ISSN 2398-2969      



Synonym(s): GN


  • Cause: deposition orin situformation of antigen-antibody complexes in the basement membranes of glomerular capillaries in the kidneys.
  • Signs: often no clinical signs until very advanced. Proteinuria leads to hypoalbuminemia and sometimes to subcutaneous edema, eg of the distal limbs. Severe glomerular loss may eventually lead to signs of acute or chronic renal failure, eg polydipsia/polyuria, inappetence, vomiting.
  • Diagnosis: urine analysis, serum chemistry profile, histopathologic examination of a kidney biopsy.
  • Treatment: detect and eliminate the underlying source of antigen, if at all possible. Special diet, low-dose aspirin, angiotensin-converting enzyme (ACE) inhibition, +/- immunosuppressant/immunomodulator therapy.
  • Prognosis: very variable. Some cases progress rapidly despite therapy, others remain stable for prolonged periods. If complicated by thromboembolism (eg pulmonary or caudal aortic), prognosis is poor.



Predisposing factors

  • An inflammatory, infectious, or neoplastic source of antigens that can contribute to immune complex formation.
  • A familial predisposition to form immune complexes in the glomeruli.
  • Altered (ie, increased) intestinal permeability has been postulated to play a role in some breeds (eg Soft-coated Wheaten terrier) and may turn out sometimes to be relevant in members of other breeds with 'sporadic' GN.


  • Ag-Ab complexes deposit or form in the glomerular capillary basment membranes → complement activation → cell membrane damage → leukocyte attraction and platelet aggregation → glomerular injury → leakage of proteins, especially albumin, through the glomerular filter → proteinuria → (if severe) hypoalbuminemia, weight loss, ascites, peripheral edema and hypercholesterolemia.
  • Cellular proliferation, mesangial cell contraction and glomerular obliteration → decreased glomerular filtration rate through affected glomeruli → increased glomerular filtration rate through other, less damaged nephrons → 'hyperfiltration' and glomerulosclerosis of remaining nephrons → (if sufficiently severe) chronic renal failure.
  • Loss of antithrombin III, platelet hyperactivity, and (sometimes) thrombocytosis → hypercoagulable state → thromboembolic disorders (lungs, caudal aorta).


  • Very variable. Disease can progress rapidly or remain stable for years.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Welles E G, Whatley E M, Hall A S & Wright J C (2006) Comparison of Multistix PRO dipsticks with other biochemical assays for determining urine protein (UP), urine creatinine (UC) and UP:UC ratio in dogs and cats. Vet Clin Pathol 35 (1), 31-36 PubMed.
  • Jacob F, Polzin D J, Osborne C A, Neaton J D, Kirk C A, Allen T A & Swanson L L (2005) Evaluation of the association between initial proteinuria and morbidity rate or death in dogs with naturally occurring chronic renal failure. JAVMA 226 (3), 393-400 PubMed.
  • Lees G E, Brown S A, Elliott J, Grauer G E & Vaden S L (2005) Assessment and management of proteinuria in dogs and cats: 2004 ACVIM Forum Consensus Statement (Small Animal). JVIM 19 (3), 377-385 PubMed.
  • Burkholder W J, Lees G E, LeBlanc A K, Slater M R, Bauer J E, Kashtan C E, McCracken B A & Hannah S S (2004) Diet modulates proteinuria in heterozygous female dogs with X-linked hereditary nephropathy. JVIM 18 (2), 165-175 PubMed.
  • Zaragoza C, Barrera R, Centeno F, Tapia J A & Mane M C (2004) Canine pyometra: a study of the urinary proteins by SDS-PAGE and Western blot. Theriogenology 61, 1259-1272 PubMed.
  • Littman M P (2003) Canine borreliosis. Vet Clin N Am Small Anim Pract 33 (4), 827-862 PubMed.
  • Zatelli A, Borgarelli M, Santilli R, Bonfanti U, Nigrisoli E, Zanatta R, Tarducci A & Guarraci A (2003) Glomerular lesions in dogs infected with Leishmania organisms. Am J Vet Res 64 (5), 558-561 PubMed.
  • Grauer G F, Greco D S, Getzy D M, Cowgill L D, Vaden S L, Chew D J, Polzin D J & Barsanti J A (2000) Effects of enalapril versus placebo as a treatment for canine idiopathic glomerulonephritis. JVIM 14 (5), 526-533 PubMed.
  • Littman M P, Dambach D M, Vaden S L & Giger U (2000) Familial protein-losing enteropathy and protein-losing nephropathy in Soft Coated Wheaten Terriers: 222 cases (1983-1997). JVIM 14, 68-80 PubMed.
  • Finco D R, Brown S A, Brown C A, Crowell W A, Cooper T A & Barsanti J A (1999) Progression of chronic renal disease in the dog. JVIM 13 (6), 516-528 PubMed.
  • Waters C B, Adams L G, Scott-Moncrieff J C, DeNicola D B, Snyder P W, White M R & Gasparini M (1997) Effects of glucocorticoid therapy on urine protein-to-creatinine ratios and renal morphology in dogs. JVIM 11, 172-177 PubMed.
  • Cook A K & Cowgill L D (1996) Clinical and pathological features of protein-losing glomerular disease in the dog: a review of 137 cases (1985-1992). JAAHA 32, 313-322 PubMed.
  • Lulich J P, Osborne C A & Polzin D J (1996) Diagnosis and long-term management of protein-losing glomerulonephropathy. A 5-year case-based approach. Vet Clin N Am.Small Anim Pract 26, 1401-1416 PubMed.
  • Osborne C A, Bartges J W, Polzin D J, Lulich J P, Johnston G R & Cox V (1996) Percutaneous needle biopsy of the kidney. Indications, applications, technique, and complications. Vet Clin N Am Small Anim Prac 26 (6), 1461-1504 PubMed.
  • Carter A J & Van Heerden J (1994) Aortic thrombosis in a dog with glomerulonephritis. J S Afr Vet Assoc 65 (4), 189-192 PubMed.

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