Chronic kidney disease

What it is

Chronic kidney disease (CKD) is defined as structural or functional damage to one or both kidneys present for at least three months. Whatever the initial cause, nephrons are lost and replaced by interstitial fibrosis; the remaining nephrons hypertrophy and hyperfilter, which sustains function for a time but promotes further injury, so the disease tends to progress. Clinical signs appear only when most of the renal mass is lost. Causes in the dog include chronic glomerular disease (protein-losing nephropathies), chronic tubulointerstitial nephritis, pyelonephritis, nephrolithiasis, amyloidosis, familial renal dysplasias and the after-effects of acute kidney injury; in many older dogs the cause is no longer identifiable.

Who it affects

Mainly older dogs. Familial nephropathies cause CKD in young dogs of certain breeds, for example juvenile renal dysplasia in the shih tzu and Lhasa apso, hereditary nephritis in the English cocker spaniel and Samoyed, and familial glomerulopathies in the soft-coated wheaten terrier and Bernese mountain dog.

Anatomy involved

• Kidneys: usually small, irregular and firm, with loss of corticomedullary distinction; the cortex is thin. Glomerular sclerosis, tubular loss and interstitial fibrosis are seen histologically.
• Extrarenal effects: renal secondary hyperparathyroidism (with "rubber jaw" in severe juvenile cases), non-regenerative anaemia from reduced erythropoietin, systemic hypertension that damages the eyes, heart and brain, and uraemic gastritis and oral ulcers.

Clinical signs

Early: polyuria and polydipsia, sometimes only noticed as nocturia. Later: weight loss, decreased appetite, vomiting, lethargy, poor coat, pale mucous membranes, uraemic breath and oral ulcers. Sudden blindness from hypertensive retinal detachment can be the presenting sign.

Diagnosis

• Blood work: increased creatinine and urea and SDMA (which rises earlier than creatinine); hyperphosphataemia and non-regenerative anaemia in advanced stages.
• Urinalysis: inappropriately low urine specific gravity (isosthenuria); urine protein:creatinine ratio to detect proteinuria; urine culture.
• Blood pressure measurement.
• Imaging: ultrasound shows small, hyperechoic kidneys with poor corticomedullary distinction and detects stones, cysts or obstruction.
• IRIS staging: stages 1–4 based on fasting creatinine and SDMA in a stable, hydrated patient, sub-staged by proteinuria and blood pressure.

Treatment

There is no cure; treatment aims to slow progression and control signs, and is adjusted to the IRIS stage. A renal diet (restricted phosphorus, moderate high-quality protein, omega-3 fatty acids) prolongs survival in dogs with azotaemia. Phosphate binders when phosphorus stays high, ACE inhibitors or angiotensin receptor blockers for proteinuria, amlodipine for hypertension, antiemetics and appetite stimulants, fluid therapy to correct dehydration, and erythropoiesis-stimulating agents for severe anaemia. The prognosis depends on the stage and on proteinuria.

In the cat

CKD is one of the most common diseases of older cats, and its prevalence rises steeply with age. The most frequent histological lesion is chronic tubulointerstitial nephritis, often of unknown cause; other causes are polycystic kidney disease (Persian and related breeds), pyelonephritis, calcium oxalate ureteroliths, renal lymphoma, feline infectious peritonitis and amyloidosis (Abyssinian, Oriental). Concurrent hyperthyroidism increases glomerular filtration and can mask it.

• Feline-specific signs: besides polyuria, polydipsia and weight loss, muscle wasting, constipation from dehydration and hypokalaemia, which causes weakness and ventroflexion of the neck, are common. Systemic hypertension is frequent and can cause retinal detachment and sudden blindness.
• Diagnosis and staging: the IRIS system uses creatinine and SDMA thresholds specific to the cat; proteinuria is considered significant at lower urine protein:creatinine ratios than in the dog. Total T4 should be measured in every older cat with CKD.
• Treatment: a renal diet is the measure with the strongest evidence in cats, as it reduces uraemic crises and renal deaths in stable CKD. Also: potassium supplements for hypokalaemia, amlodipine as the first choice for hypertension, telmisartan or benazepril for proteinuria, phosphate binders, home subcutaneous fluid therapy for cats that become dehydrated, antiemetics, appetite stimulants (transdermal mirtazapine) and, in severe anaemia, erythropoiesis-stimulating agents. An oesophagostomy tube makes feeding, hydration and medication easier in advanced stages. Many cats live for years with a good quality of life in the early stages.

Key studies in the cat

• iCatCare consensus (Taylor et al., 2026): the current reference guideline for the diagnosis, IRIS staging and medical and nutritional management of feline CKD, including complications such as hypertension, proteinuria, anaemia and hypercalcaemia.
• Boyd et al. (2008), retrospective study of 211 cats with CKD. Stage at diagnosis was strongly associated with survival: median survival was 1151 days in late stage 2 (IIb), 778 days in stage 3 and 103 days in stage 4.
• Syme et al. (2006), 136 cats, most of them azotaemic, hypertensive or both. Proteinuria was closely related to survival: compared with a urine protein:creatinine ratio below 0.2, the risk of death was 2.9 times higher with a ratio of 0.2–0.4 and 4.0 times higher above 0.4. Even the low-grade proteinuria typical of feline CKD has prognostic value.
• Ross et al. (2006), double-masked randomised trial in 45 cats with stage 2 or 3 CKD fed a renal diet or a maintenance diet for up to 24 months. Uraemic crises occurred in 26% of cats on the maintenance diet and in none on the renal diet, and renal deaths were fewer; deaths from all causes did not differ.
• King et al. (2006), double-blind, randomised, placebo-controlled trial of benazepril in 192 cats with CKD. Benazepril reduced proteinuria but did not significantly prolong renal survival (mean 637 versus 520 days).
• Sent et al. (2015), blinded randomised non-inferiority trial in 224 cats with CKD. Telmisartan was non-inferior to benazepril in controlling proteinuria, and only telmisartan significantly lowered the urine protein:creatinine ratio from baseline.