Glomerulonephritis remains an important cause of renal disease in dogs - DVM
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Glomerulonephritis remains an important cause of renal disease in dogs


Management considerations The management of dogs with glomerulopathies includes treatment of potentially underlying disease processes, reduction of proteinuria and management of uremia and other complications of generalized renal failure. Most glomerulopathies in dogs develop secondary to a systemic infectious, inflammatory or neoplastic disease process. The initial step in the management of a persistently proteinuric dog is to treat any potentially underlying diseases. The dog should be subsequently evaluated for resolving proteinuria. Because uncontrolled proteinuria leads to progressive tubulointerstitial damage, a reduction in proteinuria may slow the progression of glomerular disease.

The use of angiotensin-converting enzyme (ACE) inhibitors to reduce proteinuria in dogs with glomerulopathies is now considered the standard of care. Typically benazepril (0.25-0.5 mg/kg PO) is given once daily. If there is not a reduction in proteinuria after four to six weeks of administration, the frequency can be increased to twice daily or double the ACE inhibitor's dosage. Adequate blood pressure control of hypertensive dogs may also lead to a reduction in proteinuria and slow the progression of disease. Because ACE inhibitors are relatively weak antihypertensive agents, additional antihypertensive agents (amlodipine, 0.05-0.1 mg/kg q24h PO) may be needed if hypertension persists (systolic blood pressure >170 mmHg) after the initiation of ACE inhibitor administration. Low dose aspirin (0.5 to 5.0 mg/kg PO q12h) is often administered to prevent thromboembolism in at-risk dogs and may have the added benefit of attenuating progressive glomerular injury through inhibition of platelet cyclooxygenase.

Immunosuppressive drugs The use of immunosuppressive drugs is generally limited to dogs that have developed glomerulonephritis secondary to a steroid-responsive disease, such as systemic lupus erythematosus. Corticosteroids may exacerbate proteinuria and cause additional glomerular lesions; they should be used only with caution and close monitoring. The starting dose of prednisolone is 2.2 mg/kg daily PO with subsequent tapering to 1-2 mg/kg q48h or the lowest dose needed to maintain effect. Alternatively, azathioprine (2 mg/kg PO q24 hours for 10-14 days then q48h), cyclophosphamide (50 mg/m2 PO q24h for three to four days each week) or chlorambucil (2 mg/m2 PO q48h) can be used. Cyclosporine is probably not beneficial in dogs with glomerulonephritis.

The UPC, urinalysis, body weight, body condition score, and serum albumin and creatinine concentrations should be evaluated monthly whenever modifications in the therapeutic plan are being made every three to six months if the dog's clinical signs are stable and therapeutic changes are not being made. Because slight day-to-day variation can occur, the UPC may be evaluated by repeat measurement (at least two to three) over a period of days. Systemic blood pressure should be measured at least every three to six months, and more frequently if hypertension is unregulated. If the dog no longer has the ability to produce concentrated urine, a urine sample should be submitted for bacterial culture and susceptibility testing every six months. Because histologic lesions do not necessarily resolve even though renal function may improve, repeat biopsies are generally not needed. A reduction in proteinuria (ideally of >50 percent) as measured by the UPC without an increase in serum creatinine concentration indicates improvement or response to medical therapy.


Source: DVM360 MAGAZINE,
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