Autoantibody against phospholipase A2 receptor (anti-PLA2R) is a sensitive and specific biomarker of idiopathic membranous nephropathy (iMN), being found in approximately 70% of iMN patients and only occasionally in other glomerular diseases. However, whereas its diagnostic specificity vs. normal controls and other glomerulonephritides (GN) has been firmly established, its specificity vs. membranous nephropathy associated with various diseases (sMN) has given inconsistent results. The aim of our study was to evaluate the prevalence of anti-PLA2R antibodies in iMN in comparison with various control groups, including sMN. A total of 252 consecutive iMN patients, 184 pathological and 43 healthy controls were tested for anti-PLA2R antibody using indirect immunofluorescence (PLA2R IIFT, Euroimmun). Anti-PLA2R autoantibodies were detectable in 178/252 iMN patients, 1/80 primary GN, 0/72 secondary GN, 9/32 sMN and 0/43 healthy controls, with a diagnostic sensitivity of 70.6%. The diagnostic specificity of anti-PLA2R antibody vs. normal and pathological controls was 100 and 94.6% respectively. However, when the diagnostic specificity was calculated only vs. secondary forms of MN, it decreased considerably to 71.9%. Interestingly enough, 9 out of 10 anti-PLA2R positive patients in the disease control groups had membranous nephropathy associated with various diseases (7 cancer, 1 Crohn's disease, 1 scleroderma). In conclusion, anti-PLA2R positivity in a patient with MN, should not be considered sufficient to abstain from seeking a secondary cause, especially in patients with risk factors for neoplasia. The causal relationship between tumors and anti-PLA2R-induced MN remains to be established, as well as the possible mechanisms through which malignancies provoke autoimmunity.
BackgoundFungal peritonitis (FP) is one of the most important causes of peritoneal dialysis (PD) failure, often burdened by increased morbility and mortality. This study evaluates the clinical course of FP cases that arose between 1983 and 2016 in a single PD unit.MethodsWe conducted a retrospective observational analysis of FP episodes recorded in the Baxter POET (Peritonitis Organism Exit sites Tunnel infections) registry and clinical records. FP incidence rate, PD and patients’ survival and clinical characteristics of the study population were analysed, taking into account the evolution of clinical practice during the study period as a result of technical innovation, scientific evidence and guideline history.ResultsFourteen FP cases (2.8%) were detected. The overall incidence of PD peritonitis was one episode/27 patient-months. Candida parapsilosis was the most frequently (50%) detected yeast. Seventy-five per cent of cases were considered secondary FP. This group experienced 2.6±1.7 bacterial peritonitis before FP, most frequently due to Staphylococcus and Enterococcus species. Most patients were treated with fluconazole for ≥8 days. All subjects were hospitalized for a median time of 25 days. Tenckhoff catheter removal occurred in all cases of FP and all patients were transferred to haemodialysis. Two patients died. From December 2010 to December 2016, no FP episodes were recorded.ConclusionsFP is confirmed as a significant cause of PD drop out and increases patients’ mortality risk. Prompt diagnosis of FP, targeted antifugal therapy and rapid PD catheter removal are essential strategies for improved patient and PD survival.
Lanthanum carbonate, being the most potent calcium-free phosphate binder available in clinical practice, could be decisive for those cases where controlling phosphate load is complicated by poor compliance to medications, stubborn high phosphorus intake, extended VC and bone disorders.
A consistent body of evidence supports an independent association between uric acid (UA) level and the risk of chronic kidney disease (CKD) in humans. It has been observed in experimental data that UA is capable of inducing renal damage through several pathways, including activation of the renin-angiotensin-aldosterone system (RAAS), oxidative stress, and inflammation. Treatment with urate lowering agents and RAAS inhibitors prevented renal insult mediated by UA in animal models. Both of the xanthine oxidase inhibitors available in clinical practice, allopurinol and febuxostat, were efficient in controlling gout flares. However, data from randomised controlled trials are still inconsistent in relation to their benefit for slowing CKD progression. This review discusses the metabolism of urates in humans as well as the experimental and clinical evidence linking UA to CKD. Current evidence about the effect of allopurinol and febuxostat on CKD progression is also considered.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.