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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.

Abstract. Infection rates in tunneled-cuffed catheters (TCC) are reported to be higher in immunocompromised patients. The purpose of this study was to evaluate TCC-associated infection rates in patients with HIV infection (HIV+). Data were collected in 40 HIV + patients and 41 controls (C), and in 118 TCC (HIV+, 58; C, 60) for 28,146 catheter days (HIV+, 16,227; C, 11,919). There were no significant differences in the TCC bacteremia rates (HIV+, 2.23 versus C, 2.53 per 1000 TCC days, P = NS) or in the TCC exit site infection rates (HIV+, 2.20 versus C, 2.24 per 1000 TCC days, P = NS) between the groups. The number of TCC removed due to infection was also similar, (HIV+ versus C: 17 versus 15%, P = NS). In the HIV+ group, the association of hepatitis B surface antigenemia with TCC exit site infection was dependent on the history of injection drug use. Black race was a significant risk factor for higher TCC exit site infection rates, whereas prophylactic antibiotic use and high CD4 count were significantly associated with lower TCC exit site infection rates. None of the factors significantly predicted bacteremia rate in either group (HIV+ or C). In comparison to controls, HIV+ patients had a fivefold increased risk of having a Gramnegative organism (P = 0.02) and a sevenfold increased risk of a fungal isolate (P = 0.08), although the latter finding was not statistically significant. HIV infection is not a significant risk factor for TCC-associated infection but is associated with a higher prevalence of Gram-negative and fungal species.

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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.