prärenal

Prärenal, or pre-renal, refers to conditions in which reduced perfusion of the kidneys is the primary abnormality, leading to prerenal acute kidney injury (AKI) without initial damage to renal parenchyma. It is distinguished from intrinsic renal causes and post-renal obstruction.

The underlying mechanism is a fall in effective arterial blood volume or renal perfusion pressure, resulting in a decreased glomerular filtration rate. The kidney responds by conserving sodium and water through activation of the renin-angiotensin-aldosterone system and antidiuretic hormone. If perfusion is not restored, prolonged ischemia can cause tubular injury and may progress to acute tubular necrosis.

Common causes include hypovolemia from dehydration, gastrointestinal losses, or hemorrhage; reduced effective circulating volume in heart failure or cirrhosis with ascites; nephrotic syndrome; and systemic vasodilation from sepsis or anaphylaxis. Renal artery stenosis or other obstructions that limit renal blood flow can also contribute.

Diagnosis relies on clinical context and laboratory findings. Typical features include a BUN to creatinine ratio greater than 20:1, low urinary sodium (<20 mEq/L), and a high urine osmolality (>500 mOsm/kg). Fractional excretion of sodium (FeNa) is usually <1% but may be confounded by diuretics; FeUrea can be used in diuretic-treated patients. Urine sediment is typically bland.

Management focuses on treating the underlying cause and restoring renal perfusion. This often involves isotonic fluid resuscitation, careful avoidance of volume overload in heart failure, and discontinuation of nephrotoxins. In refractory hypotension, vasopressors may be used. Ongoing assessment of kidney function and urine output is essential. If perfusion is promptly restored, prognosis is generally favorable; prolonged hypoperfusion raises the risk of progression to intrinsic renal injury.