The prevalence of hepatitis C virus (HCV) infection has been as high as approximately 80% in patients with maintenance hemodialysis in public hospitals in Indonesia. However, the prevalence in private hospitals has not been examined yet. The aim of this study was to investigate the prevalence of anti-HCV antibody and the subtype distribution in patients with hemodialysis in a private hospital in Surabaya, Indonesia. Sera were obtained from 41 hemodialysis patients in a private hospital in Surabaya. The positive prevalence of anti-HCV antibody was carried out by the enzyme-linked immunosorbent assay (ELISA). Anti-HCV-positive sera were subjected to reverse transcription-PCR (RT-PCR) to detect HCV RNA and then direct sequencing. The HCV subtype was examined by phylogenetic analysis. Twenty five patients (61%) out of 41 were positive for anti-HCV antibody, and HCV-RNA was detected in 19 patients. The positive prevalence of anti-HCV antibody was 7.7% (one out of 13 patients) among patients who had undergone hemodialysis for less than one year, whereas it was 85.7% (24 out of 28 patients) among patients who had undergone hemodialysis for over one year. Phylogenetic analysis revealed HCV-1a (52.6%) was the most common subtype, followed by 1b (15.8%), 1c (15.8%), 2a (5.3%), and 3k (5.3%). In conclusion, the prevalence of HCV infection among hemodialysis patients in a private hospital was as high as that in general hospitals. The predominant subtype was HCV-1a, which is in accordance with the previous studies in general hospitals in Surabaya, Indonesia
Introduction: Patients with CKD have elevated plasma levels of Asymmetrical Dimethyl Arginine (ADMA), impaired EDRF/NO responses in isolated resistance vessels, and a marked increase in the frequency of cardiovascular events that are predicated by plasma levels of ADMA. ADMA is considered as a risk factor for endothelial dysfunction, progression of chronic kidney disease and a marked increase in the frequency of cardiovascular events that are predicated by plasma levels of ADMA. Elevated ADMA in CKD have been related to a combination of a reduced renal ADMA excretion and a reduced catabolism of ADMA by dimethylarginine dimethylaminohydrolase (DDAH). The current study was undertaken to determine whether there is a correlation between ADMA and SNPs at −449 DDAH 2. Subjects and Methods: It was a cross sectional analytic study, 56 hemodialysis patients and 30 healthy individuals were enrolled. Based on its etiology, HD patients group was further divided in to hypertension (HT) subgroup and non-HT subgroup. Genotyping of the polymorphisms was performed using PCR-based SNP detection methods based on 5'-exonuclease activity assays for rs805305. Results: Heterozygotes were observed as the most abundant genotypes in both groups, followed by GG genotype in the HD patients (30%) and CC (27%) healthy individuals. Among the HT subgroup, the mean plasma levels of ADMA were sequentially higher from genotypes CC, G/C and GG (p = 0.037). Further multiple comparisons between groups using post hoc test showed results that genotype GG and CC were different at 0.05 level of significance. These findings were not found among non HT subgroup. Conclusion: Genetic variation in the DDAH 2 genes is significantly associated with serum ADMA levels in hypertensive HD patients. We observed that carriage of a G at position −449 in the promoter region of the DDAH 2 gene is associated with higher ADMA levels.
We report an uncommon case of simultaneous cardio-cerebral infarction, due to Inferior – right ventricle ST Segment Elevation Myocardial Infarction (STEMI) with acute ischemic stroke. Incidence of cardio cerebral infarction is exceptionally rare, with an incidence rate as low as 0.009%. Hemodynamic compromise in patients with acute myocardial infarction may result in the cerebral blood flow reduction that cause hemodynamic stroke. Due to the rarity of this condition, there were no recommended therapeutics strategy. Mechanical reperfusion with PCI procedure may be a superior choice in the settings of acute cardio-cerebral infarction for restoring hemodynamic stability.
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