Introduction Apolipoprotein-L1 ( APOL1 ) risk variants G1 and G2 increase the risk of chronic kidney disease (CKD), including HIV-related CKD, among African Americans. However, such data from populations living in Africa, especially children, remain limited. Our research aimed to determine the prevalence of APOL1 risk variants and to assess the association between these variants and early-stage CKD in the general pediatric population and HIV-infected children. Methods In a cross-sectional study, we enrolled 412 children from the general population and 401 HIV-infected children in Kinshasa, Democratic Republic of Congo (DRC). APOL1 high-risk genotype (HRG) was defined by the presence of 2 risk variants (G1/G1, G2/G2, or G1/G2), and low-risk genotype (LRG) by the presence of 0 or 1 risk variants. The main outcome was elevated albuminuria, defined as a urinary albumin/creatinine ratio ≥30 mg/g. Results APOL1 sequence analysis revealed that in the general population, 29 of 412 participants (7.0%) carried HRG, 84 of 412 (20.4%) carried the G1/G0 genotype, and 61 of 412 (14.8%) carried the G2/G0 genotype. In HIV-infected children, 23 of 401 (5.7%) carried HRG, and the same trend as in the general population was observed in regard to the prevalence of LRG. Univariate analysis showed that in the general population, 5 of 29 participants (17.2%) carrying HRG had elevated albuminuria, compared with 35 of 383 (9.0%) with LRG (odds ratio [OR] 2.1, 95% confidence interval [CI] 0.6–6.0; P = 0.13). In HIV-infected children, participants who carried APOL1 HRG had almost 22-fold increased odds of albuminuria compared to those with LRG. Conclusion The APOL1 risk variants are prevalent in children living in DRC. HRG carriers have increased odds of early kidney disease, and infection with HIV dramatically increases this probability.

In the Democratic Republic of Congo (DRC), acute kidney injury (AKI) contributes to the high rate of child mortality owing to the conjunction of poverty, deficiency of qualified health-care providers in pediatric nephrology, and the lack of pediatric dialysis programs. We aimed to describe the recent experience of the first pediatric acute peritoneal dialysis (PD) program in DRC. This is a retrospective cohort study on epidemiology, clinical features and outcomes of children admitted from January 2018 to January 2019 at the University Hospital of Kinshasa for AKI and treated with PD. This pediatric PD program started by a team of one physician and one nurse who were trained in the local production of PD fluids and bedside catheter insertion technique in Benin Republic. The training was jointly supported by the Flemish Inter-University Council (VLIR) TEAM project and Saving Young Lives (SYL) program of ISN, ISPD, EuroPD, and IPNA. From January 2018 to January 2019, 49 children (aged 4 months–15 years) were admitted for AKI mainly due to severe malaria and sepsis. Dialysis was indicated in 35 of 49 (71.4%), 32 of 35 (91.4%) were treated with PD, two with hemodialysis (HD) in adult ward and one died at admission. Data of the two patients transferred for HD were not available for follow-up. The main indications were uremia and prolonged anuria. Of 32 dialyzed patients, 24 (75%) recovered normal renal function 3 months after discharge. Peritonitis was observed in 2 of 32 (6.2%) patients and the mortality was 18.7%. This promising experience proves that with simple means including use of locally produced dialysis fluids and low peritonitis rates, we can effectively save lives of children suffering from AKI.

Apolipoprotein L1 (APOL1) high-risk genotypes (HRG), G1 and G2, increase the risk of various non-diabetic kidney diseases in the African population. To date, the precise mechanisms by which APOL1 risk variants induce injury on podocytes and other kidney cells remain unclear. Trying to unravel these mechanisms, most studies have used animal or cell models created by gene editing. We developed and characterised conditionally immortalised human podocyte cell lines derived from urine of a donor carrying APOL1 HRG G2/G2. Following induction of APOL1 expression by polyinosinic-polycytidylic acid (poly(I:C)), we assessed functional features of APOL1-induced podocyte dysfunction. As control, APOL1 wild type (G0/G0) podocyte cell line previously generated from a Caucasian donor was used. Upon exposure to poly(I:C), G2/G2 and G0/G0 podocytes upregulated APOL1 expression resulting in podocytes detachment, decreased cells viability and increased apoptosis rate in a genotype-independent manner. Nevertheless, G2/G2 podocyte cell lines exhibited altered features, including upregulation of CD2AP, alteration of cytoskeleton, reduction of autophagic flux and increased permeability in an in vitro model under continuous perfusion. The human APOL1 G2/G2 podocyte cell model is a useful tool for unravelling the mechanisms of APOL1-induced podocyte injury and the cellular functions of APOL1.

No abstract

Clinical and genetic factors have been reported as influencing the development of sickle cell nephropathy (SCN). However, such data remain limited in the paediatric population. In this cross-sectional study, we enrolled 361 sickle cell disease children from the Democratic Republic of Congo. Participants were genotyped for the beta (b)-globin gene, apolipoprotein L1 (APOL1) risk variants, and haem oxygenase-1 (HMOX1) GT-dinucleotide repeats. As markers of kidney damage, albuminuria, hyperfiltration and decreased estimated glomerular filtration with creatinine (eGFRcr) were measured. An association of independent clinical and genetic factors with these markers of kidney damage were assessed via regression analysis. Genetic sequencing confirmed sickle cell anaemia in 326 participants. Albuminuria, hyperfiltration and decreased eGFRcr were present in 65 (20%), 52 (16%) and 18 (5Á5%) patients, respectively. Regression analysis revealed frequent blood transfusions, indirect bilirubin and male gender as clinical predictors of SCN. APOL1 high-risk genotype (G1/G1, G2/G2 and G1/G2) was significantly associated with albuminuria (P = 0Á04) and hyperfiltration (P = 0Á001). HMOX1 GT-dinucleotide long repeats were significantly associated with lower eGFRcr. The study revealed a high burden of kidney damage among Congolese children and provided evidence of the possible role of APOL1 and HMOX1 in making children more susceptible to kidney complications.

No abstract

No abstract

No abstract