In a rat model of p-aminophenol-induced tubular necrosis, filtration failure is driven by high fluid flow resistance in distal segments rather than tubuloglomerular feedback.
Rat model data should not change AKI management; leaves open distal tubular resistance as a hypothesis-generating mechanism in toxin-induced failure.
The p-aminophenol (pAP) model of tubular necrosis displays elevated tubular pressures equivalent to 'stop-flow', with low glomerular filtration rate (GFR) but maintained blood flow and urine output. Renal function, micropuncture, and morphological studies were performed in anaesthetized rats to examine the causes of filtration failure. 2. At the height of pAP-induced renal failure proximal tubular fluid reabsorption (Jv(a] was markedly reduced while proximal and distal free-flow rates measured by tubular fluid collections during venting of the nephron were not significantly different from saline-injected controls. Renal blood flow was maintained over the 4 h observation period despite extensive and selective proximal tubular necrosis. There was no temporal relationship between increased tubular pressure and cast formation. 3. Maintained blood and tubular fluid flow rates indicate that activation of tubuloglomerular feedback plays little or no part in pAP-induced renal failure, which is apparently due to high fluid flow resistance in the region of the connecting tubule, late distal convolution or collecting ducts. Morphological appearances were consistent with compression of these segments.
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Henry et al. (1990) studied this question.
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