prerenale

Prerenale, in medical usage, refers to conditions in which reduced blood flow to the kidneys occurs before filtration, leading to decreased renal perfusion and a decline in glomerular filtration rate without direct injury to renal parenchyma. In English, the more common term is prerenal; prerenale appears in some texts as an alternative spelling or in non-English contexts. It is a major category in discussions of acute kidney injury and is distinguished from intrinsic renal injury and postrenal obstruction.

Pathophysiology is driven by a fall in effective arterial blood volume or renal perfusion, such as from dehydration, hemorrhage, heart failure, or circulatory dysfunction. The kidneys respond by activating autoregulatory and neurohormonal mechanisms—the sympathetic nervous system, the renin-angiotensin-aldosterone system, and antidiuretic hormone—to conserve water and sodium and to maintain perfusion. These responses cause vasoconstriction of renal arterioles and heightened reabsorption of sodium and water. If perfusion is restored, GFR typically returns to baseline; if prolonged, prerenal states can progress to intrinsic renal injury, such as acute tubular necrosis.

Common causes include volume depletion (vomiting, diarrhea, bleeding, diuretic overuse), reduced circulating volume from heart failure or cirrhosis with ascites, and distributive states such as sepsis. Certain nephrotoxic agents can worsen perfusion, especially in susceptible individuals.

Clinical and laboratory features often show a high BUN-to-creatinine ratio (typically >20:1), low urine sodium (<20 mEq/L), low fractional excretion of sodium (<1%), and concentrated urine (urine osmolality often >500 mOsm/kg) with a bland sediment. Diagnosis integrates history, physical examination, and these indices, and treatment centers on restoring renal perfusion with appropriate fluid support while avoiding further nephrotoxins. Prognosis is favorable with prompt correction; delays raise the risk of progression to intrinsic kidney injury.