Comparison of nephrotoxicity between two gadolinium-contrasts, gadodiamide and gadopentetate in patients with mildly diminished renal failure.

Although gadolinium (Gd)-based contrast media have been found to be nephrotoxic, their nephrotoxicity, and the dependence of nephrotoxicity on chelate types, have not been assessed in patients with normal or mildly diminished renal failure. This prospective, randomized study compared the nephrotoxicity of low doses of the nonionic Gd-based contrast medium gadodiamide (Omniscan®) and the ionic Gd-based contrast medium gadopentetate (Magnevist®) in patients with serum creatinine < 1.6 mg/dL. Patients aged 20 to 80 years, weighing 45 to 70 kg and with normal or < 1.6 mg/dL Serum-creatinine in the 3 months prior to undergoing magnetic resonance imaging (MRI) of brain, were enrolled. Patients were randomized to receive 0.1 mol/kg gadodiamide or gadopentetate. Serum-creatinine, serum cystatin-C, estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) formula, and estimated creatinine clearance rate (eCCr) using the Cockcroft-Gault formula were measured just before and 16-80 hr after MRI. Groups were compared statistically by Mann-Whitney U-tests and Wilcoxon signed-rank tests. There were no significant differences in clinical characteristics between the gadodiamide (n = 43) and gadopentetate (n = 59) groups. Serum-creatinine, eGFR and eCCr before and 16-80 hr after MRI did not differ significantly within either group or between the two groups. Serum cystatin-C was significantly higher 16-80 hr after than before MRI only in the gadodiamide group (0.79 ± 0.21 vs. 0.74 ± 0.14 mg/L, p = 0.028). The ionic contrast medium, gadopentetate, did not affect renal function during MRI, whereas the nonionic contrast medium, gadodiamide, affected renal function transiently.

Antigen-binding abilities of anti-nephrin antibody are prescribed by signal sequence of expression vector in genetic immunization.

BACKGROUND: Nephrin is an essential protein for maintaining the normal structure of podocyte foot processes and the glomerular filtration barrier. To analyze the mechanism of proteinuria and nephrotic syndrome, we previously reported on a new method of producing polyclonal anti-nephrin antibody by genetic immunization. In the present paper, we investigate the effect of signal peptide sequence cDNA on the characteristics of polyclonal anti-nephrin antibodies induced by genetic immunization. METHODS: Five fragments of nephrin cDNA with or without signal peptide sequence were inserted into the pTARGET™ vector. Rats were immunized with these vectors by the gene gun method. Sera obtained from rats at 14 weeks following immunization were analyzed by Western blotting, immunoprecipitation, flow cytometry and immunohistochemistry. RESULTS: Four different antibodies induced by cDNA encoding nephrin protein fragments without signal peptide showed antigen site-specific binding to fragmented glycosylation-disturbed nephrin proteins. These antibodies also reacted to a glycosylation-disturbed full-length nephrin protein (inhibited by tunicamycin), but did not react to either a native nephrin protein or a fully glycosylated conformational nephrin protein. Four different antibodies induced by cDNA encoding nephrin fragments with signal peptide showed an antigen site-specific binding to glycosylation-disturbed nephrin protein fragments. In addition, these antibodies reacted to both a native nephrin protein and a full-length glycosylated conformational nephrin protein. CONCLUSIONS: The absence of signal peptide sequence cDNA in the expression vector produced antibodies specific for glycosylation-disturbed proteins, while its presence produced antibodies that bound to native or fully glycosylated conformational protein.

[Irradiation for invasive malignant thymoma led a remission of refractory minimal change nephrotic syndrome: a case report].

A 46-year-old man was diagnosed as malignant thymoma, and was treated with chemotherapy and radiotherapy in 2003. On June 2004, he had edema of his legs and nephrotic syndrome (NS). As renal biopsy revealed a minor glomerular abnormality, he was diagnosed as minimal change nephrotic syndrome (MCNS). Intravenous steroid therapy of 500 mg/day for 3 days, following oral administration of 15 mg/day prednisolone and 75 mg cyclosporine twice a day was taken from July 2004. On July 2005, he went into remission of NS with 0.6 g/day proteinuria. On January 2008, NS relapsed with left pleural effusion. Chest CT and a biopsy specimen from left pleural mass lesion revealed the pleural invasion of malignant thymoma. Sixty Gray radiotherapy diminished the pleural metastatic lesion and also improved proteinuria from 6.6 g/day to 0.4 g/day. Though there have been a few case reports of MCNS concomitant with malignant thymoma, this is the first report that radiotherapy for metastatic malignant thymoma improved NS while diminishing the tumor.

Tosufloxacin tosilate-induced thrombocytopenic purpura.

Tosufloxacin tosilate, a member of the naphthyridine group, was developed in Japan and became commercially available in 1990. We experienced a 69-year-old male who developed thrombocytopenic purpura due to tosufloxacin tosilate. The diagnosis was made when similar symptoms (petechiae and thrombocytopenia) were induced by inadvertent challenge with tosufloxacin tosilate. In this paper, we report the first case of tosufloxacin tosilate-induced thrombocytopenic purpura and present a brief published work review.