The Effect Of Alloxan-Included Hyperglycemia On The Cortical Layer Of Kidney

Frolova S., Gordienko O., Yarmolenko O.
Department of Morphology, Medical Institute, Sumy State University

Toufik’s Medical Journal
Volume 1, Supplement 1, November 2021
Abstract from Biomedical Perspectives III 

Introduction: The main reason for diabetes damage is high blood glucose level. Primarily it induces non-enzymatic glycosylation of proteins, oxidative stress, action growth factors, cytokines that cause kidney damage at the cellular level.

Aim: To investigate the effect of alloxan diabetes mellitus on kidney functions of rats.

Materials and methods: 24 white rats-7-month-old males were divided into two groups:control (6 animals) and experimental (18 animals).Experimental animals were administered alloxan alone times intraperitoneally at a dose of 40 mg / kg. Glucose level goats were measured 2, 12 and 24 hours after injection of alloxan and then weekly. Average glucose level remained 11.0 mmol / l ± 2.0 mmol / l. Animals were out of experiment on days 14, 21 and 45. Histological preparations of the kidneys were stained with hematoxylin and eosin.

Results: On the 14-th day of the observation, the capsule, medulla and cortex are microscopically distincted in the experimental rat`s kidney. There is a thickening of the glomerular capillaries walls.  The numerous glomeruli have a spherical shape with a little uneven surface. The glomerular capsule contains a rounded shape. On the 21-st day of the observation, it is more difficult to distinguish cortex from medulla. The cortex has a more uneven surface than in the previous term. The glomeruli lose their rounded shape. The cavity of the glomerular (Bowman’s) capsule slightly increases. On the 45-th day of the observation, the distal tubules lose their usual shape, become thinner and are difficult to distinguish from other tubules on the histological preparation. The cortex becomes spongy due to the cystic tubular dilatation. In addition, there is a thinning of the renal artery. The mesangial expansion and inflammation of interstitial cells in diabetic animals explains diffusely located lymphocytes and macrophages in the interstitial connective tissue of the kidney.

Conclusions. Thus, alloxan diabetes causes many early nonglomerular structural changes in the kidney. At the same time, the function of kidneys is enhanced. The changes in the cortex are increasing every day. It grows thinner, in some cases it takes on a spongy appearance. In the later stage of the experimental diabetes mellitus, disorders of the tubules of nephrons are responsible for changes in renal function.