Analysis of the prerenal contributions to acute kidney injury

Acute kidney injury (AKI) occurs frequently in hospitalized patients, and prerenal mechanisms contribute significantly to the pathogenesis of AKI. Prerenal contributions to renal dysfunction may be transient and reversible, as in volume depletion, or more persistent as observed with heart failure and liver disease. They can also act as a precursor to parenchymal kidney damage. The reductions in glomerular filtration rate are largely shared by all nephrons and are primarily mediated by reductions in nephron plasma flow and decreases in the glomerular ultrafiltration coefficient. Studies in animals suggest that adrenergic activity and angiotensin II (Ang II) are the dominant hormonal influences that independently and synergistically impact the determinants of glomerular filtration. Interactions between individual adrenoreceptors and Ang II are complex and significant. Tubular injury can also activate prerenal mechanisms via the tubuloglomerular feedback system. The effects of adrenergic and Ang II activities are counteracted by actions of nitric oxide and prostaglandins within the kidney. Bidirectional regulatory influences occur between the vasoconstrictor and vasodilatory hormonal systems. Understanding these prerenal mechanisms and the role of endogenous and exogenous vasoconstrictor and vasodilator hormones is important in the prevention, therapy and recovery of AKI in critically ill patients who commonly encounter it.