[Mitochondrial enlargement of renal proximal tubulus as a cause of microalbuminuria in non-insulin dependent diabetics].

To clarify the ultrastructural changes of renal proximal tubulus in initial nephropathy having microalbuminuria, we observed 80 biopsies of non-insulin-dependent diabetics by light and electron microscopically morphometric analysis. The patients were divided into four groups; group I; no proteinuria (p.u.) & normal serum creatinine (Cr.); less than 1.5 mg/dl, group II; p.u. less than or equal to 0.5 g/day & normal Cr., group III; p.u. greater than 0.5 g/day & normal Cr., group IV; Cr. greater than 1.5 mg/dl. Age-matched 20 normal patients and 40 patients with IgA-nephropathy (20 cases with Cr. less than or equal to 1.5 mg/dl, 20 cases with Cr. greater than 1.5 mg/dl) were used as controls. In diabetics in Group I and II, significant changes were as follow. 1) general mitochondrial enlargement in size in proximal tubular cells, and significantly related to the level of fasting blood glucose, 2) enlargement of proximal tubular cells and their nuclei in size, 3) thickening of the proximal tubular basement membrane, and in group I, it indicated to get worse in future, 4) no relationship between the mitochondrial enlargement and other parenchymal parameters such as glomerular sclerotic change, interstitial fibrosis, luminar narrowing of arterioles and prognosis. Glomerular nodular-lesion, glomerular sclerotic change, and cortical tubulointerstitial fibrosis only appeared in the advanced stages; Group III and IV. We concluded that mitochondrial enlargement could be caused by the initially urinary excretion of low molecular proteins and microalbumin in diabetics, probably due to disturbances of ATP synthesis, reduction of active transport, and finally decreased of reabsorption in the proximal tubulus.