Diabetic and Prediabetic Nephropathy in Childhood

Morphometric studies of the peripheral glomerular basement membrane in early juvenile diabetes I. Development of initial basement membrane thickening

“…The finding of a normal glomerular basement membrane in juvenile diabetics at onset, as published in a preliminary report [35] was confirmed in the present extension of the study. Results contrary to these were reported some years ago [6,17,21,23,24]. Some of the studies did not contain control patients and in some cases conclusions were drawn without measurements.…”

“…Kimmelstiel et al concluded that the primary lesion is to be found in the mesangial regions, and thickening of the peripheral basement membrane occurs as a secondary phenomenon. Other investigators have suggested the same sequence of events [7,23,26], but their conclusions were not based on quantitative data. The interrelationship between abnormalities in the peripheral basement membrane and in mesangial regions has been studied in this laboratory.…”

Protein and LDH-isoenzyme pattern of the urine from patients with diabetes mellitus determined by disc-electrophoresis

“…The absolute excretion of albumin was however slightly increased. These alterations in the excretion of protein and the protein pattern in urine from Recent JDM, can possibly be related to the electron microscopic changes demonstrable in JDM soon after the onset of the disease [12,27,5,26]. It may also be connected with the increased glomerular filtration rate in the same group of patients, demonstrated by Ditzel et al [6].…”

The role of fibrin deposition in diabetic glomerulosclerosis: a light, electron and immunofluorescence microscopy study

“…While fibrin having a periodicity of 200 to 240 A' has not, to our knowledge, been described in the early stages of diabetic glomerulosclerosis, some investigators have made reference to amorphous, electron-dense granular deposits within the peripheral capillary basement membrane or within the mesangial areas in glomeruli not severely affected by other morphological change (Suzuki, Churg, Grishman, Mautner, and Dachs, 1963;Rosenbaum, Kattine, and Gottsegen, 1963;Dachs, Chuig, and Mautner, 1964). Similar changes have been described in those few instances where glomerular lesions convincingly similar to human diabetic glomerulosclerosis have been produced in animals (0sterby Hansen, Lundbaek, Olsen, and Orskov, 1967;Bloodworth, 1965b;Gibbs, Wilson, and Gifford, 1966).…”