11 research outputs found

    Mini review: a unique case of crescentic C3 glomerulonephritis

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    Kidney involvement is an under-recognized complication of non-Hodgkin lymphomas. They occur in a variety of mechanisms and differ widely in their clinical presentation. We take this opportunity to report a case of a 65year-old man who developed a rapidly progressive glomerulonephritis within days after completing his first cycle of R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisolone) chemotherapy for newly diagnosed mantle cell lymphoma. He was odematous, hypertensive, oliguric with nephrotic range proteinuria and an active urine sediment. A renal biopsy showed a crescentic C3 glomerulonephritis (C3GN) with no evidence endocapillary or mesangial hypercellularity. He was promptly treated with immunosuppression and dialysis, with resumption of his chemotherapy. Genetic testing on complement proteins revealed a homozygous deletion spanning the CFHR1 and CFHR3 genes. Crescentic C3GN is a rare form of kidney injury, and this is the first known case of lymphoma-associated kidney involvement manifesting as C3GN. This article explores the possible mechanism of disease and reviews the literature of lymphoma-related kidney disease

    Antibiotic prophylaxis for melioidosis in patients receiving hemodialysis in the tropics? One size does not fit all

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    Melioidosis has a high case fatality rate and is more common in patients with chronic kidney disease. Some authors recommended trimethoprim/sulfamethoxazole (TMP/SMX) prophylaxis for all hemodialysis (HD) patients during the wet season in melioidosis-endemic regions. Historical data were reviewed to determine if TMP/SMX prophylaxis was warranted in the HD population of Far North Queensland, Australia. Between 1997 and 2017, there were 242 culture-confirmed cases of melioidosis in the region, three (1.2%) occurred in HD patients; all survived without intensive care support. During the study period, there were 843 HD patients in the region with 3,024 cumulative patient years of risk. Even assuming 100% efficacy, it would have been necessary to prescribe TMP/SMX for 1,008 patient years to prevent one case of melioidosis. Given the significant additional cost and potentially life-threatening side effects of TMP/SMX therapy, clinicians should review the local epidemiology of melioidosis before the implementation of universal TMP/SMX prophylaxis in their HD population

    Acute irreversible oxalate nephropathy in a lung transplant recipient treated successfully with a renal transplant

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    We report a 29 year old male cystic fibrosis patient with end stage lung disease and normal renal function who underwent a sequential double lung transplant. Medical history included: an ileal resection and pancreatic exocrine dysfunction. The postoperative period was complicated with haemorrhage and repeat surgery, requiring multiple blood transfusions and extensive antibiotic cover. Pancreatic supplements were interrupted. Acute renal failure attributed to haemodynamically-mediated acute tubular necrosis was managed expectantly. He remained dialysis dependent 8 weeks post surgery and was maintained on triple immunosuppression with tacrolimus, mycophenolate and prednisolone. A DTPA study was consistent with ATN. Renal biopsy revealed features consistent with tubular injury due to acute oxalate nephropathy (AON). Further biochemical characterization excluded primary hyperoxaluria but confirmed increased 24 hour urinary oxalate. He was maintained on enhanced frequency HDF and subsequently received an uncomplicated live related renal transplant 10 months post lung transplant with only additional Basiliximab. Calcium Carbonate was continued to manage post transplant hyperoxaluria and an early renal biopsy excluded recurrent oxalate injury. Enteric hyperoxaluria due to malabsorption in patients with CF especially with ileal resection, in addition to loss of gut Oxalobacter Formigenes due to prolonged antimicrobials, increases the risk of AON. Increased awareness of this condition and screening prior to lung transplant is recommended

    Establishing a stable platform for the measurement of blood endotoxin levels in the dialysis population

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    Background Gram-negative lipopolysaccharides are potent inducers of inflammation and have been shown to be present in patients with end-stage kidney disease. There are a variety of different manufacturers and assay types to quantify endotoxin levels; however, there is no standard methodology to demonstrate its presence in plasma. Methods A control group consisting of haemodialysis and non-kidney disease was selected. Five sets of experiments were conducted to try and ascertain the best platform for plasma endotoxin testing. This included: testing of blank tubes; the effects of freezing, thawing and storage on recovery; the effect of different buffers; use of an endpoint assay and comparison of turbidimetric vs. chromogenic kinetic assays. Results No endotoxin was detected in the blood collection tubes. Freezing and thawing per se did not affect spike recovery rates. However, the sequencing of sample dilution relative to freezing had a significant effect on endotoxin recovery. Buffers increased spike recovery at all levels of dilution. No endotoxin was demonstrated with either the turbidimetric or chromogenic kinetic assay at two different dilutions in the haemodialysis controls. The endpoint assay at a 1:5 dilution did not achieve a valid standard curve. Conclusions The findings of our study suggest that, when testing plasma samples, either a turbidimetric or chromogenic assay may be used and should be diluted with appropriate buffers to achieve optimal recovery. Studies looking to quantify the presence of plasma endotoxin need to internally validate their assays and specify their validation findings in their results
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