Background. Sevelamer carbonate is an improved, buffered form of sevelamer hydrochloride developed for the treatment of hyperphosphataemia in CKD patients. Sevelamer carbonate formulated as a powder for oral suspension presents a novel, patient-friendly alternative to tablet phosphate binders. This study compared the safety and efficacy of sevelamer carbonate powder with sevelamer hydrochloride tablets in CKD patients on haemodialysis.Methods. This was a multi-centre, open-label, randomized, crossover design study. Thirty-one haemodialysis patients were randomly assigned to either sevelamer carbonate powder or sevelamer hydrochloride tablets for 4 weeks followed by a crossover to the other regimen for an additional 4 weeks.Results. The mean serum phosphorus was 1.6 ± 0.5 mmol/L (5.0 ± 1.5 mg/dL) during sevelamer carbonate powder treatment and 1.7 ± 0.4 mmol/L (5.2 ± 1.1 mg/dL) during sevelamer hydrochloride tablet treatment. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus; the geometric least square mean ratio was 0.95 (90% CI 0.87–1.03). No statistically significant or clinically meaningful differences were observed in calcium × phosphorus product and lipid levels between sevelamer carbonate powder and sevelamer hydrochloride tablets. Serum bicarbonate levels increased 2.7 ± 3.7 mmol/L (2.7 ± 3.7 mEq/L) during sevelamer carbonate treatment. No statistically significant change in bicarbonate was observed during sevelamer hydrochloride treatment. Sevelamer carbonate powder and sevelamer hydrochloride were well tolerated during this study.Conclusions. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus and well tolerated in CKD patients on haemodialysis. Bicarbonate levels improved only during sevelamer carbonate treatment. Sevelamer carbonate powder should provide a welcomed new option for the treatment of hyperphosphataemia for CKD patients on dialysis.
Dapsone (4,4'-diaminodiphenyl sulphone) is used for a variety of dermatological conditions including immunobullous diseases and urticarial vasculitis. Side-effects are common and include lethargy, headaches, methaemoglobinaemia and haemolysis. Severe adverse effects are rare but the dapsone hypersensitivity syndrome is well recognized. Symptoms include fever, haemolytic anaemia, lymphocytosis and hepatitis. We report a near fatal case of the dapsone hypersensitivity syndrome in a patient with urticarial vasculitis. This diagnosis should be remembered in any patient who becomes unwell whilst taking dapsone.
SUMMARY
Goodpasture's disease is a rare form of glomerulonephritis characterized by the production of autoantibodies to the glomerular basement membrane (GBM). In order to understand the development of autoimmunity to the GBM, it is important to examine mechanisms underlying T cell responses to the autoantigen. A MoAb PI, with the same specificity as patients’ autoantibodies, was used to affinity‐purify the antigen from collagenase‐digested human GBM. This material was enriched in the NCI domain of the α3 chain of type IV collagen (α3(IV)NC1), known to be the principal target of anti‐GBM antibodies, but also contained lower quantities of α4(IV)NC1. In proliferation assays, T cells from 11/14 patients with Goodpasture's disease showed significant responses (SI ± 2·0) to affinity‐purified human GBM. Peak responses were demonstrated at 7 or 10 days at antigen concentrations of 10–30 μg/ml. As in other autoimmune disorders, the presence of autoantigen‐reactive T cells was also demonstrated in 5/10 healthy volunteers. Tissue typing revealed that all patients possessed HLA‐DR2 and/or ‐DR4 alleles, while normal individuals whose T cells responded possessed DR2 and/or DR7 alleles. The specificity of the T cell response in Goodpasture's disease was further investigated using monomeric components of human GBM purified by gel filtration and reverse phase high performance liquid chromatography (HPLC). Two antigenic monomer pools were obtained, which were shown by amino‐terminal sequence analysis to contain α3(IV)NC1 and α4(IV)NC1, respectively. In all patients tested, significant T cell proliferation was observed in response to one or both of these α(IV)NC1 domains. These results demonstrate that patients with Goodpasture's disease possess T cells reactive with autoantigens known to be recognized by anti‐GBM antibodies.
Two cases of systemic vasculitis complicated by microangiopathic haemolytic anaemia (MAHA) are described: this association has not previously been reported. Both patients had atypical presentations of their primary disease, one with parotitis and one with a Guillain-Barré syndrome. Other causes of MAHA were excluded and a possible link with macromolecular von Willebrands factor is speculated upon.
A 36-year-old male presented with a secondary, but anti-neutrophil cytoplasmic antibody (ANCA) (proteinase-3) positive, vasculitis with renal insufficiency due to a pauci-immune necrotizing glomerulonephritis. An infective process was initially excluded by blood cultures and an echocardiogram prior to immunosuppression. The patient's condition failed to improve and re-evaluation confirmed infective endocarditis requiring valve replacement. Subsequent tissue cultures identified Bartonella henselae. Antibiotic treatment led to full resolution of physical, biochemical and immunological markers. This is the first case of B. henselae endocarditis-associated ANCA positivity with a pauci-immune glomerulonephritis. It demonstrates the importance of revisiting standard investigations in patients not improving expectantly on conventional therapy.
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