Diabetes and hypertension are frequently associated in humans and the patie
nts run a higher risk of developing chronic renal failure. We combined stre
ptozotocin-induced diabetes with a model of experimental renovascular hyper
tension induced by restricting aortic growth between the renal arteries. Th
is model allowed us to have two kidneys in the same metabolic milieu; one e
xposed to hypertension and the other not. A moderate degree of hyperglycemi
a (2-4 g/l) was maintained with daily insulin. Determinations were made of
urinary flow (UF) creatinine clearance (GFR), urinary protein excretion (UP
), urinary glucose (UG), osmolality, and urinary electrolyte excretion. At
the end of the study perfusion pressure (PP) and weight were measured in bo
th the right and the left kidney in each group. All the kidneys were fixed
and stained for microscopic observation.
Functional study showed that urinary electrolyte excretion was higher in th
e diabetic group than in the control group from the first month. UF,UC and
GFR were higher in the diabetic group than in the control group from the be
ginning of the study UP increased slightly in the control group along the s
tudy but the increase was much higher in the diabetic group. In both in the
control and diabetic group, the right kidney was subject to a higher PP th
an the left one. Kidney weight was similar in the right and the left kidney
in the control group but in the diabetic group it was higher in the right
kidney than in the left and higher than in the control group in both kidney
s.
In the right of these results and the histology we conclude that diabetic a
nimals develop renal damage to a greater extent than non-diabetic and this
lesion occurs only in the hypertensive (right) kidney. These experiments sh
ow that both diabetes and hypertension are necessary for the development of
glomerulosclerosis.