When Sugar Damages Kidneys

Diabetes mellitus is one of the most common secondary diseases in modern society. And because it is on the rise, it is also one of the greatest challenges facing medicine today. Diabetes patients do not die as a direct result of the increase in blood sugar, but from the long-term complications of their disease, in which the increase in blood sugar causes damage to blood vessels and organs. Kidneys are particularly susceptible to damage, and this can lead to a loss in kidney function and the need to begin a dialysis treatment.

Prof. Dr. Tobias Huber is a kidney expert in the Nephrology Division of the University Medical Center Freiburg. With the support of the Cluster of Excellence BIOSS Centre for Biological Signalling Studies, Dr. Huber and his team were able to identify a signalling path that affects the progression of kidney disease in diabetes patients: mTOR is an important metabolic enzyme that controls similar functions in simple organisms, such as yeast and roundworms, as in humans; for example, it controls the growth and reproduction of cells. Diabetes causes the mTOR signalling path to become overactive, which can cause damage in highly specialized kidney cells.

The researchers in Freiburg were able to demonstrate that, although the basal activation of this enzyme may be important for the regular function of renal corpuscles during embryonic development, an overactive mTOR can result in a serious disruption of the kidney filter in diabetes patients and can lead to a total loss of function. In tests on animals, the deliberate genetic interception of this signalling path was able to halt the progression of kidney disease.This spectacular result of medical research was published as the title story in the latest edition (in June 2011) of the prestigious scientific journal, Journal of Clinical Investigation. It also gives us hope that it will be possible to prevent kidney disease in diabetes patients in the future.

Sources:
Albert-Ludwigs-Universit Freiburg, AlphaGalileo Foundation.