancreatic duct and into the pancreas, enzymes are prematurely activated and pancreatitis results. This is apparently the most common pancreatitis mechanism in humans, though it is not very common in veterinary patients.<br />
• Concurrent hormonal imbalance predisposes a dog to pancreatitis. Such conditions include: <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=631&amp;S=0&amp;EVetID=0" target="_blank">diabetes</a>, <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=461&amp;S=0&amp;EVetID=0" target="_blank">hypothyroidism</a>, and <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=1732&amp;S=0&amp;EVetID=0" target="_blank">hypercalcemia</a>. The first two conditions are associated with altered fat metabolism that predisposes to pancreatitis, and the latter condition involves elevated blood calcium that activates stored digestive enzymes.<br />
• Use of certain drugs can predispose to pancreatitis (sulfa-containing antibiotics such as <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=617&amp;S=0&amp;EVetID=0" target="_blank">trimethoprim sulfa</a> or chemotherapy agents such as <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=511&amp;S=0&amp;EVetID=0" target="_blank">azathioprine</a>).<br />
• Trauma to the pancreas as from a car accident or even surgical manipulation can cause inflammation and thus pancreatitis.</p>
<p><strong><em>Miniature Schnauzers are predisposed to pancreatitis as they commonly have altered fat metabolism.</em></strong></p>
<p><strong>Signs of Pancreatitis</strong></p>
<p>The classical signs in dogs are appetite loss, vomiting, diarrhea, painful abdomen, and fever.</p>
<p><strong>Making the Diagnosis</strong></p>
<p>A reliable blood test has been lacking for this disease. Traditionally, blood levels of amylase and lipase (two pancreatic enzymes) have been used. When their levels are especially high, this is felt to be a reasonable sign of pancreatitis, but still these tests are not as sensitive or specific as we would prefer. They can elevate dramatically with corticosteroid use, with intestinal perforation, kidney disease, or even dehydration. Some experts advocate measuring lipase and amylase on fluid from the belly rather than on blood but this has not been fully investigated and is somewhat invasive.</p>
<p>A newer test called the PLI or pancreatic lipase immunoreactivity test has come to be important. Lipase is one of the pancreatic digestive enzymes and small traces are normally present in the circulation. These levels jump dramatically in pancreatitis and the diagnosis can be confirmed with a less expensive and non-invasive test. A regular lipase level measures all forms of lipase, not just those of a pancreatic source; this is test is specific for pancreatic lipase. The problem is that technology needed to run this test is unique and the test can only been run in certain facilities on certain days. Results are not necessarily available rapidly enough to help a very sick patient.</p>
<p>More recently a new test called the SPEC cPL (specific canine pancreatic lipase) test has come to be the test of choice. This test is a newer generation immunological test for canine pancreatic lipase and can be run overnight by a reference lab. This test is able to detect 83% of pancreatitis cases (the test is 83% sensitive) and excludes other possible diseases in 98% of cases (i.e., the test is 98% specific for pancreatitis). There is no comparable test for cats at this time.</p>
<p>Radiographs can show a widening of the angle of the duodenum against the stomach, which indicates a swelling of the pancreas. Most veterinary hospitals have the ability to take radiographs but this type of imaging is not very sensitive in detecting pancreatitis and only is able to find 24% of cases.</p>
<p>Ultrasound, on the other hand, detected 68% of cases and provides the opportunity to image other organs and even collect fluid from the belly easily. When one balances rapid results and accuracy, this test may be the best.</p>
<p>In some cases, surgical exploration is the only way to make the correct diagnosis.</p>
<p><strong>Treatment</strong></p>
<p>The passage of food through the duodenum is a strong stimulus to the pancreas. In the treatment of canine pancreatitis we do not want any stimulation of the pancreas; we want the pancreas to rest. This means no food and no water for 2 to 3 days (IV fluid support prevents dehydration).</p>
<p>Fluid support will generally require potassium supplementation as potassium depletes in pancreatitis. Blood pH must be tracked as well. A critical patient with pancreatitis will need 24 hour care and blood test monitoring several times a day. A plasma transfusion represents a special type of fluid therapy and helps provide special proteins that inhibit pancreatic enzymes. Whether or not the protection afforded by plasma is real or theoretical is still being worked out but since it is difficult to go wrong with a plasma transfusion, do not be surprised if your veterinarian uses this approach.</p>
<p>Pancreatitis is a painful condition and pain management is not only humane but important in recovery. Untreated pain affects the immune system and increases mortality. Injectable pain medications, <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=534&amp;S=0&amp;EVetID=0" target="_blank">fentanyl patches</a>, and even continuous drips can be used effectively to control pain. Additional medications to control nausea are also commonly used in the management of this condition. Antibiotics are often used because even though pancreatitis is not a bacterial disease, bacterial invasion from the diseased intestine is a common occurrence.</p>
<p>Once the patient has started to eat again, a low fat diet (such as one of the prescription high fiber diets) is important to minimize pancreatic stimulation. Since there is potential for the pancreas to always have a chronic smoldering bit of inflammation, long-term use of a low-fat diet is likely to be recommended.</p>
<p><strong>Beware of Diabetes Mellitus</strong></p>
<p>When the inflammation subsides in the pancreas, some scarring is inevitable. When 80% of the pancreas is damaged, insulin cannot be produced, and diabetes mellitus results. This may or may not be permanent depending on the capacity for the pancreas’ tissue to recover. See more information on the management of <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=631&amp;S=0&amp;EVetID=0" target="_blank">diabetes mellitus</a>.</p>
<p><em>Date Published: 1/2/2006 12:27:00 PM<br />
</em></p>
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		<title>Dietary Therapy of Renal Failure</title>
		<link>http://marinpethospital.com/library/cats/dietary-therapy-of-renal-failure/</link>
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		<pubDate>Thu, 13 May 2010 19:37:07 +0000</pubDate>
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THE PET HEALTH LIBRARY
By Wendy C. Brooks, DVM, DipABVP
Educational Director, VeterinaryPartner.com


 



 



    



Dietary Therapy of Renal Failure








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There are many [...]]]></description>
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<td valign="bottom"><a href="http://www.veterinarypartner.com/Content.plx?P=SRC&amp;S=4&amp;SourceID=42&amp;EVetID=0">THE PET HEALTH LIBRARY</a><br />
By Wendy C. Brooks, DVM, DipABVP<br />
Educational Director, VeterinaryPartner.com</td>
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<p> </p>
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<p>Dietary Therapy of Renal Failure</p>
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<p> </p>
<p>There are many aspects of kidney failure that require attention. Diet can be used to help in many ways and we are lucky to have commercially available diets made specifically for renal patients. There are even diets made for different stages of kidney failure. The goal of therapy, dietary or otherwise, is to prevent or at least postpone advanced uremia (poisoning by toxins that the kidneys could not adequately remove) and extend life expectancy.<br />
In one famous study where 38 dogs in kidney failure were tracked for 2 years, dietary therapy reduced the risk of dying by 69% over dogs allowed to continue eating regular dog food.</p>
<p>Another study in dogs showed that beginning the renal diet when the creatinine was between 2.0 and 3.1 delayed the onset of uremic crisis by 5 months.</p>
<p>A study of 50 cats with stable naturally occurring renal failure were divided into two groups, one receiving renal diet and the other receiving regular food. The cats on the renal diet survived over twice as long as the others.</p>
<p>Clearly there is tremendous benefit to the patient in switching to a therapeutic renal diet. Unfortunately, these diets tend to be blander than what the pet may be used to and they are not always acceptable to the pet.</p>
<ul>
<li>Do not attempt to starve the pet into eating the new food. Change more gradually.</li>
<li>Consider using another brand that might have a different flavor. Remember, therapeutic foods are guaranteed so that even opened bags can be returned for a full refund.</li>
</ul>
<p>Let’s review some basic features of a desired diet. There are many misconceptions about an appropriate diet for renal disease. In fact, what dietary modifications should be made depend on the stage of renal disease. Some basic desired qualities in a renal diet are:</p>
<ul>
<li>Protein restriction</li>
<li>Phosphate restriction</li>
<li>Sodium restriction</li>
<li>Supplementation with omega-3 fatty acids</li>
</ul>
<p><strong>Low Protein</strong></p>
<p>Since a number of renal toxins come from the metabolism of protein, one way to give the kidneys less work to do is to eat less protein. How much less protein depends on how serious the kidney disease is. Older animals tend to require a higher dietary protein level in general when compared to their younger counterparts. Protein also adds palatability to the food so that if we try to restrict protein too much we may end up with a pet who will not eat at all.</p>
<p>Further, there is a metabolic requirement for protein below which a diet cannot dip. This has led to diets with differing protein restrictions to fit with different stages of disease, less restriction for earlier stages.</p>
<ul>
<li>There is no protective value to restricting protein prior to the onset of kidney failure.</li>
<li>High protein diets do not cause kidney failure (though they certainly make the patient worse after kidney failure is present).</li>
</ul>
<p><strong>Phosphorus Restriction</strong></p>
<p>This is an important part of a renal diet since phosphorus balance is crucial. Phosphorus comes into the body via the diet and leaves the body via the kidney, only in renal failure phosphorus is not well removed as it is supposed to. Obviously using less phosphorus in the diet may be adequate to keep the blood phosphorus levels normal, thus balancing the intake with the output, but sometimes addition of medication (i.e. a phosphate binder) is needed to further reduce intake. Restricting dietary phosphate has been shown to slow the progression of renal disease.</p>
<p><strong><em>If the goal phosphorus level has not been achieved in 2 to 4 weeks after starting the renal diet, a phosphorus binder should be utilized.</em></strong></p>
<p><strong>Omega 3 Fatty Acids</strong></p>
<p>Studies suggest that kidney failure patients taking omega 3 fatty acids are likely to live longer than patients who do not take them. This has led to the supplementation of most renal diets with fish oils. The full import of fatty acid supplementation is still being worked out.</p>
<p>Other dietary features include B vitamin supplementation (since the damaged kidneys tend to lose excess B complex), which have non-acidifying features to help control acidosis.</p>
<p><strong>At What Point Should a Special Diet be Started?</strong></p>
<p>This has been a controversial question for a long time. For many animals, changing diet to a less palatable food represents a definite reduction in life quality. There was some thinking that we are changing the diet too soon. On the other hand, if a pet is in a more advanced state of disease before the switch is made, the pet will be much less willing to change to a food of less palatability. The companies that make these foods have put a great deal of research into improving palatability over the years, which has helped tremendously and now the International Renal Interest Society finally has guidelines.</p>
<p><strong><em>They recommend changing the diet to a renal food when a dog’s creatinine level is in the 2.1-5 mg/dl range (Stage III renal failure). For cats, the diet should change when the creatinine reaches approximately 2.0 mg/dl (middle Stage II renal failure).</em></strong></p>
<p>These guidelines allow the patient to benefit the most from the preventive advantages of the diet. If the pet finds the diet palatable then there should be no life quality issues with changing foods.<br />
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<p><strong>Home Cooking a Renal Diet</strong></p>
<p>Home cooking an appropriate renal diet is a complicated task but it can be done. Because different pets experience different problems with their renal disease (potassium depletion or not, pH issues or not, different degrees of phosphorus restriction needed, etc.), the diet should ideally be tailored to the individual.</p>
<p>Your veterinarian can get you an appropriate recipe through <a href="http://www.balanceit.com/" target="_blank">www.balanceit.com</a>. (Because these are therapeutic diet formulas, you cannot access them on your own.)</p>
<p>Several recipes have been published by Dr. Donald Strombeck, one of the internal medicine specialists at the University of California at Davis. These recipes can be viewed at:</p>
<p><a href="http://users.ameritech.net/critterz/crf_recipes.htm#Strombeck%27s%20recipes" target="_blank">http://users.ameritech.net/critterz/crf_recipes.htm#Strombeck%27s%20recipes</a></p>
<p>We cannot vouch for other recipes found on this site but can say that often published recipes prove nutritionally incomplete when scrutinized. The Strombeck recipes are complete and balanced.</p>
<p>For more detailed recipe and expert adjustments, a veterinary nutritionist can be consulted. There are several university nutrition departments that offer this service but we have found the best service from a private company at<br />
<a href="http://www.petdiets.com/" target="_blank">www.petdiets.com</a>.</p>
<p>Expect a consultation with a veterinary nutritionist to cost anywhere from $150 to $200.</p>
<p><em>Date Published: 7/30/2007 10:53:00 AM<br />
</em></p>
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		<title>Glomerulonephritis</title>
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		<pubDate>Thu, 13 May 2010 19:35:01 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
				<category><![CDATA[Cats]]></category>
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		<category><![CDATA[Kidney Disease]]></category>

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		<description><![CDATA[


 



THE PET HEALTH LIBRARY
By Wendy C. Brooks, DVM, DipABVP
Educational Director, VeterinaryPartner.com


 



 



    



Glomerulonephritis








Related Articles







A Chronic Renal (Kidney) Failure Center



Anemia: Inadequate Red Blood Cells



Anorexia



Calcium Phosphorus Balance



Chronic Renal Failure Links



Dietary Therapy of Renal Failure 



Fluid Therapy



High Blood Pressure (Systemic Hypertension) in our Pets



Kidney Dialysis: Is it for your Pet?



Kidney Failure: Where to Begin



Kidney Transplants for Cats and Dogs












 
(Renal Protein [...]]]></description>
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<td valign="bottom"><a href="http://www.veterinarypartner.com/Content.plx?P=SRC&amp;S=4&amp;SourceID=42&amp;EVetID=0">THE PET HEALTH LIBRARY</a><br />
By Wendy C. Brooks, DVM, DipABVP<br />
Educational Director, VeterinaryPartner.com</td>
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<p>Glomerulonephritis</p>
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<p> </p>
<p><strong>(Renal Protein Loss Due to Inflammation)</strong></p>
<p>Most of the time when kidney disease is discussed, renal insufficiency or chronic kidney failure is the subject. In renal failure, the kidney loses its ability to conserve the body’s water as it removes the body’s daily toxin build up. Excessive water consumption is seen as an early sign of trouble as large amounts of water are required to make enough urine. Eventually toxins build up despite increased water consumption. Weight loss ensues. The classical metabolic changes that result are collectively called uremia or uremic poisoning.</p>
<p>Glomerular disease is different. Glomerular disease represents more of a filtration problem rather than a failure to excrete harmful toxins; in fact, glomerular disease is all about losing protein inappropriately through the kidneys. While it is certainly possible to have uremia without glomerular disease and glomerular disease without uremia, in many cases glomerular disease seems to represent a situation that can progress to uremia.</p>
<p><strong>What Is a Glomerulus Anyway?</strong></p>
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<p>This illustration shows the nephron, which is the functional unit of the kidney. The kidneys have thousands upon thousands of these and they serve to filter the blood, add in toxins to get rid of, and balance the blood’s electrolytes and pH by adding and subtracting salts. The round tuft-like structure at the head of the nephron is the glomerulus, where blood is filtered.</p>
<p>The delicate membranes of the glomerulus, allow salts and very small molecules to pass through while cells and large molecules (like proteins) stay in the blood. Later areas in the nephron balance the salts and small molecules to make sure we keep and dump them in appropriate amounts but the glomerulus is the filter that allows our body’s blood proteins to be conserved. Let’s take a closer look:</p>
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<p>The glomerulus is the microscopic kidney area that separates urine from blood. Blood comes in the afferent arteriole, is filtered in a tuft of capillaries, and then exits through the efferent arteriole. The fluid that has been separated out is channeled into the tubules of the nephron for further treatment. Let us emphasize that the filtration membranes are very delicate.</p>
<p>When glomerular disease exists, holes are punched out in this filtration system allowing large molecules (like the proteins that a body needs to keep) to enter the urine flow and be urinated away into oblivion.</p>
<p><strong>How Does the Glomerulus Get Leaky?</strong></p>
<p>Sources of chronic inflammation are believed to be the ultimate cause of the problem. The chronic inflammatory state leads to the circulation of antigen:antibody complexes in the blood and these complexes stick in delicate glomerular membranes like flies in fly paper. Once stuck there, they call in other inflammatory cells and soon a hole is eaten into the membrane by the ensuing reaction. The holes in the filtration membranes are big enough for proteins to traverse.</p>
<p>There are many are many possible sources of chronic inflammation which could be generating antigen:antibody complexes. Chronic ear or skin infections could be the cause. Long-standing dental disease could do it. A latent more internal infection might be the cause (such as <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=1196&amp;S=0&amp;EVetID=0" target="_blank">heartworm</a>, <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=681&amp;S=0&amp;EVetID=0" target="_blank">feline infectious peritonitis</a>, prostate infection, or <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=2103&amp;S=0&amp;EVetID=0" target="_blank">Ehrlichiosis</a>). Even a tumor might generate enough of the immune system’s attention to lead to this sort of reaction.</p>
<p><strong>Kidney failure is one thing but when it is compounded by glomerular protein loss,<br />
survival is substantially reduced and prognosis is much worse.</strong></p>
<p><strong>How Is the Diagnosis Made?</strong></p>
<p>There are several common scenarios that might lead to the diagnosis of glomerular disease.</p>
<p><em>Protein found in a routine urinalysis</em><br />
A urinalysis examines a urine sample for some of its chemical contents and properties. Protein content is one of the parameters that are checked and semi-quantified in a small, medium or large amount. On a urinalysis report this will be designated as “+, ++, or +++.”</p>
<p>This seems like it would be easy enough to interpret but unfortunately there is more to the story. A small amount of protein in a well-concentrated sample may be very normal while the same amount of protein a dilute sample would be highly significant. How dilute or concentrated the urine is depends on the patient’s water consumption and we need a method to examine urine protein that is independent of the patient’s water consumption.</p>
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<p>To complicate matters more, protein in urine may be a reflection of inflammation or infection in the urinary bladder (or even blood contamination of the sample) and not be related to the kidney at all. To determine what is going on, there are two tests that your veterinarian may discuss:</p>
<p>• Urine culture<br />
• Urine Protein:Creatinine ratio</p>
<p>The culture of the urine should find any latent infections (infection and its associated inflammation easily increases protein in the bladder). The urine protein:creatinine ratio quantifies the amount of protein loss in a way that is not dependent on the patient’s water consumption. It is helpful to do the culture first as a bladder infection will elevate the urine protein:creatinine ratio well into the abnormal range and lead to the wrong diagnosis if infection is not ruled out.</p>
<p>If the urine sediment is active, meaning there are inflammatory cells in the sample then the patient most likely has infection and culture should be pursued. If the urine is dilute from the patient’s excess water consumption, it may be prudent to culture the urine to rule out a more latent infection. Alternatively, if the sediment is not active (and especially if the sample is not also dilute), a recheck urine sample in a couple of weeks to see if the urine protein is persisting might also be a fair idea. If there is still protein in the urine 2 to 4 weeks later, further tests are definitely in order.</p>
<p><strong>Screening for Protein Loss After Diagnosing Kidney Failure</strong></p>
<p>After kidney failure has been discovered, if urine testing has not yet been done, performing urine tests can lead to important additional information. Again we come to the same two tests:</p>
<p>• Urine culture<br />
• Urine protein:creatinine ratio</p>
<p>In the kidney failure patient, urine is generally very dilute because failure includes inability to concentrate urine/conserve water. This means that urinalysis clues that there is an infection (visible bacteria, white blood cells etc.) will be diluted out. The only way to find a latent infection is to culture the sample. If infection and kidney failure are present together, there is a good chance that the infection is inside the kidney. This means the antibiotic course must be much longer (4-6 weeks) than it would be for a simple bladder infection. It also means there may be potential for the kidney to heal with time and for function to be regained. Prognosis thus improves with documented infection.</p>
<p>On the other hand, glomerular disease accompanying kidney failure is bad news. The kidney insufficiency is likely to progress much faster when the urine protein:creatinine ratio is abnormal.</p>
<p><strong>Low Blood Albumin Level Found on a Blood Panel</strong></p>
<p>Albumin is one of those proteins that the body really wants to conserve. There are plenty of substances the body needs to circulate that simply are not water soluble, which means they will not simply dissolve in the bloodstream and be pumped around by the heart. Substances that will not dissolve in water bind to albumin, and the albumin carries them around like passengers on a subway train. Albumin also is important in keeping water in the bloodstream. (This sounds odd but blood is basically a liquid and without enough water it sludges and clots abnormally.) Further, if water is not held in the vasculature, it leaks into other body cavities such as the chest and abdomen, filling these cavities with liquid.</p>
<p>There are few ways that albumin can be depleted.</p>
<p>• When an inflammatory process occurs and globulin levels rise due to antibody production, albumin levels will drop in compensation so that the overall blood protein level does not get too high. This is normal compensation and should not lead to a dangerously low albumin level.<br />
• Albumin can be lost from the intestinal tract in diseases called protein-losing enteropathies. These conditions tend to lose albumin as well as other blood proteins through GI tract leakage.<br />
• Albumin is a product of the liver. If the liver fails, there may not be adequate albumin produced.<br />
• Albumin can be lost through the holes in the kidney membranes caused by glomerular disease. Fairly advanced glomerular disease is required to produce an actual drop in blood albumin. One would need to beware of nephrotic syndrome (see below) and treatment would be needed.</p>
<ul>
<li>Urine protein:creatinine ratio of &lt;1.0 in a stable animal with normal kidney function<br />
tests (normal blood creatinine) can simply be periodically monitored.</li>
<li>A urine protein:creatinine ratio of 1-2 warrants investigation into a possible underlying cause.</li>
<li>A urine protein:creatinine ratio &gt;2 warrants not only investigation but also intervention.<br />
The International Renal Interest Society classifies the urine protein:creatinine ratio a little<br />
 differently for animals that are azotemic (have an elevated blood creatinine level):<br />
     • Ratios &lt;0.2 are considered normal<br />
     • Ratios of 0.2-0.5 in dogs and 0.2-0.4 in cats are considered borderline proteinuric and warrant a test 2 months to see if the condition is progressing.<br />
     • Ratios &gt;0.5 in dogs and &gt;0.4 in cats are considered proteinuric and require intervention.</li>
</ul>
<p>A biopsy of the kidney is needed to absolutely confirm the diagnosis of glomerulonephritis and classify the glomerular inflammation further. This is an invasive and potentially risky procedure and recently the usefulness of the information gleaned from biopsy has been questioned.</p>
<p>It is much more practical to monitor the urine protein:creatinine ratio though this is not as easy as it sounds, either. One needs to get an idea of the “baseline” urine protein:creatinine ratio, which means that at least a couple of samples should be checked. (The International Renal Interest Society recommends running the ratio on 3 samples over a two week period.) After this, how often the ratio should be rechecked depends on how the patient is doing and how the serum creatinine level is doing.</p>
<p><strong>The urine protein:creatinine ratio varies by up to 30% above or below<br />
“baseline” as a matter of course. A significant change in the ratio caused by<br />
disease progression (up) or response to therapy (down) must be greater than 30%.</strong></p>
<p><strong>If Intervention Is Recommended, What Does that Mean?</strong></p>
<p>There are several aspects to treatment and some or all of them may be instituted depending on the needs of the patient.</p>
<p><em>Low protein, low sodium diet</em><br />
Most commercial renal diets would fit in this category. It seems paradoxical that a disease that causes body protein to be lost would be treated with a protein-restricted diet but, in fact, supplementing protein causes albumin to drop faster.</p>
<p><em>ACE inhibitor</em><br />
These medications have been shown to reduce renal protein loss. Typically enalapril is recommended for dogs and benazepril is recommended for cats. These medications inherently reduce blood flow to the kidneys, so care must be taken in patients with elevated creatinine ratios to be sure the uremia does not worsen. Lower doses are used and monitoring becomes more important.</p>
<p><em>Aspirin<br />
</em>Aspirin in low doses can be used to reduce the tendency of blood to clot by inactivating blood platelets. Again, it is important to use low doses so as not to disturb the kidney’s circulation by disrupting the prostaglandin balance (which could happen with anti-inflammatory doses of aspirin typically used for pain). Patients where nephrotic syndrome is a concern (see below) would definitely need to be concerned about increased blood clotting tendency.</p>
<p>Omega 3 fatty acid supplementation<br />
Most commercial renal diets are fortified with omega 3 fatty acids. These anti-inflammatory fats have been shown to improve survival of dogs with renal disease. It is still unclear how helpful they are for cats but studies are ongoing.</p>
<p><strong>Nephrotic Syndrome</strong></p>
<p>In severe cases of glomerular disease, a complication called nephrotic syndrome can result due to the extreme urinary protein loss. Patients with nephrotic syndrome develop:</p>
<p>• High blood pressure<br />
• Tendency to form abnormal blood clots<br />
• Edema (swelling) especially of the legs and potentially fluid accumulation in a body cavity.</p>
<p>Nephrotic syndrome is defined as the combination of: 1) significant protein loss in urine, 2) low serum albumin, 3) edema or other abnormal fluid accumulation, and  4) elevated blood cholesterol level. This is a severe complication and suggests a poor prognosis especially if creatinine levels are elevated in the blood. Diuretics may be needed to supplement the other treatments listed above.</p>
<p><strong>Further Resources</strong></p>
<p>Other web pages on this subject that might be helpful:<br />
<a href="http://courses.vetmed.wsu.edu/vm552/urogenital/gn.htm" target="_blank">http://courses.vetmed.wsu.edu/vm552/urogenital/gn.htm</a><br />
A bit technical as it is meant as veterinary student education but still has excellent detail.</p>
<p><strong>Renal Amyloidosis: The Other Glomerular Disease</strong></p>
<p>There is an additional glomerular disease that bears mentioning and this is renal amyloidosis. Here instead of antigen:antibody complexes damaging the tender glomerular membranes, an abnormal protein called amyloid is deposited in the kidney. This condition is far less treatable and more rapidly progressive. We hope to have a supplemental section on this special situation in the near future.</p>
<p><em>Date Published: 12/30/2002 1:07:00 PM<br />
Date Reviewed/Revised: 09/25/2007<br />
</em></p>
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		<title>Kidney Disease</title>
		<link>http://marinpethospital.com/library/cats/kidney-disease/</link>
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		<pubDate>Thu, 13 May 2010 19:29:47 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
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		<category><![CDATA[Dogs]]></category>
		<category><![CDATA[Kidney Disease]]></category>

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THE PET HEALTH LIBRARY
By Wendy C. Brooks, DVM, DipABVP
Educational Director, VeterinaryPartner.com


 



 



    



Kidney Failure: Where to Begin







Related Articles






 
A Chronic Renal (Kidney) Failure Center


 
Anemia: Inadequate Red Blood Cells


 
Anorexia


 
Calcium Phosphorus Balance


 
Chronic Renal Failure Links


 
Dietary Therapy of Renal Failure 


 
Fluid Therapy


 
Glomerulonephritis


 
High Blood Pressure (Systemic Hypertension) in our Pets


 
Kidney Dialysis: Is it for your Pet?


 
Kidney Transplants for Cats and Dogs































 



 
The Vocabulary [...]]]></description>
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<td valign="bottom"><a href="http://www.veterinarypartner.com/Content.plx?P=SRC&amp;S=4&amp;SourceID=42&amp;EVetID=0">THE PET HEALTH LIBRARY</a><br />
By Wendy C. Brooks, DVM, DipABVP<br />
Educational Director, VeterinaryPartner.com</td>
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<p>Kidney Failure: Where to Begin</p>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2633&amp;SourceID=">A Chronic Renal (Kidney) Failure Center</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2595&amp;SourceID=">Anemia: Inadequate Red Blood Cells</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2509&amp;SourceID=">Anorexia</a></td>
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<td valign="top"> </td>
<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2622&amp;SourceID=">Calcium Phosphorus Balance</a></td>
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<td valign="top"> </td>
<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2629&amp;SourceID=">Chronic Renal Failure Links</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2615&amp;SourceID=">Dietary Therapy of Renal Failure </a></td>
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<td valign="top"> </td>
<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=2596&amp;SourceID=">Fluid Therapy</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=1352&amp;SourceID=">Glomerulonephritis</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=1216&amp;SourceID=">High Blood Pressure (Systemic Hypertension) in our Pets</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=1749&amp;SourceID=">Kidney Dialysis: Is it for your Pet?</a></td>
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<td><a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;C=&amp;A=1349&amp;SourceID=">Kidney Transplants for Cats and Dogs</a></td>
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<p> </p>
<p><strong>The Vocabulary of this Disease</strong></p>
<p><strong>Chronic</strong> means long term. <strong>Renal</strong> means kidney. <strong>Failure</strong> means inability to perform a task adequately. Chronic renal failure, also called <strong>chronic kidney failure</strong>, refers to the situation where the kidneys have not been able to perform at least one of their many tasks adequately for some time (months to years). Because the word failure evokes such a sense of doom, many clinicians opt for the term <strong>chronic renal insufficiency</strong>, as many cases can be treated successfully and can look forward to months or often years of quality life.</p>
<p>The terms renal failure or renal insufficiency imply that a condition called azotemia is present. Azotemia is the condition where toxins have built up in the bloodstream and lab tests are definitely abnormal. It does not necessarily mean the patient is experiencing reduced life quality as a result of these abnormal lab findings. The term <strong>uremia</strong> means that the patient is experiencing uremic poisoning. In other words, not only are the tests abnormal but the patient is feeling the effects of the toxic build up. Our goal in treatment is to prevent, postpone, or resolve uremia. Resolving azotemia may not be realistic.</p>
<p>In most cases, by the time the diagnosis of kidney failure has been made, the initial disease that started the kidneys on their path to failure is long gone, leaving a progressive loss of function to march unrelentingly onward. Our goal is to stop that march, and get to a stage where the patient does not feel the consequences of the disease. We cannot make failed kidneys become normal again, but we may be able to re-balance our patient’s metabolism so that he or she feels as though we did. What makes a case hopeless or hopeful depends on the patient’s ability to respond to therapy nearly as much as it depends on the stage at which the condition is discovered.</p>
<p>Many people have no idea what our kidneys do for us beyond that they have something to do with urine production. In fact, the kidneys are involved in conservation of water, stimulating red blood cell production, regulating blood pressure, balancing salts, activating Vitamin D, and more. Any of these functions may be failing in the renal failure patient.</p>
<p>The kidneys remove toxic wastes from our bodies and when these substances cannot be adequately removed, we develop excess thirst, nausea, pain, weakness, appetite loss, intestinal bleeding, even seizures. Our goal in early stage patients is to postpone or even fully prevent the development of uremia. Our goal in later stage patients is to resolve the uremia and bring the patient back to an earlier stage of disease.</p>
<p>Let’s begin with some of the relevant lab values that come up in the course of screening a pet’s kidney function. It is helpful to become familiar with these terms so you can understand what your veterinarian is tracking:</p>
<p><strong><em>Urine Specific Gravity</em></strong><br />
One of the kidney’s most important jobs is the conservation of the body’s water. The kidney must excrete the toxic by-products created by the body’s metabolism but it will want to do so in the least amount of water possible. The healthy kidney is able to make very concentrated urine.</p>
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<p>When we analyze a urine sample, one of the most important parameters is the specific gravity. This is a measure of how concentrated a urine sample is. Water has a specific gravity of 1.000. A dilute urine sample has a specific gravity less that 1.020 (often less than 1.010). A concentrated urine sample would have a specific gravity over 1.030 or 1.040. A failing kidney by definition cannot make concentrated urine and the patient must drink excessively to get enough water to excrete the day’s toxic load.</p>
<p><strong><em>Blood Urea Nitrogen (BUN)</em></strong><br />
This is a protein metabolite excreted by the kidney (it is one of the toxins we are concerned about, though it may be more of a marker for other toxins that are less easily measured). In a normal animal, the BUN is 25 mg/dl (milligram per deciliter) or so. Often at the time of diagnosis, BUN is well over 150, 200, or even 300. We’d like to keep the BUN no more than 60 to 80 mg/dl. BUN is influenced by dietary protein (including the patient’s own blood that has bled into the intestine), something which becomes important in certain situations.</p>
<p><strong><em>Creatinine</em></strong><br />
This is another protein metabolite (though this one is less dependent on dietary protein intake than is BUN). A normal creatinine is less than 1.4 mg/dl, certainly less than 2.0. Patients begin to feel sick when values meet or exceed 5.0 so we try to keep the value at 4.5 or less. BUN and creatinine will be tracked (as will several other parameters) over time and in response to different treatments.</p>
<p><strong><em>Phosphorus</em></strong><br />
The calcium/phosphorus balance becomes deranged in kidney failure due to hormone changes as well as the inability of the failing kidney to excrete phosphorus. If calcium and phosphorus levels become too high, the soft tissues of the animal&#8217;s body will develop mineralized deposits that are inflammatory, uncomfortable, and often cause intestinal bleeding. The bones will weaken as well, in some cases actually becoming rubbery. Keeping phosphorus levels in the low normal range has been correlated with improved survival.</p>
<p><strong><em>Potassium</em></strong><br />
The failing kidney is unable to conserve potassium efficiently and supplementation may be needed. The sign of hypokalemia (the scientific name for low blood potassium) is weakness, especially drooping of the head and neck.</p>
<p><strong><em>Packed Cell Volume / Hematocrit</em></strong><br />
This is a measure of red blood cell amount. More literally it represents the percentage of the blood made up by red blood cells. The hormone which stimulates the production of red blood cells is made by the kidney. The failing kidney does not make this hormone in normal amounts leading to a reduction in red blood cells, in turn leading to weakness, poor appetite, and overall poor life quality.</p>
<p><strong><em>Blood Pressure</em></strong><br />
Blood pressure is not something measured off a laboratory result sheet but it is important to monitor this parameter in kidney patients as there is a tendency for hypertension to develop in kidney failure. Special medications may be needed to manage this problem should it arise.</p>
<p><strong><em>Urinary Protein</em></strong><br />
One of the functions of the kidney is to prevent loss of the body’s proteins, in particular the blood proteins. The kidney’s filtering mechanism that enables it to remove toxins is designed to leave larger molecules (such as proteins) inside the body where they belong. But if holes develop in the filter, protein can be lost. If this complication cannot be controlled, survival time is dramatically shortened.</p>
<p>If you are a hands-on kind of pet owner, it is a good idea to request copies of monitoring lab work so you can make a chart of these parameters. In this way you can see how the disease is progressing or improving and what the problem areas are.</p>
<p><strong>IRIS Staging<br />
</strong><br />
The International Renal Interest Society (IRIS) has posed the following staging criteria for pets with kidney failure based on creatinine value in mg/dl.</p>
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<td width="101">Stage I<br />
(pre-failure)</td>
<td width="109">Stage II<br />
(mild failure)</td>
<td width="116">Stage III<br />
(moderate failure)</td>
<td width="99">Stage IV<br />
(severe failure)</td>
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<td>Dog</td>
<td>&lt;1.4</td>
<td>1.4-2.0</td>
<td>2.1 &#8211; 5</td>
<td>&gt;5</td>
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<td>Cat</td>
<td>&lt;1.6</td>
<td>1.6-2.8</td>
<td>2.8 – 5</td>
<td>&gt;5</td>
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<p>Most of what we discuss here will pertain to treating patients in Stage III and Stage IV but there is also a great deal of room to help patients still in Stage II.</p>
<p><em>Date Published: 1/1/2001<br />
Date Reviewed/Revised: 01/11/2010<br />
</em></p>
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		<title>Elbow Dysplasia</title>
		<link>http://marinpethospital.com/library/cats/elbow-dysplasia/</link>
		<comments>http://marinpethospital.com/library/cats/elbow-dysplasia/#comments</comments>
		<pubDate>Thu, 13 May 2010 19:03:05 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
				<category><![CDATA[Cats]]></category>
		<category><![CDATA[Dogs]]></category>
		<category><![CDATA[Orthopedics]]></category>

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		<description><![CDATA[


 



VP Client Information Sheets
By VIN Community Contributors


 



 



    



Elbow Dysplasia
Authored by: Dr. Greg Harasen







 





Elbow dysplasia in a dog







Elbow dysplasia is the most common cause of front limb lameness in the young dog, especially of the larger breeds. 
Dysplasia comes from the Greek dys, (abnormal) and plassein (to form).  Thus, dysplasia refers to abnormal development, in this case of [...]]]></description>
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<td valign="bottom"><a href="http://www.veterinarypartner.com/Content.plx?P=SRC&amp;S=4&amp;SourceID=62&amp;EVetID=0">VP Client Information Sheets</a><br />
By VIN Community Contributors</td>
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<p>Elbow Dysplasia</p>
<p>Authored by: Dr. Greg Harasen</p>
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<td align="center"><em>Elbow dysplasia in a dog</em></td>
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<p>Elbow dysplasia is the most common cause of front limb lameness in the young dog, especially of the larger breeds. </p>
<p>Dysplasia comes from the Greek <em>dys</em>, (abnormal) and <em>plassein </em>(to form).  Thus, dysplasia refers to abnormal development, in this case of the elbow joint.</p>
<p>The elbow is formed from the meeting of three bones:  the humerus, which is the boney support of the upper limb from the shoulder to the elbow; the ulna, which runs from the elbow to the paw along the back of the limb; and the radius, which supports the major weight-bearing along the front of the lower limb.  All three of these bones need to grow and develop normally and at the same rate such that they fit perfectly at the elbow.  If there are any abnormalities along these lines or if the cartilage lining the elbow joint does not form properly then “dysplasia” or abnormal formation is the result.</p>
<p>Elbow dysplasia can take several different forms.  Specifically, ununited anconeal process (UAP), fragmented medial coronoid process (FMCP), osteochondritis dessicans of the medial humeral condyle (OCD), ununited medial epicondyle (UME), and elbow incongruity all qualify as types of elbow dysplasia that can be present individually or in combination.  While all of the variations are distinct and probably develop in different ways, they have in common that they produce loose pieces of bone and/or cartilage within the joint that act as irritants much as a pebble does in your shoe!  All of these variations also have in common that they are primary problems that invariably lead to the secondary development of arthritis within the elbow.  The term “arthritis” simply describes inflammation within a joint.  The longer an elbow joint is ill-fitting or irregular, the more arthritis forms. </p>
<p>While traumatic episodes may affect the development of the elbow joint, the vast majority of elbow dysplasia cases are genetic in origin.</p>
<p><strong>Symptoms</strong></p>
<p>The first sign of a problem is a mild to moderate front limb lameness in a young dog between the ages of 4 to 10 months.  If the problem is not diagnosed at this stage, more marked lameness may be noted as severe arthritis sets in.  Large breed dogs predominate in the following list of commonly affected breeds:</p>
<ul>
<li>Bearded Collie</li>
<li>Bernese Mountain Dog</li>
<li>Chow Chow</li>
<li>German Shepherd</li>
<li>Golden Retriever</li>
<li>Labrador Retriever</li>
<li>Newfoundland</li>
<li>Rottweiler</li>
<li>St. Bernard</li>
<li>Bassett Hound</li>
</ul>
<p><strong>Diagnosis</strong></p>
<p>The history of front limb lameness in a young, large breed dog is suggestive of elbow dysplasia.  Examination of the elbow may show pain, thickening or swelling, and restricted movement.  Radiographs of the elbow will usually confirm the diagnosis although FMCP and OCD might not be clearly demonstrated.  Even in these cases there are usually radiographic signs that suggest the diagnosis.  Advanced imaging studies, particularly computed tomography (CT), may also be helpful.  Ultimately, surgical exploration of the joint may be needed to provide a complete diagnosis.  In recent years, such exploration is most often done with an arthroscope, a camera that is inserted in the joint without the need of major open surgery.</p>
<p><strong>Treatment</strong></p>
<p>The use of an arthroscope provides the preferred means of diagnosis and treatment for many cases of elbow dysplasia.  Some cases may be managed with open joint surgery and still others may do well with medications alone such as anti-inflammatories.  Early surgical management of these problems provides the best chance for minimizing arthritic changes in these elbows, but it must be conceded that virtually all dysplastic elbows will develop some degree of arthritis.  Older dogs, where arthritis is well established, may still benefit to some degree from arthroscopic surgery but the benefits are less predictable.  The newest generation of canine anti-inflammatory drugs along with chondroprotectives such as glucosamine and diets high in omega-3 fatty acids can also provide some relief.  Elbow replacement is an exciting new treatment that has been developed in the last couple of years and, although not widely available, holds great promise for the future.</p>
<p><em>Date Published: 4/9/2007 10:49:00 AM<br />
</em></p>
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		<title>Canine Hip Dysplasia</title>
		<link>http://marinpethospital.com/library/dogs/canine-hip-dysplasia/</link>
		<comments>http://marinpethospital.com/library/dogs/canine-hip-dysplasia/#comments</comments>
		<pubDate>Thu, 13 May 2010 18:55:08 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
				<category><![CDATA[Dogs]]></category>
		<category><![CDATA[Orthopedics]]></category>

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		<description><![CDATA[


By Wendy C. Brooks, DVM, DipABVP
Educational Director, VeterinaryPartner.com


 



 



    



Canine Hip Dysplasia
Hip dysplasia is a common condition of large breed dogs and many dog owners have heard of it but the fact is that anyone owning a large breed dog or considering a large breed dog as a pet should become familiar with this condition. The larger [...]]]></description>
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Educational Director, VeterinaryPartner.com</td>
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<p>Canine Hip Dysplasia</p>
<p>Hip dysplasia is a common condition of large breed dogs and many dog owners have heard of it but the fact is that anyone owning a large breed dog or considering a large breed dog as a pet should become familiar with this condition. The larger the dog, the more likely the development of this problem becomes, particularly as the dog ages. The following is a review of this disease. If you have additional questions, please send them through the Ask A Vet feature on the home page.</p>
<p><strong>So What is Hip Dysplasia?</strong></p>
<p>The term dysplasia means abnormal growth, thus hip dysplasia means abnormal growth or development of the hips. Hip dysplasia occurs during the growing phase of a puppy, usually a large breed puppy, and essentially refers to a poor fit of  the ball and socket nature of the hip. The normal hip consists of the femoral head (which is round like a ball and connects the femur to the pelvis), the acetabulum (the socket of the pelvis), and the fibrous joint capsule and lubricating fluid that make up the joint. The bones (femoral head and acetabulum) are coated with smooth cartilage so that motion is nearly frictionless and the bones glide smoothly across each other’s surface.</p>
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<td align="center"><em>The femoral head (the ball in the ball and socket joint) is outlined in yellow. The acetabulum (the socket in the ball and socket joint) is outlined in red. The femoral head ball is designed to fit inside the acetabulum socket.</em></td>
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<p> </p>
<p>See more detail on the structures of the <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=1438&amp;S=0&amp;EVetID=0" target="_blank">normal joint</a>.</p>
<p>When a dog has hip dysplasia, the ball and socket do not fit smoothly. The socket is flattened and the ball is not held tightly in place, thus allowing for some slipping. This makes for an unstable joint and the body’s attempts to stabilize the joint only end up yielding arthritis.</p>
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<td align="center"><em>normal hip &#8211; femoral head fits snugly inside acetabulum</em></td>
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<td align="center"><em>early stage hip dysplasia &#8211; note space between femoral head and acetabulum</em></td>
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<p> </p>
<p><strong>If this Disease Starts in Puppy hood Why are Most Affected Dogs Elderly?</strong></p>
<p>Actually, there are two sets of patients typically affected by hip dysplasia. The first group is the adolescent dog, typically 6 to 18 months of age. The radiograph on the right shows the hips of such a patient. This dog has hip dysplasia but has not yet developed arthritis. Note the shallow hip sockets. This dog was brought to the vet’s office for signs of discomfort. Radiographs were taken and hip dysplasia was discovered. Many dogs with similar radiographs will not be in pain and thus will not end up coming to the vet for an evaluation. These dogs show up as elderly dogs, after they have been walking on their poorly formed hips for many years. After many years, bony build up along the margins of the socket, mineralization of the joint capsule, cartilage wear, and inflammatory change in the joint (i.e., degenerative arthritis) has become painful and now the dog comes to the vet for an evaluation.</p>
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<td align="center"><em>bad hip dysplasia</em></td>
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<p><strong>Why Do Some Dogs Have Pain at a Young Age While Others Don&#8217;t Have Pain Until They&#8217;re Old?</strong></p>
<p>Obviously different individuals may have different degrees of dysplasia. A dog’s weight makes a difference (a lighter dog can tolerate a more abnormal hip joint). The muscle mass supporting the joint is greater in a younger dog and helps reduce the stress directly on the bones. Still, some dogs have truly shocking radiographs and virtually no symptoms while others show relative subtle changes and are very uncomfortable. We don’t know why there isn’t a better correlation between radiographs and actual pain.</p>
<p><strong>How Can an Owner Tell if their Dog is Having Discomfort?</strong></p>
<p>Do not expect a dog with dysplasia (or any other chronically painful condition for that matter) to cry or whine in pain. Instead discomfort is shown with reduced activity, difficulty rising or lying down or going up stairs. A characteristic swivel of the hips is seen from behind and classically stairs are taken in a bunny hop fashion.</p>
<p><strong>What Causes Hip Dysplasia?</strong></p>
<p>The primary cause of hip dysplasia is genetic but inheritance of this trait is not as simple as a dominance/recessive relationship like we study in high school biology. Normal dogs can breed and yield dysplastic offspring as the condition may skip generations. Until a test based on the actual DNA can be developed, the best we can do to prevent this disease is to breed only dogs with normal hips (a challenge since often dogs are not apparently dysplastic until they have already started a breeding career.)</p>
<p>Nutritional factors are also important in the development of hip dysplasia. For example, it has been popular to try to nutritionally “push” a large breed puppy to grow faster or larger by providing extra protein, more calcium, or even just extra food. Practices such as these have been disastrous, leading to bones and muscle growing at different rates and creating assorted joint diseases of which hip dysplasia is one. One study showed that when puppies of hip dysplasia prone breeds were allowed to free feed, two thirds went on to develop hip dysplasia while only one third developed hip dysplasia when the same diet was fed in meals. Another study showed German Shepherds were nearly twice as likely to develop hip dysplasia if their adult weights were above average. Studies such as these have led to the development of puppy foods designed for large breed puppies, where the optimal nutritional plane is lower than for small breed puppies.</p>
<p><strong>How Can I Find out if My Dog has Hip Dysplasia?</strong></p>
<p>There are two reasons to pursue testing: to explain a dog’s discomfort/rear weakness or to screen a dog for breeding purposes. If a dog is not going to be bred and is not in any apparent discomfort, there may be no benefit to looking at the conformation of the bones in a radiograph except possibly to look back at a future time to get a sense for progression of bony changes.</p>
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<p>The first step in diagnosis is an examination. Your veterinarian will likely extend the dog’s hind leg backward to check for pain. (Hip dysplasia causes pain on hip extension.) The dog may be asked to walk around to demonstrate the possible hip swivel. Another test involves having the dog lie on its back with a hind leg perpendicular to the body. As the leg is moved away from perpendicular to the body, a dysplastic hip will generate a pop as the femoral head slips to the center of the acetabulum. This pop, which can be felt if one’s hand is resting on the hip during the exercise, is called an Ortolani sign. You may hear this term used as hip dysplasia is discussed.</p>
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<td align="center"><em>In a dog suffering hip dysplasia, femoral head has moved away from acetabulum</em></td>
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<td align="center"><em>Ortalani sign: an audible pop is heard as the femoral head slips back to the center of the acetabulum</em></td>
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<p> </p>
<p>To find out for sure about dysplasia, radiographs are necessary and this generally involves some sort of sedation to minimize the patient’s discomfort as their hips are properly positioned for the picture. Sedation also helps the veterinary team control the dog’s position better so they can minimize the number of radiographs needed in order to get one good diagnostic view. The classical view is called a VD pelvic view where the dog is held on its back with its legs straight out. This shows the seating of the two femoral heads as well as any bony changes indicating arthritis. This is the view required by the Orthopedic Foundation for Animals for registration.</p>
<p><em>What is OFA Registration?</em></p>
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<p> </p>
<p>When purchasing a puppy, particularly one of a larger breed, often the parents will be listed as “OFA Good” or “OFA Excellent.” What this means is that the breeder has had the hips of the dog’s parents certified by the Orthopedic Foundation for Animals. The OFA is an organization with a goal of reducing the incidence of hip dysplasia (though now it is also possible to obtain certification for elbows, thyroid function, and other issues). The idea here is that a dog for breeding can have radiographs taken at age 24 months. The radiographs are sent to the OFA for review by several independent radiologists where they are graded. Hips that are rated as good or excellent receive a registration number.  Offspring of OFA-certified parents would be less likely to develop dysplasia themselves, however, it is important to realize that a dog with excellent hips at age 2 may not have such excellent hips at age 5, 7, or 10. OFA certification is no guarantee that a dog will not develop hip dysplasia symptoms in the future and does not guarantee that the offspring will not develop hip dysplasia.</p>
<p><em>What is PennHip Registration?</em></p>
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<p> </p>
<p>Many people with potential breeding dogs do not want to have to wait two years for OFA registration. The University of Pennsylvania Hip Improvement Plan, developed by Dr. Gail Smith, allows for another way to predict if a dog will develop hip dysplasia. For PennHip certification, the veterinarian taking the radiographs must receive special training and special equipment is necessary. The pet is anesthetized and two radiographs are taken: one with the femoral heads compressed (pushed into the acetabula as far as they will go) and one with the femoral heads distracted (pulled out of the acetabula as far as they will go). A measurement called a distraction index is calculated from these radiographs,  the idea being that a tighter fitting hip (one allowing less distraction) is less likely to develop dysplasia. Each dog breed has a different range of distraction indices that are considered acceptable. Puppies can be certified as young as 16 weeks of age with this system.</p>
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<td align="center"><em>view in compression</em></td>
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<p><strong>Is Surgery the Best Treatment for Hip Dysplasia?</strong></p>
<p>There are many surgical options for hip dysplasia and it is important to understand which patients benefit from which surgery. Some surgical procedures are controversial and some are not. All will entail a recovery period as well as expense. Often both hips need not be treated surgically; treating one hip is often enough to yield good results. Hip surgery is expensive, usually $2000 to $3000 in the Los Angeles area. If you are considering surgery for your dog, these are the procedures to know about:</p>
<p>• <em>Triple Pelvic Osteotomy</em><br />
This surgery is appropriate for young (age 8-18 months) dogs with dysplasia but without degenerative arthritis changes. This means that there is a window of opportunity for this surgery and if the dog develops arthritis or becomes too old, it will be too late for this surgery to be performed. In this surgery the ill-fitting acetabulum is essentially sawed free of the rest of the pelvis, re-positioned for a tighter fit on the femoral head, and then plated back into place.</p>
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<td align="center"><em>Three cuts are made to free the acetabulum from the pelvis</em></td>
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<p>Many times surgery on one hip leads to positive changes in the other hip so that surgery on the second hip is not necessary. Alternatively it is possible to do the TPO on both hips if it seems clear that ultimately both will need surgical correction. This is a surgery that requires a board certified surgeon or a surgeon with extensive orthopedic experience. After care involves a good 3 to 4 months of exercise restriction. No leashed walks are allowed for 2 months except to go outside for elimination.</p>
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<p>• <em>Femoral Head/Neck Ostectomy</em><br />
This surgery is commonly referred to as the “FHO” and is best used for smaller dogs (50 lbs or less) or very active dogs. Here, the femoral head is cut off and removed, allowing the joint to heal as a false joint (just a capsule connecting the two bones but no actual bone to bone contact. If the dog is not carrying too much weight, a false joint is strong enough. If the dog is very active, a false joint will form quickly. The pet typically does not want to use the leg for the first 2 weeks but should at least be partially using the leg after 4 to 6 weeks. The leg should be used nearly normally after a couple of months. Many veterinarians are well experienced with this surgery and often a specialist is not needed. This surgery is typically substantially less expensive than the other procedures.</p>
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<td align="center"><em>femoral head before FHO</em></td>
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<td align="center"><em>femoral head cut off after FHO</em></td>
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<p> </p>
<p><em>Total Hip Replacement</em><br />
This procedure is for dogs with established degenerative hip changes. For these dogs, the best choice may be to simply replace the hip (or hips) with a prosthetic hip. This procedure may sound radical but it has been commonly performed for nearly 20 years in dogs with great success. This is a highly invasive procedure, obviously, and infection must be avoided at all costs (no skin disease can be present in the skin over the hips, extra precautions for sterility are used). In other words, when complications occur they have potential to be disastrous. Complications have about a 10% incidence. Expect about 3 months of exercise restriction after this procedure. Usually only one hip receives surgery at a time. Often only one replacement is needed and the pet does well enough not to need surgery on the other side.</p>
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<td align="center"><em>x-ray of a bilateral (both hips) total hip replacement</em></td>
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<p> </p>
<p>• <em>DARthroplasty</em></p>
<p>“DAR” stands for dorsal acetabular rim. In this procedure, bone grafts taken from other areas of the pelvis are used to build a longer rim on the acetabulum so that the femoral head will have a deeper socket in which to fit. This procedure is best done in dogs that are too old for triple pelvic osteotomy or have just started developing degenerative arthritis. This is a fairly new procedure in the hip dysplasia arena and thus somewhat controversial. Long term success (i.e., how patients do when they are old) is not really known as the procedure has not been performed long enough to collect results from a large number of patients. A specialist is needed for this surgery.</p>
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<p> </p>
<p><strong>Juvenile Pubic Symphysiodesis</strong></p>
<p>This surgery is performed on young puppies before age 5 months, so it is generally done as a preventive procedure before it is known if the puppy will indeed have dysplastic hips. The pubic symphysis is the cartilage seem connecting the right side of the pelvis to the left side. As an individual matures, this cartilage converts to bone and the two halves of the pelvis fuse permanently. This surgery prematurely seals the symphysis, which in turn results in rotation of the developing hip sockets into a more normal alignment. While studies show promise, because this procedure is done on puppies who do not yet actually have hip dysplasia, it is hard to evaluate success.</p>
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<p><strong>What Non-Surgical Treatment is Available?</strong></p>
<p>Non-surgical treatment of hip dysplasia is essentially the same as non-surgical treatment for any other type of arthritis. There are nutritional supplements to help repair cartilage, pain medications, and anti-inflammatory medications. Physical therapy and massage are also important and helpful in non-surgical joint therapy. For details see <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=587&amp;S=0&amp;EVetID=0" target="_blank">medications for degenerative arthritis</a>.</p>
<p><em>Date Published: 2/21/2005 10:50:00 AM<br />
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		<title>Congenital Patellar Luxation</title>
		<link>http://marinpethospital.com/library/cats/congenital-patellar-luxation/</link>
		<comments>http://marinpethospital.com/library/cats/congenital-patellar-luxation/#comments</comments>
		<pubDate>Thu, 13 May 2010 18:50:44 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
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By VIN Community Contributors</td>
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<p>Congenital Patellar Luxation</p>
<p>Authored by: Becky Lundgren, DVM</p>
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<p>Patella luxation, or knee dislocation, can range in severity from a patella that can be luxated (dislocated) only in extreme extension and then snaps readily into place, to a patella that is permanently luxated medially (toward the center of the dog’s body). One of the causes of patella luxation is an abnormal shape of the distal end of the femur, resulting in a shallow patellar groove. The other major cause is a displacement of the quadriceps tendon&#8217;s attachment to the tibia, so that the patella is displaced medially when the quadriceps muscle is flexed.</p>
<p>The tendency to luxate to the medial side causes a transient lameness, at least until the patella returns to its normal position, if it is able to. The extent of patella luxation increases with time as the femur&#8217;s trochlear groove becomes flatter and flatter, as increased bowing of the leg takes place, and as the structures of the stifle joint weaken. Continued deformity of the joint results in degenerative joint disease, pain, and decreased mobility.<br />
This condition can be genetic, but not all cases are.</p>
<p>Some breeds have a higher incidence than others. Breeds known to have this condition include: Affenpinscher, Brussels griffon, Chihuahua, English toy spaniel, Greyhound, Japanese spaniel, Maltese, Manchester terrier, Miniature pinscher, Papillon, Pekingese, Pomeranian, Poodle, Pug, Shih tzu, Silky terrier, and Yorkshire terrier.</p>
<p>Patellar luxation is a common condition. Four grades of dislocation are recognized:</p>
<p>1) The patella luxates with manual pressure and returns spontaneously.<br />
2) The patella luxates with flexion and extension of the joint, but returns to the trochlear groove spontaneously. Some lameness may be present.<br />
3) The patella luxates with flexion and extension of the joint, but can be reduced manually. Considerable lameness exists.<br />
4) The patella is permanently luxated to the medial side. The limb or limbs are unable to extend and the animal walks balancing its weight on the forelimbs.</p>
<p>Treatment in mild cases may include exercise restriction, aspirin, non-steroidal anti-inflammatories (NSAIDs), polysulfated glycosaminoglycans, <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=542&amp;S=0&amp;EVetID=0" target="_blank">glucosamine/chondroitin sulfate</a> (Cosequin), and weight reduction in obese dogs. The addition of surgery to the treatment regimen is usually indicated in severe cases, and may benefit mild cases also.</p>
<p><em>Date Published: 11/14/2005 12:08:00 PM<br />
Date Reviewed/Revised: 01/06/2010<br />
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		<title>Diabetes Mellitus</title>
		<link>http://marinpethospital.com/library/cats/diabetes-melllitus/</link>
		<comments>http://marinpethospital.com/library/cats/diabetes-melllitus/#comments</comments>
		<pubDate>Thu, 13 May 2010 18:47:42 +0000</pubDate>
		<dc:creator>MPHospital</dc:creator>
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What is Diabetes Mellitus?
In order to understand the problems involved in diabetes mellitus, it is necessary to understand something of the normal body&#8217;s metabolism.
























 

























 

























 







The cells of the body require a sugar known as glucose for food and they depend on the bloodstream to bring glucose to them. They cannot, however, absorb and utilize glucose without [...]]]></description>
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<p><strong>What is Diabetes Mellitus?</strong></p>
<p>In order to understand the problems involved in diabetes mellitus, it is necessary to understand something of the normal body&#8217;s metabolism.</p>
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<p>The cells of the body require a sugar known as glucose for food and they depend on the bloodstream to bring glucose to them. They cannot, however, absorb and utilize glucose without a hormone known as insulin. This hormone, insulin, is produced by the pancreas. Insulin is like a key that unlocks the door to separate cells from the sugars in our bloodstream.</p>
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<p>Glucose comes from the diet. When an animal goes without food, the body must break down fat, stored starches, and protein to supply calories for the hungry cells. Proteins and starches may be converted into glucose. Fat, however, requires different processing that can lead to the production of ketones rather than glucose. Ketones are another type of fuel that the body can use in a pinch but the detection of ketones indicates that something wrong is happening in the patient&#8217;s metabolism. Ketones may be detected in the urine of starving animals as massive fat mobilization is required for ketone formation. Ketones can also be detected in diabetic ketoacidosis, a severe complication of unregulated diabetes so it is helpful to periodically monitor for ketones in a diabetic patient’s urine. The point, for now, is that body fat cannot be converted into glucose; in times of extreme fat burning (such as in starvation), ketones are a fat-burning byproduct.</p>
<p>Ketones in urine for three days or more in a row warrants a visit to the veterinarian.</p>
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<p><strong> </strong></p>
<p><strong>IN A DIABETIC ANIMAL THERE ISN&#8217;T ENOUGH INSULIN</strong></p>
<p>The cells cannot receive glucose from the blood because there is no insulin to permit it.<br />
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The body is unable to detect the glucose in the blood and is fooled into thinking it is starving.<br />
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Protein, starch, and fat break-down occur as they do in starvation.<br />
 <br />
Yet all along there has been plenty of glucose in the blood. In fact, by now, there is a large excess of glucose as all resources have been mobilized. Still, without insulin, this bounty of fuel cannot get to the tissues that need it.<br />
 <br />
The normal kidney is able to prevent glucose loss in urine. In a diabetic animal, there is so much glucose in the blood that the kidney is overwhelmed and glucose spills into the urine and is lost.</p>
<p>Glucose is able to draw water with it into the urine. This leads to excess urine production and excess thirst to keep up with the fluid loss.</p>
<p><strong>Thus the main clinical signs of diabetes mellitus are:</strong></p>
<ul>
<li>Excessive eating</li>
<li>Excessive drinking</li>
<li>Excessive urination</li>
<li>Weight loss</li>
</ul>
<p>It is usually fairly clear from the history and tests showing dramatic glucose elevations in the blood (and usually glucose in the urine, too) that diabetes mellitus is the diagnosis. Some pets are able to substantially raise their blood sugars from stress (such as might occur when a sensitive, sick, and anxious patient goes the vet’s office). This could create misleading test results. If there is any question about the diagnosis, a test called a fructosamine level may be requested. This test reflects an average blood glucose level over the past several weeks so if this is also elevated, a one-time elevated glucose can be distinguished from the persistent elevations of true diabetes mellitus. The fructosamine test is also used in monitoring therapy for diabetes mellitus.</p>
<p>In dogs, sugars can enter the lens of the eye causing rapid <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=659&amp;S=0&amp;EVetID=0" target="_blank">cataract</a> formation. Because a cat’s lens is different, this phenomenon occurs only in dogs.</p>
<p>Another common symptom of diabetes mellitus is urinary tract infection. All the sugar in the urine makes the bladder an excellent incubator for bacteria. Antibiotics are necessary to clear up such an infection and some monitoring may be needed to help detect these infections.</p>
<p><strong>Type I and Type II Diabetes Mellitus</strong></p>
<p>Diabetes mellitus is a classical disease in humans and most of us have heard some of the terms used to describe it. In humans, diabetes is broken down into two forms: Type I and Type II. These are also referred to as juvenile onset and adult onset diabetes, or insulin dependent and non-insulin dependent diabetes. In short, Type 1 is the type where the pancreas produces no insulin at all, and in Type 2 the pancreas produces some insulin but not enough. Virtually all dogs have insulin dependent diabetes and must be treated with insulin. Most cats have non-insulin dependent diabetes. This might suggest that most cats can get away without insulin injections but that is not the case at all. Instead, for cats, there is potential for the diabetes to actually resolve if the pancreas improves its insulin-secreting ability. Insulin injections are needed to treat most diabetic cats but for some cats, the situation is mild enough for oral medication to suffice. Good glucose control and proper diet can resolve the diabetes in some lucky cats but virtually never in diabetic dogs.</p>
<p><strong>What Happens Once a Diagnosis Is Reached</strong></p>
<p>First, an insulin type and dose will need to be selected.  There are several types of insulins and it is not possible to know how much insulin your individual pet will require. Your veterinarian can make a guess based on what works for other cats and dogs and what has been reported in the literature. Most pets require injections twice a day, approximately 12 hours apart, following a meal.</p>
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<p>You will need to learn how to give insulin injections to your pet. The technique of subcutaneous insulin administration should be thoroughly demonstrated by your doctor or an assistant. You may be surprised to find that the most common reason for a pet having difficulty achieving regulation is that the owner is not giving the injections properly. Be sure you know how to hold the bottle, manipulate the syringe, hold your pet, and give the injection. Some situations require that the pet be hospitalized for a few days for the initial regulation, but most of the time your pet will be at home receiving injections shortly after the diagnosis has been reached.</p>
<p>Some insulins are available from the neighborhood pharmacy and some kinds are available only through veterinary offices and pharmacies. You will need syringes and a bottle of insulin to begin home treatment. Your veterinarian will either provide you with supplies or will give you the necessary prescriptions. Insulin syringes are marked in insulin units so the insulin syringes must match the insulin concentrations (either U-100 syringes for 100 unit/cc insulins or U-40 syringes for 40 unit/cc insulins.) Always double check these numbers whenever you receive more supplies.</p>
<p>Never alter the insulin dose recommended by your doctor. To determine whether dose adjustments are needed (or if a different type of insulin is more appropriate), your pet will need a glucose curve where blood sugar levels are monitored every 2 to 4 hours or so for 12 to 24 hours. This kind of testing tells the doctor how long the insulin injection is lasting as well as what the lowest and highest glucose levels of the day are. It is important to find out when your pet&#8217;s curve is due. Often in the beginning, it takes several dose selections and several curves before the right dose is determined.</p>
<p><strong>What about Home Glucose Testing?</strong></p>
<p>Not every pet is amenable to getting pricked with a lancet so that a drop of blood can be harvested for testing. We do not want your pet to fear interaction with you and do not want you to get bitten or scratched; still, some pets are comfortable with periodic glucose monitoring at home. Home testing may work best for pets that become so agitated by going to the vet that their blood sugar levels are altered at the office and cannot be interpreted. Further, a pet owner can save a great of deal of money if they can produce their own glucose curve at home when the veterinarian requests one.</p>
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<p>Human glucose meters can be obtained from any drugstore but ideally the AlphaTrak glucometer should be used as it is designed for pets. The AlphaTrak is more accurate in cats and dogs than the human equipment, although certainly the human equipment was all that was available for decades and worked sufficiently. If you would like to get an AlphaTrak meter, contact your veterinarian.</p>
<p>See a <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=605&amp;S=0&amp;EVetID=0" target="_blank">video demonstration of home glucose testing</a>.</p>
<p><a href="http://www.sugarcats.net/sites/harry/bgtest.htm" target="_blank">Sugarcats.net </a>has put together an extensive review of equipment needed for home monitoring as well as picture guides for testing both dogs and cats.</p>
<p>If you choose to use a glucometer at home, be sure to keep a log of when your pet was fed, when insulin was given, and what the glucose levels were that you found. Bring this log to your veterinarian when you come for checkups. Glucose levels obtained prior to the first insulin administration of the day are particularly useful.</p>
<p>If your pet is too sensitive for a valid glucose curve at the vet’s office and you do not think you are up to blood sugar testing at home, the fructosamine blood test may be particularly useful. Again, this test looks at average glucose levels so wide fluctuations will not be discovered but at least there is a monitoring option for this situation.</p>
<p>Ketostix are used to detect ketones in urine and can be obtained at any drug store. If it is not difficult to access your pet’s urine, a first morning test is helpful. Remember, finding ketones occasionally is not a problem but a positive dipstick three days in a row is a criterion for a vet visit.</p>
<p>A bottle of insulin should last 6 to 8 weeks. After that time it should probably be replaced.</p>
<p>For more details on insulin administration and storage, see the insulin administration guide for <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=3051&amp;S=0&amp;EVetID=0" target="_blank">dogs</a> and <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=505&amp;S=0&amp;EVetID=0" target="_blank">cats</a>.</p>
<p><strong>When to Return to the Hospital/What to Watch for</strong></p>
<p>Your pet will probably require re-regulation at some point. During re-regulation periods, expect a curve to be run a week or two after each adjustment in insulin dose.</p>
<p>Bring your pet in for a re-check exam and glucose curve if your pet:</p>
<ul>
<li>seems to feel ill</li>
<li>is losing weight</li>
<li>has a ravenous appetite or loses its appetite</li>
<li>seems to be drinking or urinating excessively</li>
<li>becomes disoriented or groggy</li>
<li> has ketones in the urine for three days in a row.</li>
</ul>
<p><strong>Annual Dental</strong></p>
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<p>It is important for diabetic pets to have their teeth cleaned annually. Dental tartar seeds the body with bacteria and when blood sugar levels run high, infections in important organs can take root. The kidneys are particularly vulnerable.</p>
<p><strong>Insulin Shock</strong></p>
<p>If your pet appears wobbly or drunken, the blood sugar level may have dropped too low. This occurs after an insulin overdose. First try to get your pet to eat. If the pet will not eat, administer light Karo syrup at a dose of one tablespoon per 5 pounds. If no improvement occurs, immediately see your veterinarian for emergency treatment. When your pet is more stable, a glucose curve will be needed to determine a more appropriate insulin dose.</p>
<p><strong>Some Pets are Difficult to Regulate<br />
</strong><br />
Some pets seem to require re-regulation frequently. There may be an underlying reason to sort out. If your pet seems to fit in this category, some reasons could be:</p>
<p><em>Improper administration of insulin</em>. If possible, have your doctor observe you giving the insulin to your pet. Your insulin may be out of date.<br />
 <br />
<em>Rapid insulin metabolism</em>. Insulin wears off quickly in some animals. Your pet may require a different type of insulin or a second injection during the day.<br />
 <br />
<em>Insulin overdose</em> may actually lead to elevated glucose levels (and clinical signs of diabetes mellitus) at the end of the day. In these cases, excess drinking, eating, or urinating are seen in the afternoon and evening but not in the morning.<br />
 <br />
<em>Steroid administration</em> (such as <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=622&amp;S=0&amp;EVetID=0" target="_blank">prednisone, prednisolone</a>, etc.) will interfere with insulin.<br />
 <br />
<em>Progesterone</em>, a female hormone, also interferes with insulin. Unspayed female diabetics should be spayed once they are sufficiently regulated.</p>
<p>For more details on trouble with regulation, read about hard to regulate <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=3055&amp;S=0&amp;EVetID=0" target="_blank">dogs</a> or <a href="http://www.veterinarypartner.com/Content.plx?P=A&amp;A=1605&amp;S=0&amp;EVetID=0" target="_blank">cats</a>.</p>
<p><strong>Feeding a Diabetic Pet</strong></p>
<p>Regulation is achieved via a balance of diet, exercise, and insulin. Realizing that therapeutic diets are not always attractive to pets, there are some ideal foods which should at least be offered.</p>
<p>The most up-to-date choice for cats is a low carbohydrate high protein diet. These diets promote weight loss in obese diabetics and are available in both canned and dry formulations. For dogs, high fiber diets are still in favor as fiber seems to help sensitize the pet to insulin. Talk to your veterinarian to select an appropriate choice for your pet.</p>
<p>Avoid soft-moist diets as sugars are used as preservatives. Avoid breads and sweet treats. If it is not possible to change the pet’s diet, then regulation will just have to be worked out around whatever the pet will eat.</p>
<p><strong> </strong></p>
<p><em>Date Published: 1/1/2001<br />
Date Reviewed/Revised: 02/18/2010<br />
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