The role of hypotension in the development of acute renal failure

Abstract

Acute renal failure in critically ill patients is common and is associated with high morbidity and mortality rates [1]. When defined as a serum creatinine of 300 μmol/l (3.5 mg/dl) or more and/or a urine output of <500 ml/day, acute renal failure was shown to affect almost 25% of patients in the ICU [2]. Using the RIFLE criteria, studies have reported that between 10 and 67% of ICU patients have acute kidney injury [3]. Moreover, by increasing the hospital length of stay [2,4,5] and by inducing the need for renal replacement therapy, acute renal failure has substantial economic consequences [5,6]. Acute renal failure is typically multifactorial. The classical classification of renal diseases seen in any nephrology textbook does not apply to the vast majority of critically ill patients, who usually develop what is called ‘acute tubular necrosis’, even though the term is a misnomer as few of the tubular cells are actually necrotic [7]. The typical course of acute renal failure in a severely ill patient involves several factors including sepsis with hypovolaemia, (possibly transient) hypotension and administration of nephrotoxic therapeutic agents and/or contrast material, in a patient with co-morbidities such as diabetes and arteriosclerosis [2,8]. In this issue of Nephrology Dialysis and Transplantation, Liu and co-workers report that development of acute renal failure is usually preceded by an episode of relative hypotension [9]. The authors retrospectively selected two cohorts of patients, one with acute kidney injury as defined by the RIFLE criteria and one without. Blood pressure readings were obtained for 3 days prior to the development of acute kidney injury and for a similar 3-day period in patients without renal failure, and compared to baseline values