Acute kidney injury
Sics Editore
Okt 2014 · SICS Editore
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In acute kidney injury (AKI) the ability of the glomeruli to filtrate deteriorates, which leads to a disturbed acid-base and fluid balance as well as to the accumulation of end products of nitrogen metabolism. Within 24 to 48 hours of the onset of the injury the serum creatinine concentration will rise and urine output fall. AKI should be identified before the creatinine concentration is markedly increased and the estimated glomerular filtration rate (eGFR) falls. A typical patient is an elderly individual with pre-existing renal impairment who, for example, contracts acute diarrhoea or receives nephrotoxic drugs (e.g. NSAIDs, ACE inhibitors), i.e. acute-on-chronic kidney disease. Hypovolaemia is the most common cause of oliguria and can be reversed with fluid therapy. The urine output of a seriously ill patient must be monitored. Urinary retention must be identified and treated. The concomitant administration of an ACE inhibitor, diuretic and NSAID increases the risk of AKI.
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