To clarify the clinical and pathological significance of thin glomerul
ar basement membranes (Thin-GBM) appearing in evident diabetics, we ex
amined the renal biopsies from 179 diabetes mellitus (DM) patients wit
h urinary abnormalities in which the number of non insulin dependent d
iabetes mellitus cases was 140 cases while the remaining 39 cases had
insulin dependent diabetes mellitus. In addition, 17 of these cases we
re found to have either segmental or diffuse Thin-GBM by electron micr
oscopy. The clinical and morphological parameters between the diabetic
s with Thin-GBM (DM-Thin-GBM) and the diabetics without Thin-GBM (the
controls) were significantly different regarding DM duration (DM-Thin-
GBM vs control: 5.3 +/- 5.5 vs 9.8 +/- 6.5 years, p <0.01), Ccr (67.0
+/- 25.5 ml/min vs 45.6 +/- 24.4 ml/min, p <0.01), the incidence of he
maturia (52.9% vs 24.5%, p <0.05) and hypertension (13.3% vs 51.3%, p
<0.05). The severity of glomerular damage was mild in the DM-Thin-GBM
group as compared to the control. The renal survival rate from the ons
et of urinary abnormalities was higher in the DM-Thin-GBM group than i
n the control (p <0.01). In the case of DM-Thin-GBM, the grade of prot
einuria correlated with the mean width of the thickened GBM (p <0.01)
and the spread of the thickened GBM which was more than 500 nm in widt
h (p <0.001). The severity of microscopic hematuria correlated with th
e spread of the Thin-GBM (p <0.05). The mean GBM thickness, the fracti
onal volume of the mesangial matrix/glomerulus and the spread of the t
hickened GBM weakly correlated with the DM duration, however the sprea
d of the Thin-GBM was considered to be independent of either DM durati
on or proteinuria. The above findings thus suggest that the Thin-GBM a
ppearing in diabetics is a congenital GBM. malformation and that such
Thin-GBM changes very little during the course of the disease, however
, it may sometimes cause unexpected urinary abnormalities including he
maturia.