Akhilesh Jaiswal

Differential alteration in peripheral T-regulatory and T-effector cells with change in P-glycoprotein expression in Childhood Nephrotic Syndrome: A longitudinal study.

INTRODUCTION Childhood Idiopathic Nephrotic Syndrome (INS) responds to glucocorticoid therapy, however, 60-80% of patients relapse and some of them become steroid non responsive. INS may occur because of T cell dysfunction, abnormal cytokines and podocytopathies which reverse on steroid treatment. The reason of relapses could be imbalances in T cells phenotypes and respective cytokines. Herein, we hypothesize that relapses in INS may occur due to imbalance in T-regulatory and T-effector cell with their respective cytokines and overexpression of P-gp on lymphocytes. METHODS The frequency of peripheral blood CD4(+)CD25(+)FoxP3(+) Treg, CD4(+)IFN-γ(+) Th1 and CD4(+)IL-4(+) Th2 lymphocytes and their respective cytokines and P-gp expression on peripheral blood lymphocytes (PBLs) were analyzed in INS patients at baseline (n=26), during remission (n=24) and at relapse (n=15). RESULTS Compared to baseline, the frequency of Tregs was significantly increased at remission and decreased during relapse. In contrast, the frequency of Th1 and Th2 lymphocytes was significantly decreased during remission and increased at the time of relapse. Similarly, expression of P-gp was significantly high at baseline and at the time of relapse as compared to remission. Levels of cytokines IL-10 and TGF-β in the supernatant of stimulated PBMCs was increased during remission and decreased during relapse. In contrast, levels of IFN-γ and IL-4 were decreased during remission and increased at the time of relapse. CONCLUSIONS Steroid therapy in INS induces decreased P-gp expression on PBLs along with increased frequency and cytokine response of T-regulatory cells, and reduced frequency and respective cytokine response of Th1 and Th2 cells during remission. However, reversal in the frequency and respective cytokines of T-regs, Th1 and Th2, and P-gp expression on PBLs occurs during relapses on follow-up.

Is basiliximab induction, a novel risk factor for new onset diabetes after transplantation for living donor renal allograft recipients?

It was found that, by affecting populations of T lymphocytes and regulatory T cells, basiliximab also indirectly affects pancreatic β‐cell function and glucose homeostasis.

Urinary Kidney injury molecule-1 can predict delayed graft function in living donor renal allograft recipients

Delayed graft function is an early complication leading to impaired creatinine clearance, urine formation and determinant of long term graft outcome. The aim of the present study was to determine the earliest predictive cut‐off value of uKIM‐1 level in patients with delayed graft function and acute tubular necrosis.

FGF23 is associated with early post-transplant hypophosphataemia and normalizes faster than iPTH in living donor renal transplant recipients: a longitudinal follow-up study

Background We aimed to longitudinally analyse changes in the levels of serum fibroblast growth factor 23 (FGF23), intact parathyroid hormone (iPTH) and associated minerals in patients undergoing renal transplantation. Methods Sixty-three patients with end-stage renal disease (ESRD) who underwent living donor transplantation were recruited. Serum FGF23, iPTH, uric acid, inorganic phosphorous (iP), blood urea nitrogen and serum creatinine were measured pre-transplant and at 1 (M1), 3 (M3) and 12 months (M12) post-transplantation. Results FGF23 levels were decreased at M1, M3 and M12 by 93.81, 96.74 and 97.53%, respectively. iPTH levels were decreased by 67.95, 74.95 and 84.9%, respectively. The prevalence of hyperparathyroidism at M1, M3 and M12 post-transplantation was 63.5, 42.9 and 11.1%, respectively. FGF23 and iP levels remained above the normal range in 23 (36.5%) and 17 (27%) patients at M1, 10 (15.9%) and 5 (8%) at M3 and in none at M12 post-transplantation, respectively. A multivariate regression model revealed that, pre-transplant, iP was positively associated with iPTH (P = 0.016) but not with FGF 23; however, post-transplant, iP level was negatively associated with FGF23 (P < 0.001) but not with iPTH. Conclusions Post-transplant FGF23 levels settle faster than those of iPTH. However, 11% of patients continued to have hyperparathyroidism even after 12 months.

Long-term outcomes of hepatitis C virus infected renal allograft recipients

Background and Aim: This study aims to study the long-term outcomes of hepatitis C virus (HCV)-infected renal allograft recipients, which is still debatable. Materials and Methods: In this study (study period - January 2003 to December 2013), we studied long-term outcomes of 106 living donor renal allograft recipients - 53 HCV-infected (33 genotype 3 and 20 genotype 1) and 53 age- and gender-matched HCV-noninfected patients. Results: Thirty-nine (73.6%) patients detected HCV positive during dialysis, while 14 (26.4%) before the start of dialysis. Forty (75.5%) patients were positive for both anti-HCV and HCV RNA, while 13 (24.5%) were HCV RNA positive and anti-HCV negative. Twelve and nine patients died among HCV positive and negative groups, respectively. Major cause of death was sepsis in both groups. Hepatic failure contributed to mortality in four HCV-positive patients, two of them also had graft failure. Patient and death noncensored graft survival rates at 1, 5, and 10 years of follow-up in HCV-positive group were 100% and 100%; 79.8% and 70.8%; 58.9% and 37.8%; respectively; and in HCV-negative group were 100% and 100%; 95.9% and 91.8%; 58.9% and 27.4%; respectively. Conclusions: The long-term survival of HCV-positive renal transplant recipients was not inferior to that of HCV-negative recipients.