El estudio de la proteinuria en la insuficiencia renal aguda: nuevos marcadores

Abstract

A panel of urinary biomarkers would allow early and precise detection of acute kidney injury, thus leading to faster therapeutic decision. Acute kidney injury involves hemodynamic alterations and inflammation strongly associated with increased morbidity and mortality in critically ill patients. Renal ischemia/reperfusion results in rapid loss of cytoskeletal integrity and cell polarity as a common pathway in a variety of clinical states. A renal biopsy is indispensable to establish a diagnosis between acute tubular necrosis and allergic tubulointerstitial nephritis, the most common forms of acute kidney injury, but it cannot be performed serially because of its invasive nature. Serum creatinine, which has been traditionally used in almost all definitions of acute kidney injury, is a suboptimal marker to accurately estimate timing and severity of injury. Examination of the urine provides a readily accessible non-invasive method to detect casts and tubular cells and to confirm a tubular cell damage and death by apoptosis and/or necrosis as a hallmark of acute kidney injury in humans. Measurements of proteins and enzymes released to the urine could increase its detection. Levels of urinary β2-microglobulin indicate tubular damage in a superior way than N-acetil-β-Dglucosaminidase(lysosomal) does. Alkaline pho sphatase was proposed to evaluate early proximal tubular injury (brush border membrane). Because of its higher stability in urine during storage, α1-microglobulin proved to be the most valuable parameter in early detection, renal outcome prediction and easy inclusion in routine analytical programmes. Recently, urinary monocyte chemoattractant protein-1 levels were able to identify serious interstitial edema and inflammatory infiltration.