Determinants of coronary artery calcification progression in renal transplant recipients.

Coronary artery calcification (CAC) is associated with increased atherosclerotic burden and cardiovascular events. The objective of this study was to determine the natural history and risk factors associated with CAC progression in a cohort of incident asymptomatic renal transplant recipients with no history of coronary revascularization. Electron-beam computed tomography was performed in 82 subjects at time of transplantation and at least 1 year later. Mean (SD) and median CAC score increased for all subjects from 392.4 (747.9) and 75.8 at time of transplant to 475.3 (873.5), (p = 0.002[log]) and 98.9 (p < 0.001), respectively. Most subjects (89%) with no calcifications remained without calcification. Mean annualized rate (SD) of CAC score change was 52.5 (150) with a median of 0.5. Average yearly percent change was 67.3 (409.6) with a median of 1.4. In multivariate analysis, diastolic blood pressure at 3 months post-transplant, Caucasian race, glomerular filtration rate at 3.0, months post-transplant, body mass index and baseline CAC score were independent predictors of annualized rate of CAC change. There is significant progression of CAC post-renal transplantation in most subjects. Progression is most likely to occur in white patients and is associated with clinical factors such as blood pressure, body mass index, renal function and baseline CAC score.

Assessment of differences in HLA-A, -B, and -DRB1 allele mismatches among African-American and non-African-American recipients of deceased kidney transplants.

Among recipients of deceased donor kidney transplants, African-Americans experience a more rapid rate of kidney allograft loss than non-African-Americans. The purpose of this study was to characterize and quantify the HLA-A, -B, and -DRB1 allele mismatches and amino acid substitutions at antigen recognition sites among African-American and non-African-American recipients of deceased donor kidney transplants matched at the antigen level. In recipients with zero HLA antigen mismatches, the degree of one or two HLA allele mismatches for both racial groups combined was 47%, 29%, and 11% at HLA-DRB1, HLA-B, and HLA-A, respectively. There was a greater number of allele mismatches in African-Americans than non-African-Americans at HLA-A (P < .0001), -B (P = .096), and -DRB1 loci (P < .0001). For both racial groups, the HLA allele mismatches were predominantly at A2 for HLA-A; B35 and B44 for HLA-B; but multiple specificities for HLA-DRB1. The observed amino acid mismatches were concentrated at a few functional positions in the antigen binding site of HLA-A and -B and -DRB1 molecules. Future studies are ongoing to assess the impact of these HLA mismatches on kidney allograft loss.

Prevalence and determinants of erectile dysfunction in hemodialysis patients.

BACKGROUND: The prevalence of erectile dysfunction (ED) among patients with end-stage renal disease (ESRD) is not known. METHODS: A cross-sectional study was conducted to determine the prevalence of ED among a community-based hemodialysis (HD) population using a two-stage cluster random sampling design. The presence and severity of ED were assessed among 302 ESRD patients using the self-administered International Index of Erectile Function-5 (IIEF-5). Logistic regression was used to examine and test associations between ED and other medical conditions. RESULTS: The prevalence of any level of ED was 82% (95% CI, 76 to 87%) for all HD subjects. The prevalence of severe ED was 45% (CI, 36 to 55%). Subjects younger than 50 years had a prevalence of ED of 63% (CI, 53 to 71%), while in subjects 50 years or older, it was 90% (CI, 84 to 94%). A multivariable analysis demonstrated increasing age (50 to 59, OR = 2.04, 95% CI, 1.3 to 3.1; 60 to 69, OR = 5.5, 95% CI, 1.9 to 15.6) and diabetes (OR = 2.0, 95% CI, 1.2 to 3.3) to be independently associated with the presence of any level of ED. However, neither the subjects' age nor history of diabetes predicted the severity of ED among subjects with ED. The use of angiotensin-converting enzyme inhibitors (ACEIs) was inversely associated with ED (OR = 0.41, 95% CI, 0.17 to 0.98). Poor functional status (Karnofsky score or the Index of Physical Impairment) was not associated with ED. CONCLUSIONS: ED is extremely prevalent among HD patients. Increasing age, diabetes, and nonuse of ACEIs were associated with higher prevalence of ED. The high prevalence of ED was seen even among patients with good functional status.

Preliminary observations of sildenafil treatment for erectile dysfunction in dialysis patients.

Erectile dysfunction is common in dialysis patients. We report our experience with sildenafil citrate in patients undergoing dialysis therapy. Male subjects attending the Outpatient Dialysis Unit at the University of Pennsylvania (Philadelphia, PA) who were prescribed sildenafil by their primary physician or nephrologist were asked to complete the International Index of Erectile Function before their first dose of sildenafil and after at least 4 weeks of therapy. Subjects' mean age was 50.3 +/- 14.63 (SD) years. Ninety-three percent of the subjects were black. Based on a global efficacy question, 66.7% of the subjects believed that treatment had improved their erections. Subjects reported no increase in the sexual desire domain despite experiencing a significant increase in erectile function, orgasmic function, and satisfaction with intercourse. Sildenafil was well tolerated in a selected group of patients who reported improved sexual function with no major adverse effects.

Membranoproliferative glomerulonephritis type I, mixed cryoglobulinemia and lymphoma in the absence of hepatitis C infection.

Chronic hepatitis C virus infection has been linked to cryoglobulinemia, membranoproliferative glomerulonephritis, and malignant B-cell lymphoproliferation, suggesting a possible pathogenetic link between these disorders. We report a patient with the latter clinical triad in the absence of hepatitis C infection. We postulate that the persistent and dysregulated immunologic activity associated with chronic antigen stimulation, inflammation and/or B-cell malignancy induces nephritogenic autoantibodies, including cryoglobulins, that produce a similar clinical syndrome in genetically susceptible individuals.