Posttransplant proteinuria is associated with higher risk of cardiovascular disease and graft failure in renal transplant patients.

In this study, we sought to determine whether proteinuria after renal transplantation was associated with cardiovascular disease (CVD), patient survival, and long-term allograft survival. One hundred twenty-six patients included 102 males and 24 females of mean age 30.7 +/- 8.9 years. Their mean follow-up was 63.21 +/- 19.9 months. All patients were evaluated for CVD, namely, ischemic heart disease, cerebrovascular disease, and peripheral vascular disease. Proteinuria was defined as urinary protein >or=500 mg/d which persisted for >6 months after transplantation. We retrospectively examined pre- and posttransplant data, including sex, age at transplantation, smoking, pretransplant dialysis duration, donor status, number of acute rejection episodes, body mass index, systolic and diastolic blood pressure levels, lipid profile and other biochemical parameters, immunosuppressive regimens, as well as pulse steroid dose. Proteinuria was significantly associated with CVD (P = .001; RR = 6.43; confidence interval [CI] 2.15-19.22). Patients with proteinuria showed significantly lower graft survival rates than those without proteinuria (58.62% vs 80.41%; P = .02). The mean time to appearance of proteinuria was 14.1 +/- 11.4 months (range, 1-36 months). There was no significant association between proteinuria and patient survival. Patients with persistent proteinuria displayed a greater number of acute rejection episodes (1.20 +/- 1.17 vs 0.62 +/- 0.85; P = .004) and higher pulse steroid dosages (4380.0 +/- 3123.4 vs 2800.0 +/- 2766.7; P = .022). In conclusion, persistent proteinuria is a strong risk factor for CVD among renal transplant patients. Therefore, an etiologic search and antiproteinuric strategy should be considered routinely to improve patient and graft outcomes.

Renin-angiotensin system polymorphisms: a risk factor for progression to end-stage renal disease in vesicoureteral reflux patients.

Aim. Renin-angiotensin system (RAS) gene mutations have been implicated as a risk factor for the presence and progression of renal disease in vesicoureteral reflux (VUR). However, the results are contradictory, and the effects of RAS polymorphisms in VUR patients with end-stage renal disease (ESRD) have not been defined yet. This study was designed to evaluate the angiotensin-converting enzyme insertion/deletion (ACE-I/D), angiotensinogen (AGT) M235T, and angiotensin II receptor type 1 (ATR1) A1166C and type 2 (ATR2) C3123A gene polymorphisms as risk factors for progression to ESRD in patients with VUR. Methods. ACE-I/D, AGT-M235T, ATR1-A1166C, and ATR2-C3123A were identified in 161 ESRD patients (52 female, 109 male; 77 renal transplant, 84 dialysis; age: 34.4 +/- 11.2 years). VUR was the ESRD etiology in 40 patients. Genetic polymorphisms of the ACE gene I/D, AGT gene M235T, ATR1 gene A1166C, and ATR2 gene C3123A were identified in all of the patients. Results. We detected no linkage between genetic polymorphisms of ATR1-, ATR2-, AGT-, and VUR-related ESRD. When ACE gene was considered, VUR(+) patients had 63.6% DD, 36.4% ID, and no II alleles, whereas VUR(-) patients had 48.6% DD, 43.2% ID, and 8.1% II alleles. Conclusion. A striking feature of VUR-related ESRD patients was the absence of II alleles, so the DD genotype may be accepted as a genetic susceptibility factor for progression to ESRD in VUR patients.

Diagnostic pitfalls in the evaluation of fine needle aspiration cytology of the thyroid: correlation with histopathology in 260 cases.

OBJECTIVES: Fine needle aspiration cytology (FNAC) of the thyroid is a non-invasive, cost-effective screening procedure that is valuable for distinguishing neoplastic lesions from non-neoplastic nodules. The aim of this study was to determine the diagnostic accuracy of FNACs performed at our institution by correlating FNAC results with histopathological diagnoses. METHODS: Two hundred and seventy-one aspiration cytology specimens followed by thyroidectomy were included in the study, and the results of 260 adequate FNACs were compared with their histological diagnoses. RESULTS: The sensitivity and specificity of thyroid FNAC for detecting neoplasia were 92.6% and 91.6%, respectively. There were 15 (5.7%) false positives and six (2.3%) false negatives. CONCLUSIONS: The results showed that follicular cells that exhibit some of the features of papillary carcinoma could be observed in a cytology slide of Hashimoto's thyroiditis, leading to a diagnostic pitfall. In addition, cellularity and overlapping cytological criteria in hyperplasia might lead to a false diagnosis.

Muscular and condylar response to rapid maxillary expansion. Part 1: electromyographic study of anterior temporal and superficial masseter muscles.

INTRODUCTION: In this prospective clinical study, we investigated the effects of rapid maxillary expansion (RME) on the electromyographic (EMG) activities of the anterior temporal and superficial masseter muscles. METHODS: The sample included 18 subjects (11 girls, 7 boys; mean age, 12.54 years) with unilateral or bilateral posterior crossbites involving 3 or more posterior teeth. There was no control group in this study because of the short observation period. The EMG activity was recorded simultaneously from both muscles during swallowing a sip of water and unilateral gum chewing. RESULTS: The mean EMG (mEMG) activities of the right and left anterior temporal muscles showed no statistically significant difference during swallowing and unilateral chewing. The mEMG activities of the right and left masseter muscles showed a statistically significant difference at unilateral chewing (P <0.01). There were a decrease of the mEMG activities for both muscles after RME and an increase during the observation period for unilateral chewing (P <0.05). Swallow-related mEMG activities of both muscles showed increases after RME and during the observation period (P <0.05). CONCLUSIONS: RME affected the EMG activities of the anterior temporal and superficial masseter muscles during swallowing and unilateral chewing. These findings suggest that the alterations in the EMG activities of these muscles should be considered in both the treatment and the the stability of maxillary transverse deficiencies.

Muscular and condylar response to rapid maxillary expansion. Part 2: magnetic resonance imaging study of the temporomandibular joint.

INTRODUCTION: In this prospective clinical study, we used bilateral temporomandibular joint (TMJ) magnetic resonance images (MRIs) to investigate the condylar response to rapid maxillary expansion (RME). METHODS: Bilaterial MRIs of the TMJs of 18 subjects (11 girls, 7 boys; mean age, 12.54 years; range, 9.75-14.8 years) were assessed. All subjects had unilateral or bilateral posterior crossbites involving 3 or more posterior teeth. There was no control group because of the short observation period. The MRI protocol included closed-mouth parasagittal proton density weighted spin echo and fat-suppressed short T1 inversion recovery sequences. The MRIs were taken before treatment (Tx 1), and at 6 weeks (Tx 2) and at 18 weeks (Tx 3) after treatment. Alterations in the signal intensities of the TMJ region were examined visually by a radiologist who was blinded to the subjects' characteristics. RESULTS: Increased signal intensities appeared as bright areas on the MRIs, indicating red bone marrow edema that is a sign of condylar remodeling. There were no bright areas in the condylar regions at Tx 2 in the 36 TMJs. Bright areas at the condylar region were observed both in proton density and fat-suppressed spin echo sequences at Tx 3 in 32 TMJs. Twenty-two TMJs had bright areas localized at the condylar head, and 10 TMJs had bright areas that extended through both the condyle and the mandibular ramus. No bright areas were seen at Tx 2 or Tx 3 for 4 TMJs. CONCLUSIONS: A condylar response to RME was observed in 32 TMJs at 18 weeks after expansion. Both the extensive orthopedic and the functional occlusal forces associated with RME have roles in condylar and ramal responses.

Muscular and condylar response to rapid maxillary expansion. Part 3: magnetic resonance assessment of condyle-disc relationship.

INTRODUCTION: The aim of this prospective study was to assess temporomandibular joint (TMJ) condyle-disc positions at the sagittal and coronal planes of magnetic resonance images (MRIs) before and after rapid maxillary expansion (RME). METHODS: The study included 18 subjects (11 girls, 7 boys) with a mean age of 12.54 years with unilateral or bilateral posterior crossbite that included at least 3 posterior teeth. The clinical and radiographic assessments of the TMJ were done before (T1) and 18 weeks after (T2) RME. A Haas-type expansion appliance was used for an average treatment time of 3.5 weeks. RESULTS: A visual MRI analysis of pretreatment condyle-disc positions showed that 8 TMJs had medial disc displacement, 3 had anteromedial disc displacement, and 2 had lateral disc displacement. The disc positions remained unchanged at T2 except in 1 subject, who developed unilateral anterior disc displacement. Unilateral joint sounds developed in 3 subjects without changes in the disc positions. CONCLUSIONS: Posterior crossbite can be considered a minor risk factor for temporomandibular disorder (TMD). RME is neither a risk factor nor a prevention for TMD. Coronal MRIs contribute complementary information for optimal diagnosis of TMD.

Impact of hepatitis serology on development of leukopenia after solid organ transplantation.

BACKGROUND: Homologous organ transplantation is an accepted therapeutic modality for end-stage disease of the kidney and liver. In posttransplantation periods leukopenia is a common problem with a wide range of differential diagnoses. Not only can it lead to an increased incidence of infections, but preclude the use of adequate immunosuppressive therapy and antimicrobial regimens because of their potential leukopenic side effects. One reason for leukopenia is viral hepatitis, which is frequently seen in transplant recipients. Herein this report, we searched for the relationship of leukopenic bouts among kidney and liver transplantation recipients to hepatitis serology. METHODS: We retrospectively evaluated the records of 569 patients who received solid transplants between January 1996 and October 2006. Because 27 patients did not come for follow-up examinations, their data were excluded, and 14 patients had 2 transplantations, yielding 556 primary transplantation cases for leukopenic attacks. RESULTS: Leukopenic attacks showed a strong relationship with hepatitis B virus (HBV) infection, but were independent of HBV DNA status (P = .002). No relationship with hepatitis C virus (HCV) infection status was found. CONCLUSIONS: Leukopenia is a common, important complication that can be seen during the posttransplantation period of recipients affecting both mortality and morbidity. HBV infection is a risk factor for development of leukopenia after transplantation. Adequate treatment of HBV infection in transplant recipients is important to obtain leukocyte counts in the normal range, allowing easier and safe antibacterial and immunosuppressive therapy in the posttransplantation period.

Relevant histopathologic findings that distinguish acute cellular rejection from cholangitis in hepatic allograft biopsy specimens.

BACKGROUND AND AIM: Histopathologic differential diagnosis of acute cellular rejection (ACR) and cholangitis continue to pose important problems following liver transplantation. The purpose of the present study was to evaluate the histopathologic features of ACR versus cholangitis. METHODS: The following variables were evaluated among 36 hepatic allograft biopsy specimens, consisting of 21 with ACR (group 1) and 15 with cholangitis (group 2) for ductal neutrophilic infiltration, presence/density of portal eosinophilia, centrilobular necrosis, central/portal vein endothelialitis, pericentral inflammation, hepatocyte ballooning, hepatocanalicular/ductular cholestasis, hepatocyte apoptosis, lobular inflammation, ductular proliferation, periductal fibrosis/edema, ductular epithelial damage, and portal inflammation. Only the first biopsy samples of the ACR group were included in this study. RESULTS: The incidences of ductal neutrophilic infiltration (93.3% vs 19%), hepatocanalicular cholestasis (86.7% vs 47.6%), ductular cholestasis (60% vs 0%), ductular proliferation (93.3% vs 4.8%), and periductal fibrosis/edema (93.3% vs 19%) were significantly greater in group 2 than group 1 (P < .05). In contrasts the incidences of portal eosinophilia (mean +/- SD, 3.37 +/- 3.9 vs 0.73 +/- 0.8), dense portal eosinophilia (mean +/- SD, 0.33 +/- 0.31 vs 0.11 +/- 0.16), central vein endothelialitis (0% vs 57.1%), portal vein endothelialitis (20% vs 95.2%), apoptosis (40% vs 71.4%), and necroinflammation (0% vs 90.5%) were significantly higher in group 1 (P < .05). The other parenchymal histopathologic changes and features of portal inflammation were similar in the 2 groups. CONCLUSION: In the differential diagnosis, ductal changes (cholestasis, neutrophilic infiltration, proliferation, and periductal fibrosis/edema) favor cholangitis, whereas the presence and density of portal eosinophilia favor ACR. Portal inflammation is not a distinctive morphological finding.

Relationship of preoperative venous and arterial imaging findings to outcomes of brachio-basilic transposition fistulae for hemodialysis: a prospective clinical study.

PURPOSE: To evaluate the maturation and patency of transposed brachio-basilic fistulae that had been chosen based on the results of preoperative imaging techniques. METHODS: Among 215 patients admitted to our clinic requiring arteriovenous fistulae between May 2004 and September 2005, 59 were scheduled for a transposed brachio-basilic fistula procedure. The relationship between demographic data, laboratory values, invasive and noninvasive imaging studies with patency and maturation time of the fistulae were evaluated by univariate analyses. RESULTS: Primary and secondary patency rates were 82% and 97% at 6 months 72% and 92% at one year respectively. The only parameter found to affect maturation time was basilic vein diameter. The maturation time was 59.3+/-22.3 days (range 32-92 days) for veins less than 3mm in diameter and 24.7+/-4.4 days (range, 21 to 34 days) for those with larger diameters. The number of previously failed fistulae correlated with a decrease in primary patency time. The primary patency rate at 1 year was 58.9% for patients whose preoperative arterial flow rate was below 70cm/sec, while it was 93.3% when the flow was greater. CONCLUSION: We believe that this type of fistula should be the first option in patients in whom the cephalic vein is inappropriate for a vascular access. Preoperative evaluation of the arterial system as well as a history of previous access failure may be considered predictive parameters for the patency of the fistulae.

Malnutrition inflammation score is associated with coronary artery disease in hepatitis C virus-infected hemodialysis patients.

OBJECTIVE: Hepatitis C virus (HCV) infection exerts diverse effects on atherogenesis. We investigated whether malnutrition inflammation score (MIS) is associated with the presence of coronary artery disease (CAD) in anti-HCV-positive hemodialysis (HD) patients. SUBJECTS/METHODS: Twenty-two anti-HCV-positive HD patients with CAD and 61 anti-HCV-positive HD patients without CAD (as controls) were included. Data were obtained from hospital records, patients were evaluated for risk factors for CAD. The same physician performed MIS evaluation. RESULTS: MIS of anti-HCV-positive HD patients with CAD were significantly higher than patients without CAD (8.8+/-4.0 vs 6.5+/-2.6, P=0.02). In patients with CAD, basal (P=0.002) and peak C-reactive protein (P=0.03) and serum ferritin (P=0.01) concentrations were higher, serum albumin concentrations (P=0.003) were lower than those patients without CAD. MIS was positively correlated with age (r=+0.359, P=0.001) and viral load (r=+0.629, P<0.0001). In univariate logistic regression analysis, advanced age (odds ratios (OR)=1.093, confidence interval (CI): 1.039-1.150, P=0.001), hypertension (OR=3.143, CI: 1.084-9.116, P=0.035), diabetes mellitus (OR=5.344, CI: 1.343-21.269, P=0.017), low triglyceride (OR=0.992, CI: 0.984-0.999, P=0.026) and high MIS (OR=1.259, CI: 1.066-1.488, P=0.007) were associated with the presence of CAD. Multivariate logistic regression analysis identified age (OR=1.090, CI: 1.007-1.179, P=0.033) and MIS as the factors associated with the presence of CAD (OR=1.232, CI: 1.004-1.511, P=0.04). CONCLUSIONS: MIS may be associated with CAD in anti-HCV-positive HD patients.

Pretransplantation systolic blood pressure and the risk of delayed graft function in young living-related renal allograft recipients.

Delayed graft function (DGF) is associated with decreased long-term renal allograft survival, however, the entire mechanism of action of DGF has not yet been established. The goal of this study was to determine possible risk factors for DGF in young living-related renal allograft recipients. We retrospectively analyzed the outcome of 142 renal transplant recipients (115 men and 27 women; mean age, 29.7 +/- 9.43 years; 114 living-related donors and 28 cadaveric donors). Data recorded for each patient and donor included gender, age at transplantation, duration of pretransplantation dialysis (recipients only), body mass index, number of human leucocyte antigen mismatches, panel-reactive antibodies, donor creatinine clearance, body weight, systolic and diastolic blood pressure levels, lipid profile, and biochemical parameters. Having obtained the transplant from a cadaveric donor (P<.000, odds ratio [OR]=17.556, confidence interval [CI]=5.961-51.743) and a pretransplantation systolic blood pressure level in the recipient of <120 mm Hg (P<.021, OR=3.600, CI=1.214-10.672) were possible risk factors for DGF. When only living-related recipients were considered, the systolic blood pressure level was significantly associated with DGF. We concluded that a pretransplantation systolic blood pressure level <120 mm Hg is a risk factor for DGF and that preoperative blood pressure control and intervention may help to decrease the risk of DGF.

Serum C-reactive protein surge in renal transplant recipients: link with allograft survival.

The restoration of kidney function by transplantation improves the common finding of chronic inflammation in patients with end-stage renal disease (ESRD). The C-reactive protein (CRP) level is a reliable marker of inflammation in renal transplant recipients. We analyzed the predictive value of posttransplant CRP surges on renal allograft survival among 141 ESRD patients who underwent renal transplantation between May 1999 and September 2001 at our institution. Twenty-seven cadaveric and 114 living donors were also studied. The subjects' demographic, clinical, and laboratory data were recorded. The renal transplant recipients were divided into three groups defined by the type of serum CRP surge: a normal, intermittently high, or consistently high serum CRP concentration. Renal allograft survival rates were 90.0% among recipients with normal serum CRP concentrations, 72.6% among those with intermittently high concentrations, and 11.1% in those with consistently high concentrations. A Cox regression analysis of factors that affect allograft survival showed that acute rejection, advanced recipient age, and consistently high serum CRP concentrations were associated with a high risk of renal allograft loss. Intermittent elevations in the serum CRP level were not associated with an increased risk of allograft loss, according to the Cox regression model. We concluded that consistently high serum CRP concentrations in renal allograft recipients showed a high negative predictive value for renal allograft survival. In recipients who exhibited ongoing inflammatory process in the 5-year posttransplant period, additional efforts are necessary to manage inflammation and therefore prolong renal allograft survival.

Early onset proteinuria after renal transplantation: a marker for allograft dysfunction.

The objective of this study was to determine whether early proteinuria after renal transplantation affected long-term allograft survival. The 130 patients included 105 men and 25 women of overall mean age, 29.6 +/- 9.6 years. There were 105 living related and, 25 cadaveric donor transplants. Proteinuria was defined as a level in of more than 300 mg/d. Donor and recipient age at transplantation, duration of pretransplant dialysis, donor type (living related or cadaveric), the presence of delayed graft function or acute rejection, panel-reactive antibodies, the number of human leukocyte antigen mismatches, and the systolic blood pressure level were retrospectively recorded for the study subjects. Cox regression analysis was used to determine the effects of proteinuria on allograft survival. Patients with proteinuria demonstrated significantly lower graft survival rates than did those without proteinuria (54.17% vs 82.62%, respectively; P<.002). Proteinuria at the third month after transplantation (P<.004, odds ratio [OR]=3.26, confidence interval [CI]=1.46 to 7.29), donor age (P<.001, OR=1.06, CI=1.02 to 109), and panel-reactive antibodies (P<.041, OR=1.06, CI=1.00 to 1.12) were significantly associated with decreased allograft survival. Early proteinuria after renal transplantation was indicative of a high risk for allograft dysfunction. A reduction of proteinuria may be associated with improved graft survival.

The association between cytomegalovirus infection and atherosclerotic events in renal transplant recipients.

Cytomegalovirus (CMV) infection is a risk factor for arteriosclerosis in renal transplant recipients. We sought to investigate the effects of CMV infection on atherosclerotic events (AE) in renal transplant recipients. This retrospective analysis included 200 patients: 52 women and 148 men of overall mean age of 36.18 +/- 10.23 years who were transplanted at our center between 1998 and 2001. We analyzed demographic features, dialysis duration, diabetes, blood pressure level, body mass index (BMI), medications, and lipid parameters. CMV infection was diagnosed in 23.5% of patients in the first 2 years after transplantation; these patients were followed for 4 years. All patients had been assessed for AE, including previous myocardial infarction, angina, revascularization procedures, intermittent claudication, stroke, or transient ischemic attack. AE occurred in 13% during the follow-up period. CMV infection was more frequent among these patients compared to those without AE, namely 42.3% versus 20.6%, respectively. Although the gender, dialysis duration, serum cholesterol level, presence of acute rejection, and BMI were not associated with AE, age, hypertension, and CMV infection did show a relation. A multivariate analysis by logistic regression revealed mean age and CMV infection to be independent risk factors for AE: odds ratio (OR)=5.6, 95% confidence interval (CI)=1.3 to 24.6 (P=0.02) and OR=4, 95% CI = 1.3 to 12.3 (P=.01). This study suggested that the presence of CMV infection may be a triggering factor for AE in renal transplant recipients.

Is uric acid a predictive factor for graft dysfunction in renal transplant recipients?

Hyperuricemia is a common complication in renal transplant recipients, and uric acid (UA) may play a role in renal dysfunction. The aim of this study was to evaluate the effects of UA on chronic allograft nephropathy (CAN) in renal transplant recipients. The 133 study subjects included 34 women and 99 men of overall mean age of 34.7 +/- 9.9 years. They underwent renal transplantation between 1998 and 2000. Serum UA levels were measured in the first month after transplantation and then at yearly intervals throughout a 3-year follow-up. In the first month after transplantation, 55.3% of recipients had hyperuricemia (UA >7 mg/dL in men; UA >6 mg/dL in women), but, 3 years after transplantation, 84.6% of the subjects had that disorder (P<.001). CAN was diagnosed in 31.5% of the patients at a mean onset of 31.8 +/- 14.3 months after transplantation. Fifty-two percent of these individuals experienced graft failure within 43.3 +/- 20.8 months after transplantation. UA levels were recorded before the development of CAN. There was no association between UA levels and CAN according to a Cox regression analysis (P>.05; relative risk, 1.082; 95% confidence interval [CI] 0.9-1.3). We concluded that the prevalence of hyperuricemia was higher among recipients than in healthy individuals, but that the UA level did not affect the development of CAN during first 3 years after transplantation.

Additional effect of hyperparathyroidism on inflammatory status and rHuEPO requirements in hemodialysis patients.

BACKGROUND: The aim of this study was to analyze the effects of elevated parathyroid hormone (iPTH) and C-reactive protein (CRP) on rHuEPO requirements and associated clinical and biochemical parameters of hemodialysis patients. METHODS: A total of 127 hemodialysis patients were included. Laboratory values from the previous 3 months (monthly measured CRP, iPTH, albumin, prealbumin, calcium, phosphorus, and hemoglobin) and clinical findings (rHuEPO requirements, iron supplements, Kt/V) were recorded retrospectively. Patients were subgrouped according to presence of hyperparathyroidism (mean iPTH > 350 pg/mL) and chronic inflammation (mean CRP > 8.5 mg/L) as group I (low iPTH, low CRP, n = 32), group II (high iPTH, low CRP, n = 32), group III (low iPTH, high CRP, n = 32), and group IV (high iPTH, high CRP, n = 31). RESULTS: We found that group IV had lowest hemoglobin (P < .0001, .0001, .01, respectively), albumin (P < .0001), prealbumin (P < .0001, .0001, .02, respectively), and highest rHuEPO requirements (P < .0001, .0001, .01, respectively) compared to other groups despite of similar iron indices. Group III also had lower albumin (P < .002, .0001, respectively), prealbumin (P < .001, .01, respectively), hemoglobin (P < .001, .005, respectively), but higher rHuEPO requirements (P < .01) compared to group I and group II. CONCLUSIONS: We propose that hyperparathyroidism increases rHuEPO requirements and aggravates the negative effects of chronic inflammation in hemodialysis patients.

1,25-dihydroxyvitamin D(3) therapy is protective for renal function and prevents hyperparathyroidism in renal allograft recipients.

1,25-Dihydroxyvitamin D(3) (calcitriol) therapy has been extensively used for posttransplant osteoporosis. Beside its effect on bone metabolism, calcitriol has an important immunomodulatory effect. We evaluated the effects of oral calcitriol therapy on allograft function and parathyroid hormone levels after renal transplantation. The patients were retrospectively selected from a renal transplant patient population who received calcitriol (group 1, n = 59, 36 male/23 female, follow-up: 52.8 +/- 12.2 months) compared with group (group 2, n = 52, 42 male/9 female, follow-up: 62.0 +/- 24.4 months) without calcitriol therapy after renal transplantation. Calcitriol therapy was started 24.0 +/- 19.1 months posttransplantation. All patients were under three-drug immunosuppression. The pretransplant and posttransplant data were studied retrospectively. Additionally, creatinine levels before and after the initiation of calcitriol therapy were recorded at 6 months intervals for 3 successive years. Our results were analyzed according to the first and third year on therapy data. According to the first year data, there were no differences in patient groups in terms of creatinine and iPTH levels. In the third year, the patients in group 1 showed significantly lower creatinine (P = .01) and iPTH (P < .04) levels and needed lower pulse steroid doses (P < .04). According to a Friedman repeated measures variance test, the creatinine level was significantly lower among group I (P < .04) at 3-year follow-up. In conclusion, even a delayed start of calcitriol therapy after renal transplantation exerts a protective effect on renal allograft function and prevents the development of hyperparathyroidism.

Predictors of vascular access thrombosis among patients on the cadaveric renal transplantation waiting list.

Acute thrombotic complications remain a constant, proportionally increasing complication before and after renal transplantation. We sought to investigate predictors for a prothrombotic state that increased the risk of vascular access thrombosis, among chronic renal failure patients during the waiting period prior to cadaveric renal transplantation. Chronic renal failure patients awaiting cadaveric renal transplantation and followed between January 2002 and January 2005 were included in this study. The 109 subjects including, 61 females and 48 males of mean age: 47.4 +/- 12.9 years; There were 36 continuous ambulatory peritoneal dialysis and 73 hemodialysis patients. Serum albumin, prealbumin, CRP, d-dimer, fibrinogen, antithrombin III, anticardiolipin antibodies (immunoglobulins G and M), homocystein, vitamin B12, folic acid, total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total platelet count were measured in each patient. Factor V Leiden, prothrombin 20210, ACE and MTHFR gene mutations were studied in all patients. Vascular Access thrombosis was detected in 62 patients. During follow-up 31 of 109 patients died. Vascular access thrombosis occurred in 78 patients who survived and 31 who died. The patients who died showed a significantly higher rate of thrombosis than those who survived (P = .003, OR: 4.61, CI: 1.70 to 12.50). Among the above biochemical risk factors, multiple regression analysis and backward logistic analysis revealed that d-dimer was the strongest biochemical predictor of thrombosis (P = .013, RR: 17.8). Upon evaluation of genetic risk factors, only factor V Leiden mutation was related to vascular access thrombosis (P = .001). In conclusion, the presence of vascular access thrombosis is a risk factor for mortality during the waiting period for cadaveric renal transplantation. As patients with factor V Leiden mutation or high serum d-dimer levels are at high risk for vascular access thrombosis, we recommend close monitorizing of these patients and use of anticoagulant therapy during the waiting period prior to renal transplantation.

Risk factors for development of posttransplant diabetes mellitus in renal transplant recipients.

Diabetes mellitus appearing after kidney transplantation--posttransplant diabetes mellitus (PTDM)--is a common complication associated with poor graft and patient survival. The purpose of the current study was to determine the risk factors for developing PTDM in 204 renal transplant recipients who had been followed for at least 30 months. Posttransplant diabetes mellitus was diagnosed according to the American Diabetic Association/WHO criteria, or a requirement for insulin, an oral hypoglycemic agent, or both. Analyses of possible risk factors for PTDM included demographic features, dialysis and posttransplantation duration, smoking, body mass index, medications, co-morbid diseases, HLA mismatches, as well as laboratory metrics of serum creatinine, albumin, calcium, phosphorus, C-reactive protein, parathyroid hormone, and lipid profiles. Twenty-six patients displayed PTDM. Univariate analysis showed that older age, greater body mass index, presence of hepatitis C virus (HCV) infection, and smoking at the time of renal transplantation were associated with PTDM development. In a multivariate analysis, HCV infection, smoking, and patient age at the time of transplantation were independent risk factors for PTDM. In conclusion, the presence of HCV infection or a smoking habit in addition to older age at the time of transplantation were the main predictors for developing PTDM. Patients should be closely followed regarding their smoking habit and weight gain as modifiable risk factors for PTDM.

Posttransplant diabetes mellitus: Impact of good blood glucose regulation on renal transplant recipient outcome.

Posttransplant diabetes mellitus (PTDM) is a frequent complication among renal transplant recipients. This study sought to compare clinical outcomes of patients with PTDM who had strict glucose control with nondiabetic patients and to identify risk factors for atherosclerotic disease in both groups. We retrospectively examined 204 renal allograft recipients transplanted at our center between 1996 and 2002. Demographic features, dialysis and posttransplantation duration, smoking, body mass index, medications, comorbid diseases, number of HLA mismatches, and laboratory parameters including serum levels of creatinine, albumin, calcium, phosphorus, C-reactive protein, lipid parameters, and parathyroid hormone were analyzed as possible risk factors for atherosclerotic disease. Patients were followed for a mean of 59.7 +/- 23.6 months. PTDM was diagnosed according to the American Diabetic Association criteria or the need for an insulin/oral hypoglycemic agent. Twenty-six patients developed PTDM, and these patients had very good diabetes control. One patient with poorly regulated PTDM was excluded. Adverse events which were documented in 24 patients were more frequent among patients with PTDM. Mean age was found to be an independent risk factor for atherosclerotic disease, whereas PTDM was not. There were no differences regarding other atherosclerosis-related or other risk factors (including serum C-reactive protein levels and lipid profiles) between the groups. Nondiabetic subjects tended to have longer graft survival than patients with PTDM, but this finding was not statistically significant. PTDM is an important risk factor for developing atherosclerotic disease. Good control of blood glucose levels can decrease the high morbidity rates and negative influence of PTDM on patient and graft survival rates in this population.