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Biomedical subjects

R Feingold

Publications and source records attributed to R Feingold.

4 recordsLinked to original sources
PubMed1990

Acute hyperuricemic nephropathy and renal failure after transplantation.

This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.

Adult↗
PubMed1989

Glomerular hemodynamics in cyclosporine nephrotoxicity following uninephrectomy.

Experiments were performed to determine the cause of the reduced glomerular filtration rate (GFR) in cyclosporine nephrotoxicity during compensatory renal growth. Sprague-Dawley rats were uninephrectomized and given daily injections of cyclosporine (30 mg/kg, i.m.) or vehicle (olive oil), and studied 7 or 14 days later. In cyclosporine treated rats GFR was lower seven days (1.34 +/- 0.10 vs. 1.68 +/- 0.07 ml/min) and 14 days (1.19 +/- 0.08 vs. 1.58 +/- 0.04, P less than 0.025) following uninephrectomy. Arterial blood pressure, cardiac output and renal blood flow (RBF) were not different in cyclosporine and control rats. Kidney mass increased to the same extent in cyclosporine and control rats. Micropuncture of the glomerular microcirculation in similarly prepared Munich-Wistar rats demonstrated low whole kidney GFR (1.10 +/- 0.07 vs. 1.55 +/- 0.13 ml/min, P less than 0.01), and single nephron GFR (31.07 +/- 2.27 vs. 42.36 +/- 2.47 nl/min, P less than 0.005) in cyclosporine treated rats as compared to controls. Single nephron plasma flow, afferent and efferent arteriolar resistance, the transglomerular hydrostatic pressure gradient, and arterial blood pressure were the same in both groups. The glomerular capillary ultrafiltration coefficient (Kf) was lower in cyclosporine treated rats compared to controls [0.039 +/- 0.002 vs. 0.075 +/- 0.013 nl/(sec.mm Hg), P less than 0.025]. We conclude that in this model of cyclosporine nephrotoxicity the low GFR is caused solely by a reduction in Kf, and that cyclosporine can reduce GFR without causing renal vasoconstriction.

Animals↗
PubMed1982

Effects of repeated, small aliquot, same donor transfusions of HL-A defined blood on prospective recipients.

A series of HL-A defined, nonrelated blood transfusions given in small aliquots from the same donor to prospective cadaveric and living-related donor recipients has been presented. The results to date show 100% kidney survival in this small series over a relatively short period of time. The rejections noted have been very mild, and easily reversed. Nonspecific antibodies appear to be produced by the recipients in response to the blood, and these antibodies seem to have no negative effect upon kidney survival. This method of small aliquot transfusion to produce the desired effect is cheaper, wastes less blood, is less likely to lead to a CMV or HAA infestation in the transfusion recipient, and appears to be a highly efficient method of producing the desired effect.

Blood Transfusion↗