Acute kidney injury (AKI) is defined as an abrupt decline in the glomerular filtration rate with accumulation of nitrogenous
waste products and the inability to maintain fluid and
electrolyte homeostasis. Occurring in 7% of all hospitalized patients and 28% to 35% of those in intensive care units, AKI increases hospital mortality. Early evaluation should include differentiating prerenal and postrenal components from intrinsic renal disease.
Biological markers can give early warning of AKI and assist with differential diagnosis and assessment of prognosis. The most effective preventive measure is to maintain adequate circulation and cardiac output, avoiding
ischemia- or nephrotoxin-induced injury. To that end, patients and situations of risk must be identified, hemodynamics and diuresis monitored,
hypovolemia reversed, and nephrotoxins avoided.
Protective agents such as
sodium bicarbonate,
mannitol, prostagiandins,
calcium channel blockers,
N-acetyl-L-cysteine,
sodium deoxycholate,
allopurinol, and
pentoxifylline should be used. Treatment includes the elimination of prerenal and postrenal causes of AKI; adjustment of doses according to renal function; avoidance of both
overhydration and low arterial pressure; maintenance of electrolytic balance, avoiding
hyperkalemia and correcting
hyperglycemia; and
nutritional support, assuring adequate
protein intake. For severe AKI, several modalities of
renal replacement therapy, differentiated by mechanism and duration, are available. Timing--neither the best moment to start dialysis nor the optimal duration--has been not established. Early detection of AKI is necessary for preventing progression and starting
renal replacement therapy at adjusted doses that reflect metabolic requirements.