Renal autoregulation and vulnerability to hypertensive injury in remnant kidney

Abstract

The remnant kidney model is characterized by moderate hypertension, proteinuria, and progressive glomerular scarring, which are ameliorated by a low-protein diet or antihypertensive drugs. The role of renal autoregulation, in determining vulnerability to hypertensive injury was investigated. After right nephrectomy and infarction of two-thirds of the left kidney, rats were fed an isocaloric normal (NP) or low-protein (LP) diet. After 3-4 wk blood pressure was not significantly different between NP and LP rats (171 +/- 8 vs. 155 +/- 6 mmHg), but urinary protein excretion was higher in NP rats (32.3 +/- 7.3 vs. 7.0 +/- 1.2 mg/24 h P less than 0.05). Measurement of renal plasma flow and glomerular filtration rate (GFR) after graded changes in renal perfusion pressure (100-160 mmHg) demonstrated poor autoregulation in NP but not in LP rats. Morphological evidence of severe injury in the form of fibrinoid necrosis and thrombosis of arterioles and glomeruli was largely confined to NP rats and became more severe after 6-8 wk. We conclude that remnant kidney rats fed NP diet autoregulate poorly, which may account for the malignant hypertensive injury to "unprotected" glomeruli, despite only moderate systemic hypertension, and contribute to the progressive nephron loss that is encountered.