Diabetic Recipients (diabetic + recipient)

Distribution by Scientific Domains


Selected Abstracts


Diabetes Mellitus: A Risk Factor for Delayed Graft Function after Deceased Donor Kidney Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2010
J. Parekh
Early graft function is a major determinant of long-term outcomes after renal transplantation. Recently, recipient diabetes was identified as a risk factor for poor initial graft function in living donor renal transplantation. To further explore this association, we performed a paired analysis of deceased donor renal transplants from January 1994 to December 2005. A total of 25,523 transplant pairs were analyzed via conditional logistic regression. Diabetic recipients were older (53.16 vs. 46.75 years, p < 0.01), had a lower average panel reactive antibody (12% vs. 15%, p < 0.01) and fewer prior transplants (0.07 vs. 0.12, p < 0.01). Recipient diabetes, age, male gender, African American race, elevated peak panel reactive antibody and increased cold ischemia time were independent risk factors for delayed graft function. Specifically, diabetic recipients had increased risk of DGF on univariate analysis (odds ratio [OR] 1.32, 95% confidence interval [CI] 1.23,1.42, p < 0.01). Multivariable analysis confirmed this association but the risk differed by recipient gender; with diabetes having a greater effect in women (OR 1.66, 95% CI 1.45,1.91, p < 0.01) compared to men (OR 1.28, 95% CI 1.15,1.43, p < 0.01). It is unknown whether the deleterious impact of recipient diabetes on graft function after renal transplantation results from perioperative hyperglycemia or the chronic sequelae of diabetes. [source]


Allograft diabetic nephropathy may progress to end-stage renal disease

PEDIATRIC TRANSPLANTATION, Issue 4 2004
Moro O. Salifu
Abstract:, Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8,9) post-transplantation and increased to the nephrotic range (3.7,4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10,14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression. [source]


Diabetes Mellitus: A Risk Factor for Delayed Graft Function after Deceased Donor Kidney Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2010
J. Parekh
Early graft function is a major determinant of long-term outcomes after renal transplantation. Recently, recipient diabetes was identified as a risk factor for poor initial graft function in living donor renal transplantation. To further explore this association, we performed a paired analysis of deceased donor renal transplants from January 1994 to December 2005. A total of 25,523 transplant pairs were analyzed via conditional logistic regression. Diabetic recipients were older (53.16 vs. 46.75 years, p < 0.01), had a lower average panel reactive antibody (12% vs. 15%, p < 0.01) and fewer prior transplants (0.07 vs. 0.12, p < 0.01). Recipient diabetes, age, male gender, African American race, elevated peak panel reactive antibody and increased cold ischemia time were independent risk factors for delayed graft function. Specifically, diabetic recipients had increased risk of DGF on univariate analysis (odds ratio [OR] 1.32, 95% confidence interval [CI] 1.23,1.42, p < 0.01). Multivariable analysis confirmed this association but the risk differed by recipient gender; with diabetes having a greater effect in women (OR 1.66, 95% CI 1.45,1.91, p < 0.01) compared to men (OR 1.28, 95% CI 1.15,1.43, p < 0.01). It is unknown whether the deleterious impact of recipient diabetes on graft function after renal transplantation results from perioperative hyperglycemia or the chronic sequelae of diabetes. [source]


2202 Kidney Transplant Recipients with 10 Years of Graft Function: What Happens Next?

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2008
A. J. Matas
The ultimate goal of clinical transplantation is for the recipients to achieve long-term survival, with continuing graft function, that is equivalent to that of the age-matched general population. We studied subsequent outcome in kidney transplant recipients with 10 years of graft function. In all, 2202 kidney transplant recipients survived with graft function >10 years. For 10-year survivors, the actuarial 25-year patient survival rate for primary transplant living donor (LD) recipients was 57%; graft survival, 43%. For primary transplant deceased donor (DD) recipients, the actuarial 25-year patient survival rate was 39%; graft survival, 27%. The two major causes of late graft loss were death (with graft function) and chronic allograft nephropathy (tubular atrophy and interstitial fibrosis). The two major causes of death with function were cardiovascular disease (CVD) and malignancy. For nondiabetic recipients, the mean age at death with function from CVD was 54 13 years; for diabetic recipients, 53 7 years. By 20 years posttransplant, morbidity was common: >40% recipients had skin cancer (mean age for nondiabetic recipients, 53 13 years; for diabetics, 49 8 years), >10% had non-skin cancer (mean age for nondiabetic recipients, 53 16 years; for diabetics, 46 9 years), and >30% had CVD (mean age for nondiabetic recipients, 53 15 years; for diabetics, 47 9 years). We conclude that long-term transplant recipients have a high rate of morbidity and early mortality. As short-term results have improved, more focus is needed on long-term outcome. [source]


Prolonged Insulin Independence After Islet Allotransplants in Recipients with Type 1 Diabetes

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2008
M. D. Bellin
We sought to determine the long-term outcomes in type 1 diabetic recipients of intraportal alloislet transplants on a modified immunosuppressive protocol. Six recipients with hypoglycemia unawareness received one to two islet infusions. Induction therapy was with antithymocyte globulin (ATG) plus etanercept for tumor necrosis factor-, blockade. Recipients received cyclosporine and everolimus for maintenance immunosuppression for the first year posttransplant, with mycophenolic acid or mycophenolate mofetil subsequently substituted for everolimus. Recipients have been followed for 1173 270 days since their last infusion for islet graft function (insulin independence, hemoglobin A1c levels and C-peptide production) and for adverse events associated with the study protocol. Of the six recipients, five were insulin-independent at 1 year, and four continue to be insulin-independent at a mean of 3.4 0.4 years posttransplant. None of the six recipients experienced recurrence of severe hypoglycemia. Measured glomerular filtration rate decreased from 110.5 21.2 mL/min/1.73 m2 pretransplant to 82.6 19.1 mL/min/1.73 m2 at 1 year posttransplant. In conclusion, islet transplants restored insulin independence for a mean of >3 years in four of six recipients treated with ATG and etanercept induction therapy and with cyclosporine and, initially, everolimus for maintenance. Our results suggest this immunosuppressive protocol may allow long-term graft survival. [source]


Pancreas after living donor kidney transplants in diabetic patients: impact on long-term kidney graft function

CLINICAL TRANSPLANTATION, Issue 4 2009
Francois Kleinclauss
Abstract:, In this single-institution study, we compared outcomes in diabetic recipients of living donor (LD) kidney transplants that did vs. did not undergo a subsequent pancreas transplant. Of 307 diabetic recipients who underwent LD kidney transplants from January 1, 1995, through December 31, 2003, a total of 175 underwent a subsequent pancreas after kidney (PAK) transplant; 75 were deemed eligible (E) for, but did not receive (for personal or financial reasons), a PAK, and thus had a kidney transplant alone (KTA); and 57 deemed ineligible (I) for a PAK because of comorbidity also had just a KTA. We analyzed the three groups (PAK, KTA-E, KTA-I) for differences in patient characteristics, glycemic control, renal function, patient and kidney graft survival rates, and causes of death. Kidney graft survival rates (actuarial) were similar in the PAK vs. KTA-E groups at one, five, and 10 yr post-transplant: 98%, 82%, and 67% (PAK) vs. 100%, 84%, and 62% (KTA-E) (p = 0.9). The long-term (greater than four yr post-transplant) estimated glomerular filtration rate (GFR) was higher in the PAK than in the KTA-E group: 53 20 mL/min (PAK) vs. 43 16 mL/min (KTA-E) (p = 0.016). The patient survival rates were also similar for the PAK and KTA-E groups. We conclude that the subsequent transplant of a pancreas after an LD kidney transplant does not adversely affect patient or kidney graft survival rates; in fact, it is associated with better long-term kidney graft function. [source]