Clinicopathologic and pathologic characteristics of feline proteinuric kidney disease

Abstract

Objectives The aim of this study was to describe the causes, clinicopathologic features and outcomes of feline protein-losing nephropathy (proteinuria secondary to glomerular disease [PLN]). Methods Kidney biopsy/necropsy samples from proteinuric cats submitted to the International Veterinary Renal Pathology Service were retrospectively reviewed. Diagnoses based on histopathology were categorized by primary disease compartment. Clinicopathologic variables at diagnosis, development of hypoalbuminemia, anemia, hypertension, azotemia and effusion/edema, and survival were compared between cats with immune-complex glomerulonephritis (ICGN) and other causes of PLN. Results Fifty-eight percent (n = 31/53) of proteinuric cats had ICGN and 74% (n = 31/42) of cats with PLN had ICGN. Cats with glomerular diseases other than ICGN had a higher median urine protein:creatinine ratio than ICGN cats (14.5 vs 6.5; P <0.001). Onset of PLN occurred at a young age; median age at diagnosis was 3.5 years in ICGN cats vs 1.3 years in cats with other glomerular diseases ( P = 0.026). Development of complications such as hypoalbuminemia, anemia, hypertension, azotemia and effusion/edema were common, regardless of the cause of PLN, and were not different between ICGN and cats with other glomerular diseases. Male cats were over-represented in the ICGN group ( P = 0.003). Median survival time (MST) for all cats with PLN was 94 days (range 3–1848 days). Survival was not different between cats with ICGN and cats with other glomerular diseases. MST in ICGN cats that developed effusion was shorter (94 days) than cats that did not (700 days; P = 0.035). MST in IGCN cats that received immunosuppressive medications was longer (244 days) than cats that did not (17 days, P = 0.039). Conclusions and relevance Taken together, these data suggest that clinical suspicion for glomerular proteinuria should increase in young, male cats with higher degrees of proteinuria, and immune-mediated disease is common. Further studies are needed to determine the effect of immunosuppression on morbidity and mortality in cats with ICGN.

2022 Update of the Consensus on the Rational Use of Antithrombotics and Thrombolytics in Veterinary Critical Care (CURATIVE) Domain 1‐ Defining populations at risk

“…Several of the reports describing histopathologic changes in cats with PLN or glomerulonephritis had evidence of fibrin deposition; however, none of the studies that reported histopathology described any micro‐ or macrovascular thrombosis 84,85 . Numerous studies were considered neutral to the PECO question because they did not include a control group, they described arterial thrombosis and did not mention PLN, or they were reports focused on PLN that did not discuss or describe thrombosis 45,48,49,54,59,62,63,66–68,70,86–110 . Although these reports were considered neutral, their collective weight suggests that there is either no association or a very weak association between PLN and arterial thromboembolic complications in cats and that the overall risk of thrombosis in cats with PLN is seemingly low.…”

Drug-Dosing Adjustment in Dogs and Cats with Chronic Kidney Disease

“…The prevalence of PLN seems to be lower in cats and, conversely to dogs, there is no evidence supporting the adoption of antithrombotic medications [8,185,187]. Although it is not licensed for use in cats and its efficacy remains unproven, acetylsalicylic acid at low doses has been encountered as antiplatelet agent in cats for the prevention of thrombosis and in particular ATE; reported dosages range widely (i.e., 5-80 mg per cat every 72 h), and special attention should be paid to the prolonged time of excretion in feline species [85,86].…”

The use of telmisartan in combination therapy in the management of nephrotic syndrome due to non‐immune‐mediated glomerulonephropathy in a young cat

“…Serum biochemistry revealed hypoalbuminaemia (11.3 g/L; 25-45), with normal globulin (30 g/L; 25-45), hypercholesterolemia (9 mmol/L; 2.2-4), increased urea of 17.7 mmol/L (<9.9) and hyperkalaemia (5.84 mmol/L; 3.5-5.5). Creatinine was normal (89 µmol/L; 80-203) and symmetric dimethylarginine (SDMA) was normal (9 µg/dl; [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. Haematology showed lymphocytosis (13.28 × 10 9 /L; 0.85-5.85).…”

“…1,2 Primary glomerular disease is, however, a relatively rare cause of PLN in cats. 3,4 Glomerular disease is more common in dogs, often associated with severe proteinuria. 5 There are occasional reports of immune-mediated glomerular disease in cats, with invariably poor outcomes.…”

“…The most common presentation of protein‐losing nephropathy (PLN) in cats is typically mild and associated with chronic kidney disease due to tubulointerstitial inflammation and fibrosis 1,2 . Primary glomerular disease is, however, a relatively rare cause of PLN in cats 3,4 . Glomerular disease is more common in dogs, often associated with severe proteinuria 5 .…”