Browsing by Subject "Proteinuria"
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Item Open Access APOL1 channel blocker reduces proteinuria in FSGS.(Kidney international, 2023-08) Olabisi, Opeyemi AItem Open Access Prevalence and correlates of proteinuria in Kampala, Uganda: a cross-sectional pilot study.(BMC Res Notes, 2016-02-16) Lunyera, Joseph; Stanifer, John W; Ingabire, Prossie; Etolu, Wilson; Bagasha, Peace; Egger, Joseph R; Patel, Uptal D; Mutungi, Gerald; Kalyesubula, RobertBACKGROUND: Despite the increasing prevalence of chronic kidney disease (CKD) in sub-Saharan Africa, few community-based screenings have been conducted in Uganda. Opportunities to improve the management of CKD in sub-Saharan Africa are limited by low awareness, inadequate access, poor recognition, and delayed presentation for clinical care. Therefore, the Uganda Kidney Foundation engaged key stakeholders in performing a screening event on World Kidney Day. METHODS: We conducted a cross-sectional pilot study in March 2013 from a convenience sample of adult, urban residents in Kampala, Uganda. We advertised the event using radio and television announcements, newspapers, billboards, and notice boards at public places, such as places of worship. Subsequently, we screened for proteinuria, hypertension, fasting glucose impairment, and obesity in a central and easily-accessible location. RESULTS: We enrolled 141 adults most of whom were female (57 %), young (64 %; 18-39 years), and had a professional occupation (52 %). The prevalence of proteinuria (13 %; 95 % confidence interval [CI] 7-19 %), hypertension (38 %; 95 % CI 31-47 %), and impaired fasting glucose (13 %; 95 % CI 9-20 %) were high in this study population. Proteinuria was most prevalent among young (18-39 years) adults (n = 14; 16 %) and among those who reported a history of alcohol intake (n = 10; 32 %). CONCLUSIONS: The prevalence of proteinuria was high among a convenience sample of urban residents in a sub-Saharan African setting. These results represent an important effort by the Ugandan Kidney Foundation to increase awareness and recognition of CKD, and they will help formulate additional epidemiological studies on NCDs in Uganda which are urgently needed and now feasible.Item Open Access Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis.(Kidney Int, 2014-12) Malone, Andrew F; Phelan, Paul J; Hall, Gentzon; Cetincelik, Umran; Homstad, Alison; Alonso, Andrea S; Jiang, Ruiji; Lindsey, Thomas B; Wu, Guanghong; Sparks, Matthew A; Smith, Stephen R; Webb, Nicholas JA; Kalra, Philip A; Adeyemo, Adebowale A; Shaw, Andrey S; Conlon, Peter J; Jennette, J Charles; Howell, David N; Winn, Michelle P; Gbadegesin, Rasheed AFocal segmental glomerulosclerosis (FSGS) is a histological lesion with many causes, including inherited genetic defects, with significant proteinuria being the predominant clinical finding at presentation. Mutations in COL4A3 and COL4A4 are known to cause Alport syndrome (AS), thin basement membrane nephropathy, and to result in pathognomonic glomerular basement membrane (GBM) findings. Secondary FSGS is known to develop in classic AS at later stages of the disease. Here, we present seven families with rare or novel variants in COL4A3 or COL4A4 (six with single and one with two heterozygous variants) from a cohort of 70 families with a diagnosis of hereditary FSGS. The predominant clinical finding at diagnosis was proteinuria associated with hematuria. In all seven families, there were individuals with nephrotic-range proteinuria with histologic features of FSGS by light microscopy. In one family, electron microscopy showed thin GBM, but four other families had variable findings inconsistent with classical Alport nephritis. There was no recurrence of disease after kidney transplantation. Families with COL4A3 and COL4A4 variants that segregated with disease represent 10% of our cohort. Thus, COL4A3 and COL4A4 variants should be considered in the interpretation of next-generation sequencing data from such patients. Furthermore, this study illustrates the power of molecular genetic diagnostics in the clarification of renal phenotypes.