Microalbuminuria can predict the development of acute kidney injury in critically ill septic patients

Sepsis is a leading cause of morbidity and mortality in the critical care setting. Millions of people are affected by this devastating illness each year, and it is reported that at least 1 in 4 of such patients will die from this disease (1, 2). Patho-physiologically, sepsis is characterized by uncontrolled sys-temic inflammatory responses and subsequent increases in vascular permeability to plasma protein triggered by inflam-matory mediators (3, 4), resulting in loss of plasma volume, increase in extravascular lung water (EVLW), hypotension, multiorgan failure, shock and even death. Acute kidney in-jury (AKI) is a life-threatening complication of severe sepsis. As demonstrated by Chertow et al (5), even mild forms of AKI (>0.5 mg/dL increase in serum creatinine) were associ-ated with a sevenfold increase in mortality. Despite recent advances in management of septic AKI, the morbidity and mortality rates for this disease entity have not been substan-tially improved. Treatment failure is largely due to the lack of a reliable biomarker for early recognition of AKI. Serum creatinine (sCr)–based evaluation of renal function lags be-hind renal injury because sCr rises only after more than 50% kidney function has been lost (6). It is proposed that AKI can be prevented and treated if adequate strategies have been taken early after renal insult. Thus, early recognition of renal injury after insult is clinically important and potentially useful to improve clinical outcomes (7). Microalbuminuria (MA), typically defined as albumin excre-tion in urine of 30-300 mg/24 hours, occurs rapidly after acute inflammatory insult and is shown to be associated with outcomes in many clinical settings, including sepsis, multiple trauma and intracranial hemorrhage (8-10). The mechanisms of MA development have been extensively