Sub-Saharan Africa is the epicentre of the HIV pandemic but there are few reports of HIV-related kidney diseases in children in this region. This study aimed to determine the prevalence of proteinuria in HIV-infected children at the Lagos University Teaching Hospital. Proteinuria was determined using urine protein-creatinine ratio. CD4+ cell count was determined for all the HIV-infected children. The mean age of the HIV-infected children was 74.4 +/- 35.6 months with a male: female ratio of 3:2. Compared with 6% of the 50 controls 20.5% of the 88 HIV-infected children had proteinuria (p = 0.026). Of 20 children with advanced clinical stage 40% had proteinuria compared with 14.7% of 68 children with milder stage (p = 0.004). Similarly, proteinuria was commoner among those with severe immunosuppression (p = 0.014). HAART use was not associated with significant difference in proteinuria prevalence (p = 0.491). Proteinuria was frequent among HIV-infected children, especially among those with advanced disease.
BackgroundLimited data is available on kidney function in HIV-infected children in sub-Saharan Africa. In addition, malnutrition in these children further reduces the utility of diagnostic methods such as creatinine-based estimates of glomerular filtration rate. We determined the serum cystatin C level and estimated glomerular filtration rate of 60 antiretroviral-naïve, HIV-infected children and 60 apparently healthy age and sex matched children.MethodsSerum cystatin C level was measured using enzyme-linked immunosorbent assay technique, while glomerular filtration rate was estimated using Filler's serum cystatin C formula. Student t test, Mann Whitney U test, Pearson chi square and Fisher's exact test were used, where appropriate, to test difference between groups.ResultsCompared to the controls, the HIV-infected group had significantly higher median (interquartile range) serum cystatin C levels {0.77 (0.29) mg/l versus 0.66 (0.20) mg/l; p = 0.025} and a higher proportion of children with serum cystatin C level >1 mg/l {10 (16.7%) versus one (1.7%); p = 0.004}. The HIV-infected children had a mean (± SD) eGFR of 96.8 (± 36.1) ml/min/1.73 m2 compared with 110.5 (± 27.8) ml/min/1.73 m2 in the controls (p = 0.021). After controlling for age, sex and body mass index, only the study group (HIV infected versus control) remained a significant predictor of serum cystatin C level (β = -0.216, p = 0.021). The proportion of HIV-infected children with eGFR <60 ml/min/1.73 m2 was eight (13.3%) versus none (0%) in the control group (p = 0.006). However, the serum cystatin C level, eGFR and proportions of children with serum cystatin C level >1 mg/l and eGFR <60 ml/min/1.73 m2 were not significantly different between the HIV-infected children with advanced disease and those with milder disease.ConclusionsHIV-infected children in Nigeria have higher serum cystatin C level and lower eGFR compared to age and sex matched controls.
Hepatitis B virus is a well described cause of nephrotic syndrome (NS) worldwide, the typical lesion being membranous glomerulonephropathy. HBV associated NS has been successfully treated with intravenous alpha interferon (IFN), an anti-viral agent. In recent times there have been reports of treatment with lamivudine, an orally administered nucleoside analogue inhibitor of HBV DNA polymerase in Caucasian children. Data is however limited and it's actual efficacy and safety in children is yet to be determined. We present the case of an 8-year-old Nigerian boy with NS and active hepatitis B virus infection. He went into remission 3 months after commencing oral lamivudine which he had for a year with no significant side effects observed. He remains in remission 3 years later. This, to our knowledge is the first report in literature of successful treatment in an African child.
Background: Blood pressure readings of adult Nigerians with sickle cell disease (SCD) are reported to be lower than that of the general population but similar studies in children are unavailable. Objectives: To determine the systolic blood pressure (SBP) of children with SCD and compare it with that of healthy controls. Also, to correlate the SBP of children with SCD with age, gender, height and weight. Methods: Children with SCD were recruited from the Paediatric Haematology Clinic of the Lagos University Teaching Hospital. Data collected included bio-demographic details, social classification, height and weight measurements and present clinical status. SBP was measu r e d u s i n g a D o p p l e r (VASCUTRACK 120 ®) and a mercury sphygmomanometer. Similar data were obtained from age and sex matched apparently healthy children. Results: One hundred and twenty three children with SCD and 62 apparently healthy controls were studied; 62% were females. The mean age of the children with SCD was 8.93±3.91years (range 1-17 years) and was similar to the controls. SBP was similar in both groups of children (90.9±12.7 versus 92.2±15.2 mmHg; p=0.53) and increased with age. In 91 (74%) children with SCD the SBP was below the 50 th centile for the general population. Multiple linear regressions involving sex, age, height and weight found no independent factor to be a significant predictor of the SBP in children with SCD. Conclusion: The SBP of children with SCD is similar to that of age and sex-matched controls. The sex, age, weight and height did not significantly predict SBP in multiple linear regression.
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