Glomerular size and structure in diabetes mellitus. II. Late abnormalities.
A study of autopsy kidney material from six long-term diabetics and four controls was performed in order to elucidate the mechanism of the glomerular enlargement in long-term diabetics. The volume and the severity of the glomerular lesions were measured in each of a number of randomly selected, open glomeruli. The relative amount of solid material was taken as an expression of the severity of the glomerular lesion. In the long-term diabetics the volume of open glomeruli was almost doubled compared to that of controls and in the individual subject the enlargement was found to be inversely related to the relative amount of solid material in the glomeruli. This indicates that the enlargement of open glomeruli in long-term diabetics is due to a compensatory hypertrophy rather than to the excessive deposition of basement membrane material. The number of nuclei per open glomerulus was increased in long-term diabetics, but nuclear size was unchanged. Most of the long-term diabetics had a large number of occluded glomeruli and the individual, relative number of such glomeruli correlated closely both with the duration of diabetes above 15 years and the concentration of creatinine in serum. It is concluded that the destruction of glomeruli due to diabetic microangiopathy is compensated for some years by hypertrophy of the least affected glomeruli. This compensatory hypertrophy of glomeruli might well account for the preservation of renal funtion in long-term diabetics for a number of years despite the progressive basement membrane lesions of diabetic microangiopathy.
D000328:Adult; D001699:Biometry; D003928:Diabetic Nephropathies / Q000473:pathology*; D005260:Female; D006801:Humans; D006984:Hypertrophy; D007620:Karyometry; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D013997:Time Factors