| pubmed-article:7216700 | pubmed:abstractText | Proposed causes of renal papillary necrosis (RPN) include tubular toxicity due to hyperconcentration of toxins in the renal medulla and vasoconstriction of medullary vessels with ischemic necrosis. The authors studied these mechanisms in bromoethylamine hydrobromide-induced RPN in rats by microvascular and tubular micropuncture injection studies. During early stages of RPN, microvascular studies revealed reduced perfusion of vasa recta, and tubular injection studies showed unobstructed tubules and collecting ducts. In the late stage, medullary vascular obliteration and intratubular debris with tubular obstruction were seen. This evidence suggests that RPN in this model is initiated by vasoconstriction rather than direct tubular toxicity. | lld:pubmed |
