Acute renal failure pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Pathophysiology
Pre-renal Failure
- Pre-renal and renal failure fall on a spectrum of manifestations of renal hypoperfusion.
- Hypovolemia from any cause leads to a fall in systemic blood pressure. This causes several auto-regulatory mechanisms to come into play. Kidneys maintain their perfusion during low pressure states by increasing the inflow of blood into the glomerulus through the afferent renal arteriolar and selective constriction of the efferent renal arteriole.
- Reduced renal blood flow causes activation of stretch receptors in the wall of the afferent renal arteriole. This results in relaxation of smooth muscles of the vessel wall which in turn causes increased blood flow, consequently increasing the filtration pressure across glomeruli. Synthesis of prostaglandins (PGE2 and prostacyclin) is also enhanced, and these compounds preferentially dilate the afferent renal arteriole.
- Hormones like angiotensin II, aldosterone and vasopressin (ADP) cause constriction of efferent renal arteriole, resulting in decrease outflow causing increased filtration pressure in the glomeruli.
- Renal filtration function is preserved during low pressure/ low volume states. However, more severe decrease in renal perfusion results in decreased urine output, causing nitrogenous waste products to accumulate in the body (acute renal failure).
- The kidney maintain their structural integrity in prerenal failure. If the renal blood flow/ filtration pressure is restored before permanent damage occurs, the kidney function normally without any compromise in the its functions.
- However, if the decline in renal blood flow is severe, ischemia of tubular cells results in intrinsic renal failure.