Chronic progressive renal disease in the cat: Recognition and management (Proceedings)


Chronic progressive renal disease in the cat: Recognition and management (Proceedings)

Aug 01, 2009

Renal insufficiency/failure is the most common cause of morbidity and mortality in older cats. There are some specific degenerative renal diseases (e.g. polycystic kidney disease of Persians and Persian-crossbreds, amyloidosis of Abyssinians), infectious causes (e.g. FIP, chronic pyelonephritis), and neoplastic renal disease (most commonly LSA) that may lead to renal failure in cats. However the most common cause of eventual renal failure is referred to as Chronic Progressive Renal Disease (CPRD). By the time this condition is recognized, renal histopathology usually reflects end-stage renal disease and any initiating insult usually cannot be identified. The most common histologic findings are those of chronic interstitial nephritis and lymphoplasmacytic nephritis.


The first step in managing feline patients with CPRD is identification of affected individuals. All middle-aged to older cats should receive at least once yearly historical assessment, thorough physical examination, and appropriate laboratory screening for patient age. Lethargy and decreased appetite may be important owner observations. Owners should be asked about changes in water consumption and urinary habits although these signs may not be noticed by some owners, particularly if cats spend significant time outside. Subtle weight loss is often one of the first physical findings in CPRD. Other physical findings might include reduced renal size, changes in renal consistency, renal irregularity or disparity in renal sizes, halitosis, stomatitis, and constipation. Retinal examination may reveal hemorrhages or retinal detachment secondary to renal-associated systemic hypertension.

We encourage "senior cat" profiling after the age of 8 years. However, the decision to perform laboratory testing should not be based on age alone. Our minimum baseline laboratory evaluation includes a complete blood count, serum biochemistry profile and electrolytes, total T4, and urinalysis (by cysto). Beware of over- or under-interpretation of marginal elevations of BUN and creatinine levels and remember that these measures of renal function must always be assessed with respect to patient hydration status and urine specific gravity. Cats do not follow the 66% (isosthenuria) - 75% (azotemia) rule of dogs. That is, cats do not become isosthenuric when they lose 2/3 of their renal mass and they can be in overt renal failure without isosthenuria. Because cats are descended from desert animals, they have much better normal renal concentration abilities than do dogs. A normally hydrated cat can produce urine with a specific gravity of 1.095 or greater. Therefore, in order to be considered to have adequate urine concentration abilities, a cat should have a USG of > 1.035.

If abnormalities are recognized that indicate the presence of CPRD, additional studies are performed including abdominal radiography and ultrasonography, and blood pressure measurement (Doppler). The earliest change seen on US examination is lack of corticomedullary differentiation. Because cats with CPRD do not concentrate urine well, they are more prone to developing true urinary tract infection. For whatever reason, inflammatory sediment is often not seen in the urine sediment on UA in these patients. We submit a urine culture in all cats with CPRD to detect those with occult infection. Cats with protein-losing nephropathy have a poor prognosis and additional interventional steps may be important in their management. Dipstick assessment of urine protein is often misleading and the ERD test is not sufficiently quantitative to critically assess the true severity of protein loss. We perform a urine protein/creatinine ratio in all cats with CPRD. Kidney biopsy is rarely performed if CPRD is suspected because there is no specific therapy other than to address the changes associated with the disease that are identical regardless of the underlying etiology of the renal damage.

Early management

Increase water consumption/maintain hydration

Older cats have a decreased thirst drive and a decreased thirst response to dehydration compared to younger cats. This will contribute to and aggravate the impact of CPRD-associated azotemia. In addition, these cats will be doubly prone to developing significant azotemia if water intake is restricted for any reason. Efforts to increase voluntary water consumption include providing clean, fresh water at all times, feeding a canned food diet (with added water if possible), offering beef or chicken broth (low sodium), bottled clam juice, or "tuna juice". Many cats enjoy drinking the water squeezed from cans of tuna. I have owners use a blender to mix a can of tuna with water, pour the mixture into ice cube trays and freeze, then pop cubes out into a plastic bag for freezer storage. These tuna juice cubes can be thawed out one at a time for the cat to enjoy. Cats that like to drink from running water sources (faucets, etc) may drink more enthusiastically from a recirculating water fountain than a water bowl. These drinking fountains are available at many pet stores.


There is no question that dietary protein and phosphorus restriction are important aspects in the management of advanced renal insufficiency. However, there are many opinions about when in the course of the disease a "renal diet" (protein and phosphorus restricted) should be given to cats with CPRD. A recent study does show improved longevity and fewer uremic crises when a low protein diet is started early in the course of azotemia. Because renal diets tend to be less palatable to cats than their "regular" food and because cats have a high dietary protein requirement, I usually wait to institute a special diet until the BUN > 35 mg/dl and creatinine is > 2.0 mg/dl. A good early choice is g/d (Hill's) which is slightly protein/phosphorus restricted compared to regular adult diets but less restricted than the renal diets. There are several excellent feline renal diets now available and generally one can be found that the patient will eat. I send owners home with baggies of different dry formulas and cans of different foods to try. Ideally, canned formulas are better because of their higher fluid content. For some cats, the diet cannot be changed for other reasons such as concurrent disease (e.g. hypoallergenic diet for IBD, etc). In those cases, we just have to work around the diet as best we can. Some cats would rather starve rather than eat the prescription renal diet. In that case, it is better to keep the cat eating a food he/she likes than to attempt to force a change to one he/she will not eat. It may not be ideal, but a cat that is eating a little bit of something is better off than one eating a whole lot of nothing.


I am a proponent of the initiation of calcitriol therapy early in the course of CPRD, in fact, even before azotemia becomes apparent. I have been impressed with the improvement in attitude, appetite, and sense of well-being in many of my patients with these subtle signs of early disease. A complete discussion of the many effects of calcitriol is beyond the scope of this discussion. In brief, it acts to lower PTH levels and helps to prevent the development of renal secondary hyperparathyroidism with its attendant negative effects. In order to use calcitriol, the serum calcium value should be normal and the serum phosphorus value < 6.0 mg/dl. I start at a calcitriol dose of 2.5 to 3.5 ng/kg PO q24h. Our pharmacy makes a suspension of calcitriol in a concentration of 25 ng/ml so it can be measured accurately and the volume administered is not excessive. Cats receiving calcitriol should have serum calcium/phosphorus levels monitored periodically to assure that the agent is working and that hypercalcemia has not occurred. If hypercalcemia is a concern, the daily dose can be multiplied by 3.5 and given twice weekly on Wed PM and Sunday AM. This regimen will have the same beneficial effect on managing PTH but with less potential for hypercalcemia. If hypercalcemia persists or serum phosphorus levels rise above the normal range and cannot be managed with diet/phosphate binders, calcitriol treatment must be discontinued.