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There are 6 basic principles to therapy in glomerulonephropathies: 1) If a cause of immune-complex disease can be identified, it should be treated. 2) Manifestations of the nephrotic syndrome, if present, should be managed with dietary salt restriction and judicious use of diuretics. 3) Antithrombotics (eg, aspirin) should be considered for hypoalbuminemic (plasma albumin <1.0 g/dL) animals as well as those with low serum levels of antithrombin III (<30% of normal). In dogs with marked proteinuria and serum albumin <2 g/dL, low-dose aspirin therapy is appropriate, unless melena is present or gastric ulceration is suspected. However, aspirin is bound to plasma proteins and is eliminated via the kidneys, so the dosage may need to be adjusted. 4) Because proteinuria may promote interstitial fibrosis, treatment to limit glomerular loss of protein is warranted and may include dietary protein restriction and administration of an ACE inhibitor. 5) Efforts to reduce the magnitude and consequences of glomerular immune complex deposition should be considered, especially in animals with biopsy-confirmed glomerular inflammation and no known primary antigenic stimulus. Immunosuppressive drugs (eg, azathioprine, cyclophosphamide, cyclosporine) can be used in dogs with glomerulonephritis, although results are variable. For amyloidosis, dimethylsulfoxide and colchicine have been tried, but without consistent results. These anti-inflammatory drugs should be administered only on a trial basis with owner consent. Corticosteroids seem to be beneficial only in mild glomerulopathy; they may worsen proteinuria in other glomerulopathies and should be avoided in animals with amyloidosis, as they are reported to enhance amyloid deposition. 6) Manifestations of chronic kidney disease will be observed in accordance with the stage of disease. Appropriate therapy has been discussed elsewhere (see Urolithiasis: Overview).
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