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Background . HIV-associated nephropathy (HIVAN) in sub-Saharan Africa remains a significant cause of morbidity and mortality in children. Early detection of kidney injury is essential for injury-specific interventions that may avert permanent kidney damage and delay progression of kidney injury. Kidney biopsy is presently the gold standard for diagnosis of related kidney disease; however, it is pervasive with attendant complications, and may not be representative owing to sampling error. Serum creatinine is an insensitive and non-specific marker for the diagnosis of various kidney diseases, particularly in HIV-infected patients, who usually have varying degrees of muscle wasting. Therefore, a non-invasive approach using additional biomarkers for early detection of HIV-related kidney diseases, particularly HIV-associated nephropathy (HIVAN), is urgently needed. Objective . To determine the urinary concentrations of kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18) and glutathione-Stransferase- π (GST-π) in children with idiopathic focal segmental glomerulosclerosis (FSGS) and HIVAN. Methods . The study group comprised 34 children: 13 with HIVAN and 21 with idiopathic FSGS. The control groups were 19 HIV-positive and 16 HIV-negative children with no kidney disease. Urine samples collected from these 69 children were stored at –80oC. Urinary concentrations of KIM-1, IL-18 and GST-π were quantified using Bio-Plex assay. Results . A significant increase in urinary KIM-1 levels was observed in the HIVAN group compared with the HIV-positive (p=0.0039) and HIV-negative (p=0.0438) control groups. There was no significant increase in KIM-1 levels on comparison of the idiopathic FSGS group with the control groups (HIV-positive and HIV-negative children) (p=0.0737 and p=0.1757, respectively). No statistically significant differences were noted in urinary IL-18 and GST-π levels across all study groups. Conclusion . Urinary KIM-1 levels are significantly elevated in children with HIVAN and may be a useful biomarker to detect kidney disease in HIV-1-infected children.

The Role of Kidney Injury Molecule-1, Interleukin-18 and Glutathione-S-Transferase-π in Paediatric HIVAN.