The number of podocyte and slit diaphragm is decreased in experimental diabetic nephropathy

Mauro Masson Lerco,César Tadeu Spadella,Reinaldo José Silva,Daniela De Oliveira Pinheiro,Célia Sperandéo Macedo

doi:10.1590/s0102-86502006000200006

Mauro Masson Lerco, César Tadeu Spadella + Show 3 more

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https://doi.org/10.1590/s0102-86502006000200006

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Abstract

To determine the number of podocyte, slit diaphragms, slit diaphragm extensions and GBM thickness in diabetic nephropathy. Sixty "Rattus Wistar"of both sexes weighing 200-300 g were divided in two experimental groups: normal group 10 animals, and alloxan diabetic rats--50 animals. Alloxan was administered in a single IV dose of 42 mg/kg body weight. Body weight, water and food intake, diuresis, and blood and urine glucose were determined in both groups before alloxan injection and two weeks, six and twelve months after alloxan injection. Proteinuria was measured at 12 months in both groups. After 12 months animals were sacrificed, and the right kidney processed for electron microscopy. Clear clinical and laboratory signs of severe diabetes were seen, in all alloxan-diabetic rats at all follow-up times. Glomerular basement membrane (GBM) thickening, podocyte number, and slit diaphragm number and extension were determined. GBM of all diabetic rats was significantly thicker (median=0.29 microm; semi-interquartile range=0.065 microm) than in the normal rats (0.23 microm; 0.035 microm). Diabetic rat podocyte number (8; 1), slit diaphragm number (4; 1), and slit diaphragm extension (0.021 microm; 0.00435 microm) were significantly lower than in normal rats (11; 1) and (7; 1.5), and (0.031 microm; 0.0058 microm). Diabetic rat proteinuria (0.060 mg/24 h; 0.037 mg/24 h) was higher than in normal rats (0.00185 mg/24 h; 0.00055 mg/24 h). Experimental diabetes is associated with significant (p<0.05) changes in podocyte foot process, slit number, slit diaphragm extension, and GBM thickness.

Highlights

Morphometric studiesNowadays, diabetes is considered a worldwide public health problem, either in terms of number of people affected and premature mortality, or the costs involved in controlling it and treating complications.[1]
Experimental diabetes is associated with significant (p
Other studies have shown that structural podocyte alterations occur at the initial stages of diabetic nephropathy and that this is related to albumin urinary excretion.[8]

Summary

Introduction

Diabetes is considered a worldwide public health problem, either in terms of number of people affected and premature mortality, or the costs involved in controlling it and treating complications.[1] Diabetic nephropathy develops in 25 to 35% type 1 and 8 to 10% type 2 diabetic patients, and is the mean cause of chronic renal disease (CRD) in the USA.[2] More than 44% of US patients who start treatment for renal disease are diabetic.[3]. Diabetic nephropathy is one of the most frequent systemic diseases; it causes chronic renal insufficiency in 10 to 15 % of patients starting dialysis in Brazilian metropolitan areas.[4] There is evidence to show that diabetic nephropathy results from metabolic alterations which occur in the renal glomeruli after long exposure to high glycemic levels (DCCT).[5]. Other studies have shown that structural podocyte alterations occur at the initial stages of diabetic nephropathy and that this is related to albumin urinary excretion.[8]

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