In humans, type 1 and 2 diabetes mellitus (DM) are important causes of renal damage. Glomerular lesions are typical in type 1 DM whereas heterogeneity of renal lesion is observed in type 2 DM, with glomerular, tubulointerstitial and arteriolar being alternatively prevalent. In cats, although diabetes is the most frequent endocrinopathy, it is yet unknown whether DM contributes to renal damage. The aim of the present study was to compare renal histopathological features and clinical parameters of kidney function in diabetic cats against a control population. Formalin-fixed, paraffin-embedded kidney samples were retrieved from diabetic and control cats that died at the Clinic for Small Animal Internal Medicine, University of Zurich (Switzerland). Control cats were selected from the archive to be matched for age, sex, breed and body weight. From all clinical records serum creatinine and urea levels were gathered if obtained within 10 days before death. Kidney slides were stained with hematoxilin-eosin, periodic acid-schiff (PAS), Masson’s trichrome, acid fuchsine orange-g (AFOG), and periodic acid methenamine silver (PAMS). At optical microscopy various glomerular, tubulointerstitial and vascular parameters were identified and scored using a tie-grade scale. Data were analyzed with non-parametric tests. Thirty-two diabetic cats and 20 controls were included. On histopathology, scores of glomerular lesions (i.e., sclerotic glomeruli, mesangial or endocapillary hypercellularity, increased mesangial matrix, immunodeposits, glomerular basement membrane thickening, mesangial interposition), tubulointerstitial lesions (i.e., inflammation, fibrosis, tubular atrophy, necrosis or lipidosis, intratubular mineralizations) and vascular lesions (i.e., small or large artery hypertrophy) were equally represented in the 2 groups. Serum creatinine and urea levels were not different between diabetic cats and controls (creatinine: 197 ± 42 vs. 199 ± 46 μmol/l, reference: 98-163 μmol/l; urea: 18.2 ± 2.5 vs. 18.4 ± 4.6 mmol/l, reference: 7.4-12.6 mmol/l). Creatinine and urea levels were similar in diabetic cats irrespective of the presence of glomerular or tubulointerstitial lesions. The same was observed in control cats. The results suggest that DM in cats does not lead to microscopically detectable renal lesions or clinically relevant renal dysfunction. In addition, creatinine and urea are not associated with glomerular and tubulointerstitial lesions in cats. A possible bias for this finding might be the mild degree of creatinine and urea increase documented in the present series.

Renal histopathology and function in cats with diabetes mellitus

ZINI, ERIC;COPPOLA, LUIGI MICHELE;ARESU, LUCA
2012

Abstract

In humans, type 1 and 2 diabetes mellitus (DM) are important causes of renal damage. Glomerular lesions are typical in type 1 DM whereas heterogeneity of renal lesion is observed in type 2 DM, with glomerular, tubulointerstitial and arteriolar being alternatively prevalent. In cats, although diabetes is the most frequent endocrinopathy, it is yet unknown whether DM contributes to renal damage. The aim of the present study was to compare renal histopathological features and clinical parameters of kidney function in diabetic cats against a control population. Formalin-fixed, paraffin-embedded kidney samples were retrieved from diabetic and control cats that died at the Clinic for Small Animal Internal Medicine, University of Zurich (Switzerland). Control cats were selected from the archive to be matched for age, sex, breed and body weight. From all clinical records serum creatinine and urea levels were gathered if obtained within 10 days before death. Kidney slides were stained with hematoxilin-eosin, periodic acid-schiff (PAS), Masson’s trichrome, acid fuchsine orange-g (AFOG), and periodic acid methenamine silver (PAMS). At optical microscopy various glomerular, tubulointerstitial and vascular parameters were identified and scored using a tie-grade scale. Data were analyzed with non-parametric tests. Thirty-two diabetic cats and 20 controls were included. On histopathology, scores of glomerular lesions (i.e., sclerotic glomeruli, mesangial or endocapillary hypercellularity, increased mesangial matrix, immunodeposits, glomerular basement membrane thickening, mesangial interposition), tubulointerstitial lesions (i.e., inflammation, fibrosis, tubular atrophy, necrosis or lipidosis, intratubular mineralizations) and vascular lesions (i.e., small or large artery hypertrophy) were equally represented in the 2 groups. Serum creatinine and urea levels were not different between diabetic cats and controls (creatinine: 197 ± 42 vs. 199 ± 46 μmol/l, reference: 98-163 μmol/l; urea: 18.2 ± 2.5 vs. 18.4 ± 4.6 mmol/l, reference: 7.4-12.6 mmol/l). Creatinine and urea levels were similar in diabetic cats irrespective of the presence of glomerular or tubulointerstitial lesions. The same was observed in control cats. The results suggest that DM in cats does not lead to microscopically detectable renal lesions or clinically relevant renal dysfunction. In addition, creatinine and urea are not associated with glomerular and tubulointerstitial lesions in cats. A possible bias for this finding might be the mild degree of creatinine and urea increase documented in the present series.
2012
Proceedings of ECVIM 2012
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2659336
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