Chronic renal failure is a common occurrence in our companion animals - especially in cats. Diet and medical management are very closely linked in prolonging survival and in ensuring good quality of life. Major clinical signs observed by owners manifest late in disease. Polyuria and polydipsia manifest initially, before azotaemia, and progress to weight loss and uraemia (anorexia, vomiting, gastritis and dehydration).
In the dog, CKD is rapidly progressive and survival is generally measured in months. In cats, the disease is more insidious in onset and they can survive many years and have good quality lives with renal azotaemia.
Treatment has 2 aims – 1. Delaying progression of disease thus prolonging survival and (2) improving quality of life.
1 - Prolonging Survival
We seldom are able to find the cause of CKD but lymphoma, pyelonephritis and urolithiasis should be tested for, as they can be managed. Progression of CKD is self-inflicted due to compensatory mechanisms, which results in ongoing glomerular injury due to glomerular hypertension. Risk factors for progression of renal disease in cats are a high UPC, high plasma creatinine, high plasma phosphate levels, high plasma urea, high blood leukocyte counts and anaemia.1 Factors having no effect on progression are breed, plasma calcium, bicarbonate, potassium, bacterial cystitis and systemic hypertension.1 The information regarding the effect of body weight and plasma albumin are conflicting.
There is no direct association with hypertension (SBP > 160 mm Hg in stages 2–4 CKD and SBP > 180 mm Hg in stage 1 CKD) and survival - but it is positively associated with proteinuria, which in turn is negatively associated with survival.2 Amlodipine (0.625 mg/cat < 4 kg OID and 1.25 mg/cat > 4 kg OID) - reduces hypertension and proteinuria, improves quality of life and has a rapid onset of action with few side effects.
Therapies to decrease proteinuria are indicated in cats with UPC > 0.4 and in dogs with UPC > 2. An ACEI is initiated at 0.25–0.5 mg/kg every 12–24 h. Small stable increases in creatinine may occur due to decrease in GFR. If the increase is > 25%, then treatment should be reduced or discontinued.3
Dietary modification has been shown to have the most positive long-term effect on outcome with patients also developing fewer uraemic episodes.3 Dietary modification should be initiated at stage 2 CKD.3
2 - Improving Quality Of Life
Appetite, nausea, hydration, electrolyte balance and anaemia need to be managed to improve quality of life.
Gastrointestinal signs. H2-blockers, antiemetics and sucralfate are used to try and manage these symptoms. Initially, an H2-blocker is used and if that is insufficient an antiemetic is added. Ondansetron is twice as effective as metoclopramide in humans. Maropitant, ondansetron and metoclopramide are used in animals. Sucralfate is added if there is evidence of GIT haemorrhage. In cats especially, constipation may develop due to the chronic dehydration. Due to the development of food aversion in cats, it is important to transition to the renal diet slowly and if possible only at home, when the nausea is under control.
Hyperphosphataemia - Aim to decrease serum phosphate levels to normal over 4 weeks using dietary modification. If ineffective, then phosphate binders need to be added. Collect the blood samples after a 12-hour fast to prevent postprandial elevation. This strategy is effective up to stage 3 CKD - in stage 4, CKD phosphate binders will always be necessary. Binders should be given with meals to be effective and include aluminium hydroxide 30–100 mg/kg/day and lanthanum carbonate 30 mg/kg/day; may cause vomiting at the higher doses. The use of calcitriol is risky and may predispose to soft tissue mineralisation and doesn't appear to reduce PTH in cats.
Cats especially are prone to develop dehydration, and prevention and correction is critical. In cats, SQ fluids can be administered by the owner at home - up to 100 ml/cat every 24–48 h to twice weekly. The procedure seems to cause minimal discomfort, and animals show a marked clinical improvement including a reduced constipation and improved appetite. Balanced fluids such as Ringer's lactate are used. Fluid overload can occur, so volumes administered should be cautiously increased. Monitor electrolyte levels, as a mild sodium overload may occur.
Hypokalaemia is common in feline stages 2–3 CKD and causes muscle weakness, lethargy ileus and progression of renal disease. Serum levels may be normal with low total body potassium depletion resulting in clinical signs - treat and see what happens. Oral replacement is the safest route for long-term administration of potassium. Potassium is incorporated into renal diets. Additional chronic supplementation of potassium gluconate or potassium citrate (40–60 mg/kg/day divided TID) may be needed.
Malnutrition - In cats, mirtazapine is effective within 30 min of administration; cyproheptadine and Valium are less reliable. Naso-oesophageal or oesophagostomy tubes are helpful to initially maintain food and water intake. I recommend that cats with severe dental disease are treated as soon as they can cope with an anaesthetic - if the cat will not or cannot eat, you will struggle to stabilise the CKD.
The anaemia of CKD can be minimised by decreasing GIT haemorrhage, preventing malnutrition and vitamin deficiencies and limiting uraemia. Darbepoetin-alpha is currently recommended for stimulating erythrocyte production.
1. Reynolds B, Lefebvre H. Feline CKD – pathophysiology and risk factors - what we know? J Fel Med Surg. 2013;15(S1):3–14.
2. Polzin DJ. Evidence-based step-wise approach to managing chronic kidney disease in dogs and cats. J Vet Emerg Crit Care. 2013; 23(2):205–215.
3. Korman R, White J. Feline CKD - current therapies - what is achievable? J Fel Med Surg. 2013;15(S1):3–14.