Prerenal azotemia

Prerenal ARF is consequent to renal hypoperfusion and denotes a functional impairment without renal parenchymal damage. The injury is reversible once perfusion is restored.

Multiple disturbances precipitate the prerenal state (Table.!). In response to effective hypovolemia, several compensatory neurohumoral mechanisms are activated in concert to preserve arterial blood pressure, namely the sympathetic nervous system, the renin-angiotensin-aldosterone system, ADH release, and endothelin production. The enhanced sympathetic response to hypovolemia and cardiac failure serves to reduce renal blood flow, while glomerular filtration rate is initially maintained due to a disproportionate increase in efferent arteriolar tone (angiotensin-mediated). Moreover, renal production of vasodilatory prostaglandins attenuates afferent arteriolar vasoconstriction ( .B..a.lle.r.m.,a.n.„ 1991). Pharmacological agents such as angiotensin-converting enzyme inhibitors and non-steroidal anti-inflammatory drugs are particularly hazardous in the setting of decreased effective blood volume, as they interfere with renal compensatory mechanisms and precipitate a decline in glomerular filtration rate.

Hepatic disease results in pooling of blood within the portal circulation and diminished serum albumin levels, hence lowering effective blood volume and renal perfusion. As liver failure progresses, renal cortical vasoconstriction and systemic vasodilatation further reduce glomerular filtration rate. This combined liver and kidney failure (called hepatorenal syndrome) is probably related to vasoactive substances. Among the many putative mediators are vasoconstrictors (e.g. catecholamines, thromboxane, endothelin) and systemic vasodilators (e.g. nitric oxide), and diminished intrarenal synthesis of prostaglandin and bradykinin may also play a role. Patients with hepatic failure are exquisitely sensitive to further hemodynamic insults (volume depletion from paracentesis or diuresis, hemorrhage, sepsis, cyclo-oxygenase inhibitor administration) which often induce ARF.

Renal impairment, characterized by oliguria, is often observed in sepsis. Despite apparent maintainance of arterial blood pressure in early sepsis, the kidney construes a volume-depleted state and responds by enhancing sodium reabsorption. Elevated renin, angiotensin, catecholamines, or nitric oxide (with peripheral vasodilation) may account for the stimulation of sodium retention. Endotoxins contribute to the initiation of ARF by many effects, including sympathetic vasoconstriction, increased production of cytokines, angiotensin, endothelin, or nitric oxide, volume contraction, and disseminated intravascular coagulation. Unfortunately, direct antagonists of lipopolysaccharides or cytokines have not been conclusively effective in alleviating the renal dysfunction of sepsis, which often degenerates to acute intrinsic renal failure.

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