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      Fulminant Emphysematous Pyelonephritis by Candida glabrata in a Kidney Allograft

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          Emphysematous pyelonephritis (EPN) is a rare and serious necrotizing infection that is potentially life-threatening. It has been seldom reported in kidney grafts and is usually caused by Gram-negative bacteria, with some case reports caused by anaerobic bacteria, and has been closely associated with poorly controlled diabetes mellitus (DM) and urinary tract structural abnormalities. There are no reports of EPN of fungal etiology in kidney grafts. We present a case of a 53-year-old kidney transplant recipient with a history of DM, active vesicoureteral reflux, and recurrent urinary tract infections who developed EPN in the kidney allograft caused by Candida glabrata, 3 weeks after starting treatment with empagliflozin, with an aggressive course that required urgent transplant nephrectomy.

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          Most cited references 31

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          Efficacy and Safety of Empagliflozin in Renal Transplant Recipients With Posttransplant Diabetes Mellitus

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            Caspofungin in the treatment of symptomatic candiduria.

            Because the urine concentrations achieved by echinocandin antifungal agents are low, drugs from this class are excluded from consideration when candiduria treatment is selected.
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              Characterization of echinocandin-resistant mutants of Candida albicans: genetic, biochemical, and virulence studies.

              The pneumocandins are potent antifungal agents of the echinocandin class which are under development for use as broad-spectrum antimycotic therapy. One important consideration for any new therapeutic class for treating serious fungal infections is the potential for drug resistance development. In this study we have isolated and characterized four independent spontaneous Candida albicans mutants resistant to the potent semisynthetic pneumocandin L-733,560. These mutants have many of the properties of FKS1/ETG1 echinocandin-resistant mutants of Saccharomyces cerevisiae, including (i) cross-resistance to other 1,3-beta-D-glucan synthase inhibitors, such as papulacandin and echinocandins, but no change in sensitivity to other antifungal agents; (ii) in vitro glucan synthase activity that is more resistant to pneumocandins than the wild-type parent enzyme; and (iii) semidominant drug resistance in spheroplast fusion strains. The mutants were compared with C. albicans echinocandin-resistant mutants isolated by mutagenesis by L. Beckford and D. Kerridge (mutant M-2) (abstr. PS3.11, in Proceedings of the XI Congress of the International Society for Human and Animal Mycology, Montreal, Canada, 1992) and by A. Cassone, R. E. Mason, and D. Kerridge (mutant CA-2) (Sabouraudia 19:97-110, 1981). All of the strains had resistant enzyme activity in vitro. M-2 grew poorly and had low levels of enzyme activity. In contrast, CA-2 and the spontaneous mutants grew as well as the parents and had normal levels of glucan synthase activity. These results suggest that these resistant mutants may have alterations in glucan synthase. CA-2 was unable to form germ tubes, an ability retained by the spontaneous mutants. The virulence of the spontaneous mutants was unimpaired in a mouse model of disseminated candidiasis, while M-2 and CA-2 were 2 orders of magnitude less virulent than their parent strains. Significantly, mice challenged with the spontaneous mutant CAI4R1 responded therapeutically to lower levels of L-733,560 than would he predicted by the increase in in vitro susceptibility.

                Author and article information

                S. Karger AG
                June 2020
                28 April 2020
                : 144
                : 6
                : 304-309
                aNephrology Department, Hospital Universitario Fundación Alcorcón, Madrid, Spain
                bInternal Medicine Department, Hospital Universitario Fundación Alcorcón, Madrid, Spain
                cNephrology Department, Hospital Clinico San Carlos, Madrid, Spain
                Author notes
                *Dr. Amir Shabaka, Servicio de Nefrología, Hospital Universitario Fundación Alcorcón, C/Budapest, 1, ES–28922 Alcorcón, Madrid (Spain),
                507259 Nephron 2020;144:304–309
                © 2020 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 3, Pages: 6
                Clinical Practice: Case Report


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