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Hyperuricemia [serum uric acid (SUA) >7.0 mg/dL] which is common in chronic renal diseases is associated with augmented vascular events. In addition to nonpharmacological therapy, hypouricosuric drugs reduce UA levels. The current study was a prospective observational study of six months duration November 2016 to April 2017 done to determine the efficacy of febuxostat in patients with hyperuricemia in chronic kidney disease (CKD) stage G3a to G5 and to correlate any association with reduction of hypertension, improvement in glomerular filtration rate (GFR), and reduction in comorbidities. The study was carried out at the Department of Nephrology, Owaisi Hospital and Research Center, Hyderabad. One hundred and ten patients were screened, of which 53 patients wherein stage G3a to G5 were recruited and SUA levels were obtained after inclusion criteria. SUA >6.0 in females and 7.0 in males were recruited. The drug febuxostat 40 mg was given once day to all patients with stage G3a to G5D with elevate uric acid levels >7.0 in males and more than 6.0 in females and three samples of UA were obtained monthly. The mean of GFR, blood pressure (BP), and SUA levels were obtained before and after the therapy. Of the 53 patients, males were 32 (60.3%), and females were 21 (39.6%). Mean age of the patients were 36.5 years. Mean UA levels before the start of febuxostat therapy were 8.6, and after adding febuxostat, it was 5.10 at the end of the third visit. The mean BP drop was 7.2 ± 2.1 mm in systolic BP (from 154-147 mm Hg) and diastolic BP drop was 93 ± 2.5 mm Hg (5.1 mm Hg). The mean GFR improved from 50.3 to 53.3 mL/min after the start of febuxostat. Febuxostat in asymptomatic CKD patients improves UA levels, BP and estimated GFR at low dose without any adverse events and no cardiac-related events.

Recurrence of FSGS in renal allo grafts is a major cause of graft loss. In this context, we tried to diagnose and classify FSGS in renal allografts. Indications for biopsy included graft dysfunction and/or proteinuria. Three hundred and sixty-three graft biopsies were studied over a period of 2 years. We classified FSGS into recurrent FSGS, new-onset primary FSGS and FSGS secondary to chronic humoral rejection, calcineurin inhibitor toxicity, and nephron loss and hyperfiltration injury. Twenty-four cases were diagnosed as FSGS, constituting 6.6%. Secondary FSGS was the most common FSGS in grafts in our study. Incidence of recurrent FSGS may not be accurate as pretransplant biopsy is available in very few cases.

Thrombotic microangiopathy (TMA) is a serious complication of renal transplantation. It is a morphological expression of various etiological factors. In a renal allograft, TMA can occur de novo or be a recurrent disease. The aim of this study was to analyze the etiological factors and observe the changing trends of TMA with respect to emerging new etiological factors. We evaluated 131 graft biopsies over a period of 2½ years (2010-2012). All the renal biopsies were formalin fixed, paraffin embedded. Twenty serial sections were studied. Stains routinely used were Hematoxylin and Eosin, Periodic Acid Schiff, Massons Trichrome and Silver Methenamine stains. C4d by immunohistochemical method was done on all graft biopsies. Incidence of TMA in our series was 9.1%. Out of the 12 cases, five were associated with calcineurin inhibitor toxicity, three were diagnosed as acute antibody-mediated rejection, and two were recurrent haemolytic uremic syndrome. One patient developed haemolytic uremic syndrome on treatment with sirolimus and one patient was cytomegalovirus positive on treatment with ganciclovir, developed haemolytic uremic syndrome during treatment course. This study describes a spectrum of etiological factors for thrombotic mciroangiopathy ranging from common cause like calcineurin inhibitor toxicity to rare cause like ganciclovir induced TMA.

Despite the endemic distribution of visceral leishmaniasis in certain parts of our country, there are only a few reports of this infection in renal transplant recipients. We report one renal transplant recipient from non-endemic area with visceral leishmaniasis and graft dysfunction that responded to treatment with stibogluconate. The infection should be considered in the differential diagnosis of a febrile transplant recipient with pancytopenia and allograft dysfunction.