The story of the African Association of Nephrology (AFRAN)

The African Association of Nephrology was founded in Cairo on 28 February 1987, during the ISN-sponsored “African Kidney and Electrolytes Conference”, being hosted and co-sponsored by the Egyptian Society of Nephrology. Twenty-five physicians interested in kidney disease, from 13 African countries, constituted the core assembly that selected a steering committee composed of five members, representing the five geographical zones in Africa. The committee proposed the name the African Association of Nephrology (AFRAN), approved its logo, defined its mission, and drafted its constitution. All were ratified at the first General Assembly meeting held in London in July of the same year. The steering committee was re-elected to continue as the Executive Committee for the first cycle and mandated to set the scene for future meetings, publications and programmes. AFRAN congresses have been held regularly ever since, triennially for three cycles, then biennially with a few exceptions. Scientific meetings including Continuing Medical Education activities and hands-on workshops addressing local kidney and electrolyte disorders, have been held in most African countries, with generous logistical and financial support by the International Society of Nephrology (ISN). The abstracts of the first congress were published in Kidney International. Meeting proceedings were usually distributed by hand, thanks to representatives of pharmaceutical companies in the various African countries. A quarterly newsletter was edited and published in the Sudan, upgraded to a journal (the African Journal of Nephrology) in 1997 and self-published from Egypt until the editorial office moved to South Africa in 2012. A registry of nephrologists and dialysis units in Africa was compiled and published from Algeria in 1989, then updated in the Sudan a few years later. More recently, an African Renal Registry was established, now hosted in South Africa. Numerous fellowships were offered by the better-off countries to their emerging neighbours, being sponsored by international organizations, mainly the ISN. Joint research has been conducted mainly through these fellowships. By its 10th birthday, AFRAN had encompassed all African countries, to become the official pan-African federation of national renal societies. The ISN initiatives for supporting the developing world, originally operated under the umbrella of the Commission for the Global Advancement of Nephrology (COMGAN), were instrumental in supporting AFRAN’s foundation and sustainability. Besides the ISN, AFRAN became affiliated to many other regional and all national societies of nephrology, which qualified it to serve as the principal liaison between African nephrology and that in the rest of the world

Immunoglobulin-A and the pathogenesis of schistosomal glomerulopathy

Immunoglobin-A and the pathogenesis of schistosomal glomerulopathy. Several observations suggest that the evolution of schistosomal glomerulopathy into clinically overt and progressive disease may involve pathogenetic mechanisms other than simple glomerular deposition of parasitic antigens. In a previous study, IgA was suggested tobe a mediator of late glomerular lesions in this disease. This issue is further addressed in this work. The study includes 32 patients with hepatosplenic schistosomiasis, of whom 16 had overt glomerular involvement, along with four control groups: (a) 15 healthy volunteers; (b) 15 patients with simple intestinal mansoniasis; (c) 17 patients with non-schistosomal chronic liver disease; and (d) 21 subjects with primary nephrotic syndrome not associated with schistosomiasis. Routine assessment was done for all subjects including confirmatory tests for schistosomal infection, liver and renal function tests, hepatitis viral markers and abdominal ultrasonography. The total serum concentrations of IgG, IgM, IgA were measured, as well astheir respective circulating immune complexes, rheumatoid factors, anti-gliadin- and anti-DNA-antibodies. Liver and renal biopsies were obtained from the relevant groups and studied by light microscopy. Renal biopsies were also examined by immunofluorescence. Patients with simple intestinal schistosomiasis had a significant increase in IgM antigliadin antibodies. Those complicated with hepatosplenic involvement also had a significant increase in the mean IgG anti-gliadin antibodies, IgG rheumatoid factor and IgM anti-DNA activity. Cases further complicated by overt glomerular disease showed a distinct IgA predominance, mainly expressed in the serum anti-gliadin antibody pool and anti-DNA activity. This profile was essentially similar to that observed in control cirrhotics. There was a significant increase in the frequency of IgA glomerular deposits in renal biopsies obtained from patients with overt schistosomal glomerulopathy, in contrast to control nephrotics. The deposits were mainly mesangial, but were also encountered in subendothelial, subepithelial and peritubular locations. Their frequency was significantly higher with more advanced lesions as seen by light microscopy. The relevance of these data is discussed, leading to the following conclusions: (a) serum IgA-anti-gliadin and -anti-DNA antibodies, and glomerular IgA deposits are markers of significant renal involvement in patients with hepatosplenic schistosomiasis, (b) IgA may be involved in the pathogenesis of advanced glomerular pathology when superimposed on parasite-induced lesions, (c) There is a significant increase in serum auto-reactivity in hepatosplenic schistosomiasis, which may also have pathogentic implications, (d) Increased production by the inflammatory bowel lesions, impaired clearance by the fibrotic livers and probable switching of immunoglobulin synthesis are suggested to explain the observed IgA predominance in those who develop renal complications

Hepatitis C virus infection and global kidney health: the consensus proceedings of the International Federation of Kidney Foundations

Hepatitis C virus (HCV) infection is an important cause of major morbidities including chronic liver disease, liver cancer, acute kidney injury and chronic kidney disease (CKD). Among patients with kidney disease who have HCV infection, the clinical outcomes are worse. The prevalence of HCV infection is exceptionally high among dialysis and kidney transplant patients throughout the globe. It is estimated that 5% to 25% or more of dialysis-dependent patients are affected. Almost half of all deaths in CKD patients, including HCV-infected patients, are due to cardiovascular disease, and HCV-infected patients have higher mortality. Given the importance and impact of the HCV epidemic on global kidney health, and the status of Egypt as the nation with the highest prevalence of HCV infection in the world along with its initiatives to eradicate HCV, the International Federation of Kidney Foundations convened a consensus conference in Cairo in December 2017. This article reflects the opinions and recommendations of the contributing experts and reiterates that, with the current availability of highly effective and well tolerated pharmacotherapy, CKD patients should be given priority for the treatment of HCV, as an important step towards the World Health Organization’s goal of eliminating viral hepatitis as a public health problem by 2030

Effect of sirolimus on malignancy and survival after kidney transplantation: systematic review and meta-analysis of individual patient data

Objective To examine risk of malignancy and death in patients with kidney transplant who receive the immunosuppressive drug sirolimus.Design Systematic review and meta-analysis of individual patient data.Data sources Medline, Embase, and the Cochrane Central Register of Controlled Trials from inception to March 2013.Eligibility Randomized controlled trials comparing immunosuppressive regimens with and without sirolimus in recipients of kidney or combined pancreatic and renal transplant for which the author was willing to provide individual patient level data. Two reviewers independently screened titles/abstracts and full text reports of potentially eligible trials to identify studies for inclusion. All eligible trials reported data on malignancy or survival.Results the search yielded 2365 unique citations. Patient level data were available from 5876 patients from 21 randomized trials. Sirolimus was associated with a 40% reduction in the risk of malignancy (adjusted hazard ratio 0.60, 95% confidence interval 0.39 to 0.93) and a 56% reduction in the risk of non-melanoma skin cancer (0.44, 0.30 to 0.63) compared with controls. the most pronounced effect was seen in patients who converted to sirolimus from an established immunosuppressive regimen, resulting in a reduction in risk of malignancy (0.34, 0.28 to 0.41), non-melanoma skin cancer (0.32, 0.24 to 0.42), and other cancers (0.52, 0.38 to 0.69). Sirolimus was associated with an increased risk of death (1.43, 1.21 to 1.71) compared with controls.Conclusions Sirolimus was associated with a reduction in the risk of malignancy and non-melanoma skin cancer in transplant recipients. the benefit was most pronounced in patients who converted from an established immunosuppressive regimen to sirolimus. Given the risk of mortality, however, the use of this drug does not seem warranted for most patients with kidney transplant. Further research is needed to determine if different populations, such as those at high risk of cancer, might benefit from sirolimus.PfizerOttawa Hosp, Res Inst, Ottawa, ON K1H 7W9, CanadaUniv Ottawa, Ottawa, ON, CanadaCairo Univ, Cairo Kidney Ctr, Cairo, EgyptLimites Med Res, Vacallo, SwitzerlandUniv Manitoba, Dept Pediat & Childs Hlth, Winnipeg, MB, CanadaLund Univ, Dept Nephrol & Transplantat, Malmo, SwedenUniversidade Federal de São Paulo, Hosp Rim & Hipertensao, São Paulo, BrazilAddenbrookes Hosp, Dept Renal Med, Cambridge, EnglandNorthwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USAMaastricht Univ, Med Ctr, Maastricht, NetherlandsSt Louis Hosp, Dept Nephrol, Paris, FranceHosp JW Goethe, Div Nephrol, Frankfurt, GermanyUniv Munich, Dept Surg, Munich, GermanyGoethe Univ Frankfurt, JW Goethe Clin, Clin Dermatol Venerol & Allergol, Frankfurt, GermanyInst Klin Expt Med, Dept Nephrol, Prague, Czech RepublicUniv Cambridge, Addenbrookes Hosp, Dept Surg, NIHR Cambridge Biomed Res Ctr, Cambridge CB2 2QQ, EnglandUniversidade Federal de São Paulo, Hosp Rim & Hipertensao, São Paulo, BrazilWeb of Scienc

Urinary Schistosomiasis: Review

In this review, the clinical manifestations of urinary schistosomiasis are displayed from a pathogenetic perspective. According to the prevailing host’s immune response profile, urinary schistosomiasis may be broadly categorized into cell-mediated and immune-complex-mediated disorders. The former, usually due to Schistosoma haematobium infection, are attributed to the formation of granulomata along the entire urinary tract. As they heal with excessive fibrosis, they may lead to strictures, calcifications and urodynamic abnormalities. The main impact is lower urinary, the site of heaviest ovi-position. Secondary bacterial or viral infection is common, any may be incriminated in secondary stone formation of the development of bladder malignancy. Immune-complex mediated lesions are usually associated with hepatosplenic schistosomiasis due to Schistosoma mansoni infection. Circulating complexes composed of schistosomal gut antigens and different classes of immunoglobulins deposit in the kidneys leading to several patterns of glomerular pathology. The latter have been categorized under six classes based on the histological and immunofluorescence profile. These classes have been linked to respective clinical manifestations and depend on the stage of evolution of the host’s immune response, extent of associated hepatic fibrosis and co-infection with salmonella or hepatitis C. Secondary amyloidosis develops in 15% of such patients, representing a critical impairment of macrophage function. Conclusion: The wide clinicopathological spectrum of urinary schistosomiasis mirrors the evolution of the host’s immune response according to chronicity of infection, bacterial or viral co-infection and, in the case of glomerulonephritis, to the extent of hepatic co-morbidity