Lipectomy is a safe, effective, and durable approach to make deep arterialized forearm veins accessible for routine cannulation for hemodialysis in obese patients. It might even be hypothesized that incident obese dialysis patients will eventually have the highest proportion of radial-cephalic fistulas because they often have distal veins that have been preserved by their fat from previous attempts at cannulation for blood sampling or infusion.
Background. Fungal infections are a rare but important cause of morbidity and mortality in kidney transplantation. Fungal contamination of the kidney preservation fluid may, sometimes, be the cause of these infections. However, the clinical consequences of fungal contamination of this fluid are not completely understood and literature on this topic is controversial. The purpose of this study was to determine the incidence of preservation fluid contamination by fungi and its clinical consequences.
Endovascular treatment plays a major role in the maturation process, maintenance and salvage of radial and ulnar-basilic fistulas. The preservation of upper arm veins for the future, with low risk of hand ischaemia or hyperflow, might encourage nephrologists and surgeons to consider forearm basilic fistulas systematically in their strategy of vascular access creation.
Background: C3 glomerulopathy is a recently described entity classified as complementassociated glomerular disease. Case Presentation: We report a case of a 48-year-old man referred to the nephrology department for nephrotic syndrome with rapidly progressive kidney failure, acquired partial lipodystrophy and drusen in Bruch’s membrane of the retina. Blood tests showed low C3 and no evidence for autoimmune diseases, monoclonal gammopathy or infection. The renal biopsy revealed a proliferative endocapillary and crescentic glomerulonephritis with glomerular deposits exclusively of C3 and significant interstitial fibrosis. The electronic microscopy was consistent with dense deposit disease. The complement analysis revealed a pathogenic mutation of the complement factor B (CFB) gene not previously described in literature. Conclusions: The authors report a new mutation of CFB, in a dense deposit disease patient; this finding brings a new insight to the pathogenic pathway of C3 glomerulopathy and possibly to other complement dysregulation associated glomerular diseases. More clinical trials are needed to clarify both the pathogenicity and the optimal treatment for these entities.
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