Canis ISSN: 2398-2942

Kidney: chronic kidney disease (CKD)

Synonym(s): Chronic kidney failure

Contributor(s): Phil Nicholls, Melissa Wallace, Rosanne Jepson


  • Cause: in younger animals consider congenital or familial renal disease. In older animals usually acquired, progressive tubulointerstitial nephritis. Results in an inability of the kidney to perform normal functions of waste excretion, fluid/electrolyte/acid-base homeostasis or endocrine function. Some kidney disease may be primarily associated with dysfunction, eg nephrogenic diabetes insipidus, renal tubular acidosis, cystinuria without obvious morphological abnormalities.
  • Signs: in early stages (International Renal Interest Society (IRIS) stage I-II) clinical signs may be mild or not detected. With progressive decline in renal function (IRIS stage II-IV) clinical signs can include polyuria/polydipsia and signs associated with uremia (nausea, vomiting, anorexia, oral ulceration, weight loss, constipation). Duration >3 months implies chronicity.
  • Treatment: management should be based on IRIS staging (Table 3) but may include phosphate restricted renal diet +/- dietary phosphate binders, gastroprotectants, anti-emetics, anti-proteinuric therapy, subcutaneous/intravenous fluid therapy, erythrocyte stimulating agent, calcitriol, anti-hypertensive therapy.
  • Prognosis: early detection of CKD permits management of associated pathophysiological adaptations, eg secondary renal hyperparathyroidism, proteinuria and systemic hypertension, which may slow progression of disease. Management of clinical signs of uremia may improve quality of life.
Print off the owner factsheet on Chronic kidney disease (CKD) to give to your client. Use the interactive tools from ROYAL CANIN® UK to explain dog anatomy and disease conditions to your client. Visit ROYAL CANIN Natom Explorer to find out more.​



Table 1: Etiology of acquired chronic kidney disease
Tubulointersitial nephritis  
Chronic nephrotoxin exposure  
Obstructive nephropathy Nephrolithiasis, ureterolithiasis, spay granuloma,
transitional cell carcinoma of bladder affecting ureterovesicular junction
Drug associated NSAID, antibiotics
Immune mediated  
Renal ischemia  
Proteinuric kidney disease Amyloidosis
Primary congenital/juvenile glomerulopathy
Secondary glomerulopathy, eg immune complex mediated
Infectious Bacterial - Leptospirosis, pyelonephritis, Lyme nephritis
Mycotic - Candida albicans, blastomycosis
Metabolic Hypercalcemia
Neoplasia Renal lymphoma
Renal carcinoma
Renal pathology Breed associations
Table 2: Congenital or familial chronic kidney disease
Renal dysplasia Shih Tzu, Golden Retriever, Norwegian Elkhound,
Lhasa Apso, Chow chow, Standard poodle,
Soft Coated Wheaten Terrier, Alaskan malamute,
Miniature Schnauzer
Glomerulopathy English Cocker Spaniel, Doberman Pinscher, English bull terrier,
Soft Coated Wheaten Terrier, Samoyed, Dalmation, Bullmastiff,
Newfoundland, Beagle, Bernese Mountain dog, Pembroke Welsh Corgi
Amyloidosis Shar-pei, English Foxhound, Beagle
Polycystic kidney disease Bull Terrier, West Highland White Terrier, Cairn Terrier
Reflux nephropathy with segmental hypoplasia Boxer
Telangectasia Pembroke Welsh Corgi
Fanconi syndrome Basenji
Hereditary multifocal renal cystadenocarcinoma Hereditary multifocal renal cystadenocarcinoma


  • Reduction of functional nephrons → loss of ability to concentrate urine and retention of waste products.
  • Hyperfiltration of remaining nephrons → self-perpetuating destruction of remaining nephrons.
  • Metabolic acidosis → renal ammoniagenesis → toxic and inflammatory effect on renal interstitium.
  • Uremia → erythropoietin deficiency and shortened RBC lifespan → normochromic, normocytic, non-regenerative anemia.
  • Hyperphosphatemia Hyperphosphatemia , due to inability to excrete phosphate → hyperparathyroidism → renal osteodystrophy and soft tissue mineralisation (including nephrocalcinosis which may potentiate renal damage).
  • Lack of active vitamin D3 (calcitriol) → initiates and exacerbates hyperparathyroidism.
  • Proteinuria Proteinuria → increased tubular reabsorption potential to promote tubulointerstitial inflammation → progression of tubulointerstitial nephritis.
  • Systemic hypertension → transfer of high systemic pressure to glomerular capillaries → development of glomerular hypertension, glomerular hyperfiltration and glomerulosclerosis → perpetuating renal damage.


  • Timecourse is variable and difficult to predict. Some animals can be managed for a long period, while others may show more rapid progression of disease.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Brown S A (2013) Renal pathophysiology: Lessons learned from the canine remnant kidney model. J Vet Emerg Crit Care 23 (2), 115-121 PubMed.
  • O'Neill D G, Elliott J, Church D B, McGreevy P D, Thomson PC & Brodbelt D C (2013) Chronic kidney disease in dogs in UK veterinary practices: prevalence, risk factors, and survival. JVIM 27 (4), 814-821 PubMed.
  • Polzin D J (2013) Evidence-based step-wise approach to managing chronic kidney disease in dogs and cats. J Vet Emerg Crit Care 23 (2), 205-215 PubMed.
  • Bartges J W (2012) Chronic kidney diseases in dogs and cats. Vet Clin North Am Small Anim Pract 42 (4), 669-692 PubMed.
  • Littman M P (2011) Protein-losing nephropathy in small animals. Vet Clin North Am Small Anim Pract 41 (1), 31-62 PubMed.
  • Finco D R et al (1999) Progression of chronic renal disease in the dog. JVIM 13 (6), 516-28 PubMed.
  • Brown S A, Finco D R & Brown C A (1998) Is there a role for dietary polyunsaturated fatty acid supplementation in canine renal disease? J Nutr 128 (12 Suppl), 2765S-2767S PubMed.
  • Devaux C, Polzin D J & Osbourne C A (1996) What role does dietary protein restriction play in the management of chronic renal failure in dogs? Vet Clin North Am 26 (6), 1247-1267 PubMed.
  • Macdougall D F, Cook T, Steward A P & Cattell V (1986) Canine chronic renal disease - prevalence and types of glomerulonephritis in the dog. Kidney Int 29 (6), 1144-1151 PubMed.