The independent association between serum uric acid and graft outcomes after kidney transplantation.

BACKGROUND: Improving long-term outcomes of kidney transplantation depends on identifying novel risk factors that lead to poor outcomes. We sought to evaluate the predictive value of mean uric acid (UA) level during the first 6 months posttransplant for graft survival and function. METHODS: Two hundred twelve recipients of living donor kidneys transplanted during January 2000 to December 2001 were included. The study outcome included graft and patient survival and graft function at 1 year posttransplant. Regression models were used to adjust for the confounding variables including graft function during first 6 months. RESULTS: During 68.3 + or - 27.2 months follow-up, UA level (mg/dL) and hyperuricemia (n=45) were associated with graft loss (hazard ratio [HR]=1.26, P=0.026, 95% confidence interval [CI]=1.03-1.53, and HR=1.92, P=0.029, 95% CI=1.1-3.4, respectively) independent of graft function and other confounders. UA also seemed to be associated with risk of death with borderline significance (HR=1.2, P=0.096, 95% CI=0.97-1.46). Examining the predictive value for graft function, UA level and hyperuricemia were independent predictors of 1-year serum creatinine (beta=0.10, P=0.013, 95% CI=0.02-0.18, and beta=0.25, P<0.04, 95% CI=0.01-0.49, respectively). Similarly, both were associated with 1-year estimated glomerular filtration rate (beta=-3.9, P<0.001, 95% CI=-5.7 to -1.5 for UA, and beta=-7.6, P<0.02, 95% CI=-13.6 to -1.5 for hyperuricemia). Notably, these associations were all independent of renal function during first 6 months. CONCLUSION: The results of this study suggest that mean UA level during the first 6 months posttransplant is an independent predictor of long-term graft survival and short-term graft function. Further investigations are needed to evaluate its causal association with chronic allograft injury and cardiovascular disease.

A single center comparison of long-term outcomes of renal allografts procured laparoscopically versus historic controls procured by the open approach.

We have previously reported that renal allografts procured by the laparoscopic live donor nephrectomy (lapNx) demonstrate worse early renal outcomes but noninferior 1-year renal function as compared to those procured by the standard open nephrectomy (openNx). We undertook this study to examine whether the apparent early dysfunction will impair long-term renal allograft survival. We retrospectively updated the status of the first 132 consecutive adult left lapNx recipients at our center and the preceding 99 adult openNx recipients. With a mean follow-up of 5.8+/-2.0 years in lapNx and 8.7+/-3.3 years in openNx, we found that death-censored renal allograft survival was identical on univariate and multivariate analysis. Patient survival was worse (log rank P-value=0.048) in lapNx, but this finding did not persist in multivariate analysis. Combined graft-patient survival as well as 1-year mean serum creatinine levels were similar on univariate and multivariate analyses. We conclude that, despite having suffered early renal dysfunction, the lapNx cohort of renal allograft recipients enjoys similar long-term renal allograft survival as compared to openNx.

Corticosteroid withdrawal in kidney transplantation: the present status.

Corticosteroids (CS) have played a vital role in organ transplantation, both for prevention and treatment of allograft rejection. However, the use of CS is associated with a wide range of adverse effects. With advances in immunosuppressive drug therapy, attempts have been made to minimize the use of CS to avoid or alleviate their side effects. Withdrawal of CS months after transplantation has transitioned to days. In low to intermediate risk renal allograft recipients, use of induction therapy and modern maintenance drug combinations allows safe withdrawal of CS within the first week of transplantation. In other groups, existing potent maintenance agents permit tapering of CS to low doses over the first few months. Withdrawal of these small doses may not add to the benefits.

Anesthesia for patients with congenital long QT syndrome.

Long QT syndrome is a malfunction of cardiac ion channels resulting in impaired ventricular repolarization that can lead to a characteristic polymorphic ventricular tachycardia known as torsades de pointes. Stressors, by increasing sympathetic tone, and drugs can provoke torsade de pointes, leading to syncope, seizures, or sudden cardiac death in these patients. Beta blockade, implantation of cardioverter defibrillators, and left cardiac sympathetic denervation are used in the treatment of these patients. However, these treatment modalities do not guarantee the prevention of sudden cardiac death. Certain drugs, including anesthetic agents, are known to contribute to QT prolongation. After reviewing the literature the authors give recommendations for the anesthetic management of these patients in the perioperative period.