HYPERTENSION AFTER PANCREAS-KIDNEY TRANSPLANTATION: ROLE OF BLADDER VERSUS ENTERIC PANCREATIC DRAINAGE

Background. Recent reports suggest that hypertension may be less common after simultaneous pancreaskidney transplantation than after kidney transplantation alone. However, the mechanisms for this beneficial effect have not been delineated. We hypothesize that lower blood pressures may result from chronic volume depletion in patients with bladderdrained pancreatic allografts. Methods. We compared the incidence and severity of hypertension 12 months after transplantation in 79 bladder-drained pancreas-kidney recipients and 46 diabetic kidney-only recipients. These two groups were compared with a smaller group of enterically drained pancreas-kidney recipients. Blood pressure was also compared before and after surgical conversion from bladder to enteric drainage in 10 patients. Results. Hypertension was significantly less common and less severe after pancreas-kidney transplantation than after kidney transplantation alone, but the benefit of the pancreas transplant was evident only in bladder-drained patients. Logistic regression analysis of the bladder-drained pancreas-kidney patients confirmed the independent impact of the pancreatic allograft on the presence of hypertension, indicated an independent association with serum creatinine concentration and donor age, but suggested no correlation with recipient age, race, or number of rejection episodes. A comparison of blood pressures before and after pancreatic conversion from bladder to enteric drainage indicated no significant change in the prevalence or severity of hypertension. Conclusions. We conclude that the beneficial effect of a pancreas transplant on the prevalence and severity of hypertension after simultaneous pancreas-kidney transplantation is limited to bladder-drained patients. Although it is possible that the effect is mediated by chronic volume depletion, the observation that blood pressure does not increase after conversion from bladder to enteric drainage suggests that other factors may be involved. Hypertension occurs in more than 60% of renal transplant recipients and has been attributed to multiple factors including the presence of diseased native kidneys, acute and chronic allograft rejection, recurrence of original renal disease, transplant renal artery stenosis, and the effects of immunosuppressant drugs (1‐ 4). Recent reports suggest that the incidence of hypertension in diabetic patients after simultaneous pancreas-kidney transplantation (SPK) is lower than that observed in diabetics receiving a kidney transplant alone (KTA) (5, 6). However, the mechanisms accounting for the protective effect of the pancreatic allograft are not clear. Bladder drainage of the exocrine pancreas in SPK patients via a pancreaticoduodenocystostomy often is associated with urinary losses of sodium and bicarbonate leading to volume depletion and metabolic acidosis (7, 8). We hypothesized that chronic volume depletion in bladder-drained SPK patients accounts for the relatively low incidence of hypertension in this population of transplant recipients. In this study, we compared the prevalence and severity of hypertension in 79 consecutive SPK patients with bladder drainage of the exocrine pancreas to that of 46 consecutive type I diabetic patients receiving a KTA, and to a smaller number of SPK patients managed with primary enteric pancreatic drainage. We also studied the effects of elective bladder-to-enteric conversion of the exocrine pancreatic allograft on the prevalence and severity of hypertension.