[Aging and hypertension as factors of progressive renal failure].
BACKGROUND
This study evaluated the effects of aging on renal hemodynamic, biochemical and histological parameters in spontaneously hypertensive rats.


METHODS
Systolic blood pressure was measured in male SHR (adult--adSHR and aged--agSHR) during four weeks, indirectly, once a week At the end of the experiment 24 h urine samples were collected and hemodynamic measurements were performed. Animals were sacrificed and blood samples were collected for biochemical analysis. The left kidney was histopathologically examined.


CONCLUSIONS
Our results show that there is no difference in systolic blood pressure between adult and aged SH rats. Renal blood flow was significantly decreased (0.68+/-0.08 vs. 0.99+/-0.007 ml/min/100 g b.w.), while renal vascular resistance increased by 28.90% in aged gSH rats. Plasma creatinine (Pcr) level was decreased in agSHR compared to adSHR (p<0.001). There was no difference in creatinine clearance, because urine volume was significantly increased in the aged rats (p<0.001). Protein excretion (Pex) and filtration fraction were significantly increased in aged rats compared to adult rats (Pex: p<0.001, and FF: p<0.05). The degree of focal-segmental glomerulosclerosis measured by a semiquantitative histological technique was significantly increased in the aged rats compared to adult. Sporadic focal tubular atrophy and dilatation with periodic acid-schiff positive material were present in the aged group. Also there were changes in structure of afferent arterioles and small vessels with myointimal proliferation and reduced lumen diameter. There were no changes in lumen diameter of large renal vessels. Histopathological score of adult rats showed only minimal changes in vessel structure.


CONCLUSIONS
These results show that aging, and long-term high arterial blood pressure are risk factors associated with hemodynamic changes in renal arteries and kidney vessels, advancement of glomerulosclerosis and tubular injury, and therefore may contribute to progression of renal failure and eventually cause end stage renal disease.
Mihailović-Stanojević
Nevena
N
nevena@imi.bg.ac.yu
Varagić
Jasmina
J
Jovović
Durdica
D
Miloradović
Zoran
Z
Marković-Lipkovski
Jasmina
J
Jerkić
Mirjana
M
D000375:Aging / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D018450:Disease Progression; D006439:Hemodynamics; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D051437:Renal Insufficiency / Q000503:physiopathology*