Renal toxicity has become an important issue in HIV-infected patients receiving highly active antiretroviral
therapy (HAART). Several biomarkers are available for monitoring renal function, although no consensus exists on how
best to apply these tools in HIV infection. The best biomarker is the glomerular filtration rate (GFR), and several
creatinine-based estimates equations of GFR are widely used in HIV infection, with clinical advantages for the equation
developed by Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI). Although serum cystatin C has been
proposed as a more sensitive marker of renal dysfunction in HIV infection, it may be affected by ongoing inflammation.
Tubular dysfunction can be simple or complex, depending on whether the tubular transport of one or more substances is
affected. Multiple renal tubular dysfunction or Fanconi syndrome is characterized by alterations in the reabsorption of
glucose, amino acids, phosphate and often also bicarbonate. Therefore, Fanconi syndrome would be the tip of the iceberg,
and the most unusual and severe manifestation. In the last years, several low molecular weight proteins as markers of
tubular alteration, including retinol-binding protein, b2-microglobulin, and neutrophil gelatinase associated lipocalin have
become available. Different studies have shown differences in urine concentrations of these proteins in patients receiving
tenofovir, but again, no consistent data have shown their clinical usefulness in predicting the clinical consequences of
tubular alteration. Thus, we review findings from recent studies performed in this area to describe the performance of new
biomarkers for renal damage in HIV-infected patients.
Keywords: Biomarkers, HIV infection, kidney damage, proteinuria, tenofovir, tubular dysfunction, CKD, MDRD, plasma, HAART.
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