Streptozotocin diabetic rats were divided into two groups. One diabetic group was given an aldose reductase inhibitor (Statil) throughout the study and the other group was left untreated. An additional group of nondiabetic rats was included in the study. After 7 months, the kidneys were perfusion fixed and blocks of tissue were sampled systematically and uniformly throughout the kidney cortex. Plastic embedded blocks were sectioned and used to determine the volume fraction of tubular glycogen by light microscopy. No difference was found between the two diabetic groups in glycogen deposits in the cortical thick ascending limb of Henle's loop, expressed as volume fraction per cortex. Tubules from control animals contained no visible glycogen, as opposed to a content of about 1% in both diabetic groups. We concluded that an aldose reductase inhibitor does not aggravate this tubular lesion (i.e., the Armanni-Ebstein lesion) in rats with experimental diabetes.

Aldehyde Reductase↗

PubMedDate not supplied

Glomerular basement membrane thickening in streptozotocin diabetic rats despite treatment with an aldose reductase inhibitor.

This study concerns the possible prevention of glomerular basement membrane thickening in experimental diabetes by an aldose reductase inhibitor (ARI), Statil. ARI added to the chow was given to streptozotocin diabetic rats over a period of 6 months. Reference groups were control rats and diabetic rats on the same chow without ARI. The diabetic rats were given insulin two or three times a week, and blood glucose was measured monthly before insulin injections. There was a marked difference in the occurrence of cataracts between the two diabetic groups. ARI treated rats tended to have lower blood glucose than the diabetic reference group, but the difference was not significant. At the termination of the experiment, the left kidney was perfusion fixed, weighed, and prepared for light and electron microscopy. Systematic random sampling from the entire kidney was performed to obtain light microscopic visual fields and ultrathin sections from two glomeruli. Mean glomerular volume was estimated by light microscopy, and glomerular basement membrane thickness, by electron microscopy. Basement membrane thickness was significantly increased in untreated diabetic rats (174 nm, SD = 4.5 nm) as compared to that of controls (Mean: 154 nm, SD = 11.0 nm), and was even more so in ARI treated rats (187 nm, SD = 18.7 nm), although the ARI treated rats showed less renal and glomerular hypertrophy than did untreated diabetic rats. In conclusion, the ARI treatment over an experimental period of 6 months attenuated diabetic renal and glomerular hypertrophy, but had no effect at all on diabetic glomerular basement membrane thickening.

Aldehyde Reductase↗

PubMedDate not supplied

Renal hypertrophy in experimental diabetes.

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Animals↗

PubMedDate not supplied

New vessel formation in the renal corpuscles in advanced diabetic glomerulopathy.

Glomerular ultrastructure was studied in 12 long-term insulin dependent diabetic patients with fairly advanced nephropathy. This article discusses the observation of capillary profiles in the glomerular tuft of a deviating ultrastructure: the basement membrane (BM) is focally extremely thin and in between it presents a very loose fluffy texture, resembling the BM in immature glomeruli. Such thin-walled capillaries (TWC) constituted 1 to 5% of total capillary length and surface. The second observation reported here is the presence of vessels within the BM of Bowman's capsule. These capillaries were lined with fenestrated endothelium, and the capsular epithelium sometimes presented foot process formation. It is suggested that both types of capillaries represent new vessel formation in the renal corpuscle in these cases of advanced diabetic glomerulopathy.

Adult↗

PubMedDate not supplied

The calcium channel blocker nitrendipine attenuates renal and glomerular hypertrophy in diabetic rats.

The efficacy of the calcium channel blocker nitrendipine in preventing early renal and glomerular hypertrophy and increased urinary albumin excretion (UAE) was studied in experimental diabetes in rats, starting treatment at the onset of diabetes. Female Wistar rats were randomised into four groups: diabetic and non-diabetic rats were given either placebo or nitrendipine (250 mg/kg) in the diet for 8 weeks. After 8 weeks the kidneys in the diabetic animals had increased significantly compared to the non-diabetic controls. In the diabetic nitrendipine-treated animals renal and glomerular hypertrophy was significantly smaller than in the diabetic placebo-treated group (p < 0.05). After an initial increment within the first week, the UAE remained constant throughout the study period in the diabetic nitrendipine-treated animals, while a steady increase was seen in the diabetic placebo-treated group (p < 0.05). No differences were seen in systemic blood pressure between calcium- channel-blocker-treated groups and placebo-treated groups. In conclusion, administration of nitrendipine to diabetic rats for 8 weeks had a significant inhibitory effect on renal and glomerular hypertrophy, and showed a tendency towards a reduction in UAE (p = 0. 06) without affecting metabolic control or systemic blood pressure.

Albuminuria↗