Clinical and morphometrical interrelationships in patients with overt nephropathy induced by non-insulin-dependent diabetes mellitus - A light- and electron-microscopy study

To clarify the relationships between clinical and renal structural findings in non-insulin-dependent diabetes mellitus (NIDDM), we studied 19 renal bi opsy specimens from patients with overt diabetic nephropathy induced by NID DM. By a conventional biopsy examination using light, immunofluorescent and electron microscopy, we excluded patients with any non-diabetic renal dise ases which may have caused urinary abnormalities. Using standard stereologi cal methods, the glomerular filtration surface area per nephron (S-Filt/nep h), mesangial volume per glomerulus (V-Mes/glom), mesangial matrix volume p er glomerulus (V-MM/glom) and the width of the glomerular basement membrane (GBM) were measured in nonoccluded glomeruli. The hyaline change in the ar teriole was analyzed semiquantitatively using light microscopy as an index of arteriolar hyalinosis. Light-microscopic findings demonstrated minimal l esions in 4 cases, focal and/or segmental sclerotic lesions in 4 cases, and diffuse mesangial expansion in 11 cases (with and without nodular lesions in 9 and 2 cases, respectively). Mean glomerular volume of an open glomerul us in diabetic patients was 1.6 times the reference value obtained from non diabetic patients with mild proteinuria and/or hematuria and normal renal f unction. Clinical parameters, including the duration of diabetes, urinary p rotein excretion and creatinine clearance were all related to S-Filt/neph, V-Mes/glom, V-MM/glom and the width of the GEM. In addition, V-MM/glom, the width of the GEM and the index of arteriolar hyalinosis were closely inter related. Based on these findings, diabetic renal changes, including an incr ease in the mesangial matrix, thickening of the GEM and arteriolar hyalinos is, appeared to progress in parallel, and may reflect various clinical mani festations in patients with overt diabetic nephropathy induced by NIDDM wit hout nondiabetic renal lesions.