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.