Glomerulonephritis (GN) is the term used to describe glomerular cell proliferation and thickening of the glomerular capillary walls. The usual cause for GN is the presence of immune complexes within the glomerulus. Proteinuria is the primary clinicopathologic sign of GN. A definitive diagnosis of GN requires renal biopsy. Use of the urine protein:creatinine ratio to quantitatively estimate proteinuria has facilitated the diagnosis and treatment of GN.

Treatment objectives include: 1) identification and elimination of underlying causative antigens and/or inflammation responsible for glomerular immune complex formation; 2) suppressing the immune response; and 3) reduction of glomerular response to the immune complexes. Without treatment, GN can cause irreversible damage to the glomerulus by way of fibrin deposition and glomerulosclerosis. Irreversible glomerular damage renders the entire nephron nonfunctional and can lead eventually to renal insufficiency and failure.

Several infectious and inflammatory diseases have been associated with glomerular deposition or in situ formation of immune complexes in dogs and cats:

In dogs, infectious (brucellosis, dirofilariasis, ehrlichiosis, Rocky Mountain spotted fever, borreliosis), neoplasia and inflammatory (pancreatitis, systemic lupus erythematosus, polyarthritis, prostatitis) causes have been associated with GN. Hereditary nephritis includes a group of genetic disorders of basement membrane collagen that causes progressive glomerular disease. Familial glomerulonephropathy has been reported in Samoyeds, bull terriers, English cocker spaniels, Bernese mountain dogs, Doberman pinschers, Rottweilers, soft-coated Wheaten terriers, Newfoundlands, shar-peis and beagles. As most affected dogs develop proteinuria as puppies, it is important to include urinalysis in their health screening.

In cats, infectious causes of GN include feline leukemia virus, feline infectious peritonitis virus, and mycoplasmal polyarthritis. Neoplasia, inflammatory (pancreatitis, chronic skin disease, immune-mediated disease), and familial causes have also been associated with GN in cats.

In both species, the association of GN with diabetes mellitus and hyperfiltration remains questionable. Also, the antigen source or underlying disease process may not be identified and so the glomerular disease is referred to as idiopathic.

There are often no clinical signs associated with GN. If there is extensive involvement with 3/4 of the glomeruli nonfunctional, renal failure and resultant azotemia, polydipsiapolyuria, anorexia, nausea and vomiting may be seen. If proteinuria is severe and persistent (serum albumin < 1.5 gm/dL), edema and/or ascites may occur. The presence of significant proteinuria, hypoalbuminemia, hypercholesterolemia, and ascites/edema is defined as the nephrotic syndrome. Complications frequently observed are hypertension and hypercoagulability. Signs associated with an underlying infectious, inflammatory or neoplastic disease may be the reason the owners seek veterinary care. Rarely, pets may present with acute dyspnea or severe panting caused by pulmonary thromboembolism. Emboli may occur in other vessels (e.g., femoral arteries with caudal paresis). Acute blindness caused by retinal detachment may occur secondary to systemic hypertension.

In many cases, asymptomatic proteinuria may be detected on urinalysis during clinical evaluation of another medical problem or with routine medical screening.