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Introduction: Involvement of the kidney in children and adolescents with perinatal (HIV-1) infection can occur at any stage during the child's life with diverse diagnoses, ranging from acute kidney injury, childhood urinary tract infections (UTIs), electrolyte imbalances and drug-induced nephrotoxicity, to diseases of the glomerulus. The latter include various immune-mediated chronic kidney diseases (CKD) and HIV-associated nephropathy (HIVAN)., Discussion: The introduction of highly active anti-retroviral therapy (HAART) has dramatically reduced the incidence of HIVAN, once the commonest form of CKD in children of African descent living with HIV, and also altered its prognosis from eventual progression to end-stage kidney disease to one that is compatible with long-term survival. The impact of HAART on the outcome of other forms of kidney diseases seen in this population has not been as impressive. Increasingly important is nephrotoxicity secondary to the prolonged use of anti-retroviral agents, and the occurrence of co-morbid kidney disease unrelated to HIV infection or its treatment. Improved understanding of the molecular pathogenesis and genetics of kidney diseases associated with HIV will result in better screening, prevention and treatment efforts, as HIV specialists and nephrologists coordinate clinical care of these patients. Both haemodialysis (HD) and peritoneal dialysis (PD) are effective as renal replacement therapy in HIV-infected patients with end-stage kidney disease, with PD being preferred in resource-limited settings. Kidney transplantation, once contraindicated in this population, has now become the most effective renal replacement therapy, provided rigorous criteria are met. Given the attendant morbidity and mortality in HIV-infected children and adolescents with kidney disease, routine screening for kidney disease is recommended where resources permit., Conclusions: This review focuses on the pathogenesis and genetics, clinical presentation and management of kidney disease in children and adolescents with perinatal HIV-1 infection.

Objectives: To compare human immunodeficiency virus (HIV)-infected and HIV-uninfected children with arthritis of unknown origin to determine whether the association between HIV infection and arthritis is causal or coincidental., Method: Retrospective review of 132 children with arthritis who were tested for HIV infection., Results: Thirty-five (27%) of the children were HIV infected and the male to female ratio was 2.5:1 (P = 0.02). Arthritis was the presenting feature of HIV infection in 78% of these children. The remaining 97 (73%) were diagnosed as having juvenile idiopathic arthritis. 'Spondyloarthropathy-like' features were found in 34% of HIV-infected children compared with 5% of uninfected children., Conclusion: The high prevalence of HIV infection in 27% of children, the predominance of males and the increased prevalence of 'spondyloarthropathy-like' features, supports a causal relationship between HIV infection and arthritis.

Background. Africa has the highest rate of HIV infection, and HIV-associated nephropathy (HIVAN) is one of the most frequent kidney diseases observed in children. HIVAN in children usually presents as a form of nephrotic syndrome, predominantly focal segmental glomerulosclerosis (FSGS) on histopathology, that often leads to chronic kidney failure. Objective. This study determined the urinary concentrations of ß-2-microglobulin (ß2M) and cystatin C proteins in children with HIVAN and primary FSGS. Methods. The study group comprised 34 children; 14 with HIVAN and 20 with primary FSGS. The control groups were 20 HIV-positive and 20 HIV-negative children with no kidney disease. Urine samples collected from these 74 children were stored at -80°C. Bio-Plex technology was used to analyse the urinary protein concentration of cystatin C and ß2M. Results. A significant increase in urinary ß2M levels was observed in the HIVAN group compared with the HIV-negative group (p=0.0240). No other statistically significant differences in urinary ß2M concentrations were noted across the study groups. Urinary cystatin C levels were significantly increased in primary FSGS children compared with both HIV-negative (p=0.0041) and HIV-positive controls (p=0.0256). Urinary cystatin C displayed a significant increase in the primary FSGS compared with the HIVAN group (p=0.0150). No significant differences in urinary cystatin C levels were noted in the HIVAN group compared with the HIV-negative and HIV-positive control groups. Conclusion. Urinary cystatin C has promising prognostic value to predict primary FSGS from HIVAN. [ABSTRACT FROM AUTHOR]

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- p (GST-p) 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 -80°C. Urinary concentrations of KIM-1, IL-18 and GST-p 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-p 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. [ABSTRACT FROM AUTHOR]