Search

Background: There are limited data on the outcome of transplant recipients with familial Mediterranean fever (FMF)-associated AA amyloidosis. The aim of the present study is to evaluate demographic, clinical, laboratory, and prognostic characteristics and outcome measures of these patients., Methods: Eighty-one renal transplant recipients with FMF-associated AA amyloidosis (group 1) and propensity score-matched transplant recipients (group 2, n = 81) with nonamyloidosis etiologies were evaluated in this retrospective, multicenter study. Recurrence of AA amyloidosis was diagnosed in 21 patients (group 1a), and their features were compared with 21 propensity score-matched recipients with FMF amyloidosis with no laboratory signs of recurrence (group 1b)., Results: The risk of overall allograft loss was higher in group 1 compared with group 2 (25 [30.9%] versus 12 [14.8%]; P = 0.015 [hazard ratio, 2.083; 95% confidence interval, 1.126-3.856]). Patients in group 1 were characterized by an increased risk of mortality compared with group 2 (11 [13.6%] versus 0%; P = 0.001 [hazard ratio, 1.136; 95% confidence interval, 1.058-1.207]). Kaplan-Meier analysis revealed that 5- and 10-year patient survival rates in group 1 (92.5% and 70.4%) were significantly lower than in group 2 (100% and 100%; P = 0.026 and P = 0.023, respectively). Although not reaching significance, overall, 5- and 10-year graft survival rates (57.1%, 94.7%, and 53.8%, respectively) in group 1a were worse than in group 1b (76.2%, 95%, and 77.8%, respectively; P = 0.19, P = 0.95, and P = 0.27, respectively)., Conclusions: AA amyloidosis is associated with higher risk of mortality after kidney transplantation. Inflammatory indicators should be monitored closely, and persistent high levels of acute-phase reactants should raise concerns about amyloid recurrence in allograft.

Background: Posttransplantation diabetes mellitus (PTDM) is a metabolic complication of renal transplantation. A high prevalence of DM has been recently reported in patients with chronic hepatitis C virus (HCV) infection in the nontransplant population. The aim of this study was to investigate possible factors that may have a role in the development of DM, including HCV infection in renal transplant recipients., Patients and Methods: This case-control study included 43 patients with PTDM (36 men, 7 women; mean age, 44+/-10 years) and 43 consecutive transplant patients who did not develop PTDM (30 men, 13 women; mean age, 37+/-11 years). Age, body mass index, high-dose steroid use, family history for DM and HCV, and presence of HLA-DR2, -DR3, and -DR4 were considered as possible factors for predicting PTDM., Results: Patients with PTDM were older (P=0.002) and had a higher prevalence of family history of DM (61% vs. 9%, P<0.001) and a higher rate of HCV seropositivity (72% vs. 37%, P=0.002; odds ratio = 1.94; 95% confidence interval = 1.26-2.98). The prevalence of pancreatic autoantibodies (anti-glutamic acid decarboxylase, islet cell antibody) was similar between patients with and without PTDM. In logistic regression analysis (r = 0.61, P<0.001), age, family history, and HCV infection were independent variables for predicting development of PTDM., Conclusion: HCV infection was associated with the development of PTDM, in addition to family history and increased age. The rate of autoantibodies against pancreatic cells was not increased in patients with HCV, which suggested that nonimmunologic mechanisms were likely to have a role in the pathogenesis of PTDM.

Increased QT dispersion (QTd), predicting patients with risk of malignant arrhythmia, have recently been reported in hemodialysis patients (HDp). In this prospective study, we aimed to investigate changes in QTd and signal averaged-ECG (SAECG) in HDp after transplantation. Twenty-seven HDp (M/F:18/9, mean age 30+/-8 years) and 24 controls (M/F:14/10, mean age 33+/-6 years) were included. All QT parameters (QTmax, Qtmin, and QTd) were increased in HDp. QTmax and QTd started to decrease at the first month after transplantation. Percentage change in QTd at the third month was significantly correlated with percentage change in LV mass index (r=0.45, P=0.04), serum calcium (r=-0.47, P=0.02) and intact parathyroid hormone (r=0.68, P=0.01). In multivariate regression analysis, only percent chance in LV mass index was retained as significant. As for analysis of SAECG, 4 of the 23 (17%) HDp has abnormal late potentials which disappeared after transplantation. HDp with LV hypertrophy had higher filtered-QRS duration compared to patients without hypertrophy (110+/-12 vs. 97+/-11 msec, P=0.01). It was concluded that increased QTd and presence of late potentials improved early after renal transplantation. These changes were mainly associated with the regression of the LV mass.

Background: The aim of this prospective randomized study was to compare the safety and efficacy of enalapril (E) and losartan (L) in the treatment of posttransplantation erythrocytosis and the effect of the ACE genotype on response to therapy., Methods: Twenty-seven (24 male and 3 female, mean age 34+/-8 years) renal transplant recipients with erythrocytosis were treated either with E (15 patients) (10 mg/day) or L (12 patients) (50 mg/day) for 8 weeks., Results: The hemoglobin levels were significantly decreased in the L (17.1+/-0.7 to 15.9+/-1.3 g/dl, P=0.01) and E groups (17.4+/-1.1 to 14.9+/-2.2 g/dl, P=0.001). Among the responders who discontinued treatment, there was a trend for longer time to relapse in the L group (7.38+/-3.75 months; 95% confidence interval: 0.03-14.7) compared with the E group (2.75+/-0.70 (95% confidence interval: 1.37-4.13) (P=0.11). Decrease in hemoglobin was more prominent with E compared with L (-3.26+/-0.65 vs. -1.70+/-0.39 g/dl, P=0.05). Decrease in hemoglobin levels between DD and non-DD genotype groups was similar (-2.0+/-1.5 vs. -1.7+/-2.3 g/dl, P=0.69)., Conclusions: Enalapril caused a greater decrease but faster relapse in hemoglobin levels compared with losartan in patients with posttransplantation erythrocytosis. The DD type polymorphism had no effect on response.

The frequency and clinical characteristics of plasmodium infection were reported in 420 renal transplant recipients who were followed in the Transplantation Unit and Out-Patient Clinic of the Medical School of Istanbul. Plasmodium infection was diagnosed in eleven (9 male, 2 female) of the 420 patients (2.6%). Ten of the patients were transplanted in India, and one in our institution. The mean duration between the transplantation and the diagnosis of malaria was 21.7 + 44.4 days in patients who were transplanted in India. All of the patients were taking triple immunosuppressive drugs (CsA, AZA, PRED). Plasmodium falciparum was diagnosed in 6 patients, P vivax in 1 patient and P malariae in 1 patient. Also mixed infection with P falciparum and P malariae was diagnosed in 3 patients. After definite diagnosis, the patients were hospitalized. Chloroquine phosphate plus primaquine phosphate was administered for P vivax infection, whereas chloroquine phosphate alone was given for P falciparum and P malariae infection as a first line antimalarial therapy. As a result of therapy, infection improved clinically and the plasmodia disappeared rapidly from the thick blood film in 10 of the patients. Severe hemolysis and acute renal failure developed in one patient, who improved after hemodialysis therapy and exchange transfusions. It was concluded that malaria is quite a frequent infection of transplant recipients who get their allografts from donors living in high-risk areas, and all transplant recipients having this kind of transplantations should be suspected and examined for malaria. This may help to diagnose and treat the complication in the early period, thus resulting in an improved prognosis for this potentially life-threatening complication of the posttransplant period.

We analyzed data on renal allograft recipients over a 27-year period in order to investigate the frequency, etiology, and outcome of pericarditis developing during the first two months following renal transplantation. Of the 1497 patients receiving renal transplants between 1963 and 1990, 34 patients developed 36 episodes of pericarditis and/or pericardial effusions, for an overall incidence of 2.4%. Pericarditis was attributed to uremia in 14 episodes, cytomegalovirus infection in three, both uremia and CMV infection in four, nonspecific bacterial infection in three, and tuberculosis and minoxidil therapy in one episode each. No etiologic diagnosis could be established in 10 episodes. No statistically significant differences were found between pericarditis and case-matched control patients considering demographic features, the number of immediately functioning grafts, the duration of posttransplant acute renal failure, the number of supportive dialysis days, pre- and postoperative CMV status of the patients, and pretransplant BUN and serum creatinine levels. There were more uremic-related complications (pulmonary edema, gastrointestinal bleeding, central nervous system symptoms) in the pericarditis group. Five allografts in the pericarditis group never functioned, versus only one in the control group. Three patients with pericarditis developed pericardial tamponade. Early diagnosis, close follow-up, and in the case of cardiac tamponade early invasive treatment, should improve the prognosis of this potentially life-threatening complication.