This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.Nephrotic syndrome is one of the most common causes of kidney disease in paediatric patients, with disadvantaged populations suffering disproportionately from the disease and its complications. [1][2][3] Data on the clinical profile of paediatric nephrotic syndrome, a chronic condition characterised by proteinuria, hypoalbuminaemia, and oedema, are limited within sub-Saharan Africa (SSA). [4] Consequently, medical management and outcomes of paediatric patients with nephrotic syndrome across SSA are not well established, especially for cases of steroidresistant disease.Early age at onset is associated with an increased prevalence of steroid-resistant nephrotic syndrome (SRNS) in children. Based on information collected from the PodoNet Consortium international registry including 1 655 paediatric patients, childhood-onset SRNS manifested before the age of 5 in 64% of patients. [5] Historically, more than 50% of these patients with steroid resistance had progressed to chronic kidney disease (CKD) and end-stage renal disease (ESRD) within five years, particularly within resourcelimited settings. [6] Until the 1980s, quartan malaria nephropathy was prevalent in tropical regions of Africa, making corticosteroidresistant disease common throughout the region. [4] However, given improving access to healthcare for the treatment of malaria, nephrotic syndrome is now increasingly associated with other disease processes, including hepatitis B, HIV, sickle cell disease and systemic lupus erythematosus. [7][8][9] Response to steroid therapy has also been reported to differ according to geography. [6,10] Studies concerning associations of SRNS with ethnicity present varying conclusions. Retrospective chart reviews reported higher rates of SRNS at institutions in the Democratic Republic of the Congo and Nigeria than those reported in Asian or Western countries (around 10%). [11][12][13][14] Conversely, two recent studies in Nigeria showed improved steroid-sensitivity in cohorts of children. [15,16] Moreover, studies from Zimbabwe, Malawi and South Africa show a continued predominance of focalsegmental glomerulosclerosis (FSGS) and membranoproliferative glomerulonephritis (MPGN) in the region, a histopathologic diagnosis commonly associated with the steroid-resistant disease. [17][18][19] Considering the lack of a definitive association with SRNS within current literature, further characterisation of the clinical profile of SRNS is needed.The present study aims to address this gap by characterising the baseline clinical and demographic factors associated with steroid resistance in a cohort of Mozambican children with nephrotic syndrome.Background. First-line treatment for paediatric nephrotic syndrome, a chronic disease characterised by proteinuria, hypoalbuminaemia and oedema, is corticosteroid therapy. An association between African ethnicity and steroid resistance has been reported, but published data from sub-Saharan Africa are limited and lack...

the ability for low viral load, untreated hepatitis B to cause proliferative glomerulonephritis (GN) or the significance of anti-Ro in absence of other biochemical, histological or clinical classical lupus manifestations. Methods: We present a case of a sixty-three-year-old female who presented with an acute on chronic renal dysfunction; she was treatment naive hepatitis B positive with low viral titre, anti-Ro antibody positive and had known IgM kappa monoclonal gammopathy with stable titres. Importantly cryoglobulins and the rest of her autoimmune panel was negative. Results: Kidney biopsy light microscopy showed proliferative GN with membranoproliferative pattern. There was moderately severe arteriosclerosis and arteriolosclerosis with few vessels showing intimal fibrinoid necrosis with hyperplasia of tunica media (onion skinning). Six out of twenty glomeruli were obsolescent and there were two fibrocellular crescents. Immunofluorescence showed 4+ granular mesangial and peripheral capillary wall reaction with IgM and kappa, 3+ granular mesangial and peripheral capillary wall reaction noted with IgG, lambda and C3 only. Electron microscopy showed variable foot process effacement and a few cryoglobulinlike cylindrical organised deposits. The patient experienced improvement in renal function with mycophenolate and prednisone, however there was debate of the use of chemotherapy agents such as rituximab or traditional myeloma therapy. We are planning to do a repeat biopsy in the future to evaluate regression of renal lesions. Conclusions: This case demonstrates the increasing evidence that many patients with proliferative glomerulonephritis do not fit neatly in to one pathophysiological box and thus treatment must be tailored to the individual patient.