Feline chronic kidney disease: an update on diagnosis and treatment - Veterinary Practice
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Feline chronic kidney disease: an update on diagnosis and treatment


An estimated 15% of cats over 15 years old may be affected by chronic kidney disease (CKD), but CKD can also affect young cats as a result of congenital or hereditary disease or toxin exposure.

Diagnosis is based on history, physical examination findings, urinalysis and demonstration of azotaemia (+/- hyperphosphataemia). Concurrent problems such as hypertension, proteinuria, hypokalaemia, urinary tract infections, and anaemia may be identified with more extensive investigations.

The diagnosis of chronic kidney disease requires the identification of azotaemia, with dilute urine on two occasions at least two weeks apart.


Use of a renal diet is advocated from IRIS stage II onwards. Introducing a renal diet sooner rather than later may be easier, as the appetite is usually maintained in the early stages of CKD.

Tips to facilitate transition include:

  • feeding of the renal diet alongside the normal diet for 1-2 weeks, allowing a gradual transition;
  • warming of the food to enhance olfactory stimulation;
  • flavouring the food with a flavour enhancer such as tuna water;
  • positive reinforcement, e.g stroking the cat whilst eating or hand feeding.

Renal diets should not be offered whilst the patient is hospitalised due to the negative association between the diet and the hospital.

Remember: inadequate nutrition will lead to catabolism of muscle tissues which will worsen azotaemia, therefore if caloric intake cannot be met with a renal diet, it is better to allow the cat to eat what it wants!

The control of phosphate is important due to its contribution to on-going renal damage and the development of secondary renal hyperparathyroidism. Phosphate restriction should be initiated in cats with IRIS stage II renal disease, even if the phosphate level is within reference range. Different target levels have been proposed based on classification (see Table below).

Initially, introduction of a phosphaterestricted diet should be used, with phosphate levels checked four weeks after starting the diet. If the phosphate levels are still too high, then a phosphate binder should be introduced and again phosphate levels reassessed after four weeks.

Phosphate binders primarily act within the GI tract to reduce absorption of phosphate. Options available include aluminium salts, calcium salts, sevelamer hydrochloride and lanthanum carbonate.

Proteinuria may be reduced by the use of an ACE inhibitor, which reduces glomerular hypertension, reduces aldosterone and angiotensin II and may increase appetite and feeling of well-being. However, azotaemia may increase as a result of reduction in GFR. Treatment of systemic hypertension is primarily with the calcium channel blocker amlodipine besylate, which provides a greater reduction in systemic blood pressure (of the order of 40-50mmHg) than ACE inhibitors.

If an inadequate reduction in systemic blood pressure is achieved, then an ACE inhibitor should be introduced, or else the dilation of the afferent arteriole induced by amlodipine may result in transmission of the high systemic blood pressure to the glomerulus and exacerbation of renal damage.

Urinary tract infections should be treated with appropriate antibiotics following culture. The dose or frequency of dosing should be reduced with some antibiotics (e.g. penicillins and cephalosporins) if the patient is azotaemic, and reno-toxic drugs such as aminoglycosides should be avoided.

Potassium supplementation (citrate or gluconate) should be provided for cats that are identified to be hypokalaemic. Calcitriol supplementation may theoretically reduce renal secondary hyperparathyroidism.

The anaemia associated with CKD is considered multifactorial in origin:

  • Decreased erythropoietin production by the failing kidneys.
  • Increased blood loss from GI bleeding (uraemic gastritis).
  • Decreased life expectancy of circulating red blood cells.
  • Suppression of the bone marrow by uraemic toxins such as PTH.
  • Decreased precursor availability (e.g. iron, protein) from anorexia.

Due to problems associated with management of anaemia, treatment should only be carried out when the patient becomes symptomatic from the anaemia. Options for treatment include erythropoietin (Eprex), darbopoeitin (Aranesp) or blood transfusion. Both erythropoietin and darbopoietin may require iron supplementation to be given to enable red blood cell generation. Both may also carry the risk of inducing hypertension.

Dehydration may hasten progression of underlying renal disease. Despite polydipsia, fluid intake may not match urine output, and decreasing appetite may result in decreased fluid consumption from food. Therefore there is a slight risk of calcium deposition at the site of injection.

Cats may develop a uraemic crisis, with a sudden worsening of azotaemia. This is particularly common if they become dehydrated, e.g. if they stop eating and/or drinking or develop vomiting and/or diarrhoea. In addition to iv fluid therapy, use of antiiemetics may contribute to restoration of appetite. Metoclopramide is more efficient given as a constant rate infusion (1mg/kg/24 hours), but its metabolism may be reduced in patients with renal disease.

Uraemic gastritis can contribute to nausea and vomiting. H2 blockers and sucralphate can be used to reduce this, and consideration may be given to appetite stimulants such as cyproheptadine or mirtazepine.


Feline CKD is a multifactorial disease, and patients may be presented at different stages, which in turn can affect prognosis. Cats may live with stable disease for a number of years, then decompensate suddenly.

Accurate evaluation of all aspects of this disease ensures an improved level of care for feline CKD patients, much of which can be performed in general practice.

  • References available on request from nreed1@staffmail.ed.ac.uk.

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