Abstract
Ureteral ligation, mechanical trauma, scar formation after staphylococ-cal infection, and localized thermal injury to the renal medulla have been shown to predispose to the development of coliform pyelonephritis in the experimental animal. Other renal insults such as nephrosclerosis and necrotizing arteriolitis may act similarly. In humans, pyelonephritis may be superimposed on hypertensive disease more frequently than isat present suspected. The present investigation was designed to test this hypothesis. Female Sprague-Dawley rats weighing 45-60 gm had left nephrectomy, 3-4 fortnightly injections of desoxycorticosterone trimethylacetate (DCA), and drank 1% NaCl. K depletion was prevented by supplementary KC1 as shown by muscle analyses. Control animals had left nephrectomy, but drank tap water and received no DCA. Experimentals and controls were pair-fed on Ralston Laboratory Chow. Weight curves were practically identical. Systolic blood pressure was indirectly determined in the unanesthetized state by means of a micro-phonic manometer. The DCA-treated animals became hypertensive within 2-3 weeks and developed diffuse arteriolarsclerosis, most evident in the kidney, soon thereafter. The animals were then inoculated intravenously with 1 ml of a suspension of Escherichia coli containing75-150 million organisms. Twenty-three of 33 hypertensives, but only 3 of 33 controls, developed varying degrees of pyelonephritis. These data support the interpretation that DCA- and saline-induced hypertension renders rats more susceptible to hematogenous renal infection.