Dog And Cat Kidney Failure Explained

Friday we discussed our Pearl being in kidney failure based on laboratory test results within the Chemistry Profile.

Geographically, the first result on our laboratory’s report that relates to the kidneys is BUN, or Blood Urea Nitrogen. Put most simply BUN is a measure of one waste product of protein metabolism. When dietary protein is used by the body, molecules of nitrogen are given off as a waste ingredient if the nitrogen is not used for building new dog or cat protein. The kidneys should “filter” that and many other waste products from the bloodstream. When they fail to, BUN measurement rises above accepted normal levels. For our laboratory, normal BUN is considered to be 6-31 for the dog and 14-36 for the cat.

Pearl’s BUN is 65, slightly more than twice the maximum of normal.

Another measurement of filtering ability of the kidneys is creatinine. Creatinine is a breakdown product of creatine phosphate (or phosphocreatine), a phosphorylated source of energy for skeletal muscle. Creatinine is created at a fairly constant rate through the day, then is removed by the kidneys. Like BUN, then, elevations in blood levels of creatinine reflect a lower filtration rate of the kidneys and, thus, increasing kidney failure. For our laboratory, normal creatinine is considered to be 0.5-1.6 for the dog and 0.6-2.4 for the cat.

Pearl’s creatinine is 3.1, slightly less than twice the maximum of normal.

Blood electrolytes that are not normally controlled by the kidneys but which may become elevated in kidney failure include phosphorous and potassium. Like BUN and creatinine, these elements become elevated simply because of failure to be removed by the kidneys. For our laboratory, normal phosphorous is considered to be 2.5-6.0 for the dog and 2.4-8.2 for the cat and dog potassium 3.6-5.5, cat potassium 3.4-5.6.

Pearl’s phosphorous is 5.9, just under the maximum of normal. Her potassium is 6.1, a little higher than normal.

Renal Uremia or azotemia are terms that refer to the buildup in the blood of protein-breakdown waste products that have not been removed by failing kidneys. For the pet owner, the most notable sign of uremia is a strong odor to the breath. As these waste products build up in the bloodstream some are transformed into a gaseous state that crosses from the blood into expired air in the lungs.

Water intake is crucial to the long-term survival of the kidney failure pet. Dehydration may cause poor, sluggish blood flow to the kidneys, pushing the kidney failure patient into a downward spiral from which he cannot recover.

Further, the more water a pet with bad kidneys drinks, the more “flushing action” is effected onto the kidneys and the more waste products are removed from the bloodstream. Indeed, in later stages we often administer fluid therapy to pets for that very reason. Change drinking water at least daily and keep the water clean and inviting to encourage maximum intake.

Special diets, such as the Hill’s Prescription Diet k/d that Pearl eats, help to prolong the kidney failure pet’s life by limiting protein intake. Of course, a dog or cat with bad kidneys needs to eat protein to live just like everyone else. What he doesn’t need, though, is excess protein that his body can’t use anyway.

For ease of explanation and understanding we will use large, round numbers in this analogy. Let’s say your pet eats 20 pounds of food each day of a 50% protein diet. So, he takes in 10 pounds of protein each day. However, only half of that protein is usable by the body. Still, all 10 pounds of protein have to be “processed” by the kidneys. If, though, we feed a special diet that has protein that is nearly 100% digestible, he can eat half as much protein and the kidneys have only half as much work to do, but still get all of the protein nutrition he needs. The net result is that there is less waste from protein metabolism for the aging kidneys to process, and uremia is avoided.

Oral medications called “phosphate binders” can also be added to a diet to “bind” the dietary phosphate in the gastrointestinal tract, thus reducing the load of excessive phosphorous in the bloodstream.

If phosphorous levels are not controlled, the body reacts to raise calcium levels to maintain a balance of the two ions. The result is a condition called renal secondary hyperparathyroidism, which results in soft, malleable bones that can break easily.

Anemia can result from kidney failure. The extent of anemia is typically proportional to the physical size of the kidneys. Kidneys have many, many functions beyond making urine and getting rid of waste products. One of those functions is forming a hormone, erythropoietin. As erythropoietin circulates through the bloodstream it bathes the bone marrow and stimulates it to produce red blood cells (RBCs). Anemia results in lethargy, shortness of breath and paleness. Erythropoietin is available commercially, and may be injected in the late stages of renal failure. Pets may create protective antibodies to erythropoietin, thinking it is a foreign substance that might be dangerous to the body, causing it to be broken down before it can do its work. That is why erythropoietin treatment is reserved for patients in late-stage kidney failure.

Weight loss typically accompanies kidney failure because aging kidneys do not return all of the protein they filter back to the bloodstream as healthy kidneys do. As that protein is lost in the urine, the body “borrows” protein from muscles and other structures, but has no reserves to “pay it back.” Thus, a pet in kidney failure tends to get bony and skinny as muscle wasting occurs.

Perhaps the most noticeable factor to pet owners is the change in water intake and urine output. Most pets in kidney failure lose the ability to control urine specific gravity. As a result, they drink water constantly and that water “goes right through them.” Though stated above, is bears repeating that water must be kept fresh and available at all times to prevent dehydration.

Caught in the early stages, renal failure such as Pearl’s is not an immediate death sentence, though it seems likely that, in the absence of other life-threatening conditions, it will be the ultimate cause of Pearl’s demise.

Prognosis is difficult because of the nature of kidneys. We are born with about ten times as much functional kidney tissue as we need. Losing a little here and a little there as years go by means that we have plenty of kidney function until 90% is lost. Therefore, it is only when 9% or less remains that we have abnormalities that we can detect on laboratory tests. Determining whether there is 9%, 8%, 7% or some other quantity is impossible, though it can be approximated with ultrasound and a radiographic dye test called intravenous pyelography or IVP.

The most important factor to remember if your pet’s kidneys are failing is to control the diet and follow your pet’s doctor’s advice exactly. Treatment of dog and cat chronic renal failure is far more complicated than can be explained here, and every element of that treatment must be exact if your pet is to maximize his survival time.
MMRENALFAIL

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