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Background/Aims: Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute renal failure. However, the pathogenesis of CIN remains unclear. This study evaluated the role of anti-inflammatory cytokine interleukin-10 (IL-10) and pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) gene polymorphisms as CIN susceptibility markers after percutaneous coronary intervention (PCI). Methods: Four IL-10 tag SNPs (rs1554286, rs3021094, rs3790622, rs1800896) and three TNF-α tag SNPs (rs1799964, rs1800630, rs1800629) were analyzed by MALDI-TOF mass spectrometry in 53 CIN patients and 455 control subjects. Serum IL-10 and TNF-α were detected using ELISA. Results: When compared to controls, the CIN patients showed increased frequencies of CC (rs1554286) and AG+GG (rs1800896) genotypes in IL-10 and GA+AA (rs1800629) genotype in TNF-α (OR = 2.24 (1.13–4.44), p = 0.018; OR = 2.61 (1.30–5.26), p = 0.005, and OR = 2.11 (1.08–4.09), p = 0.025, respectively). Baseline serum IL-10 levels in CIN patients were significantly lower (1.02 ± 1.14 vs. 2.78 ± 4.73 pg/ml, p = 0.008). Patients with CIN had a higher rate of decline in renal function than those without CIN (0.89 ± 1.67 vs. 0.30 ± 0.95 ml/min/1.73 m2 per month, p = 0.002). Significantly higher rates of decline in creatinine clearance were noted in patients with TNF-α (rs1800629) GA+AA than GG genotype (0.88 ± 1.83 vs. 0.36 ± 0.70, p = 0.03), and with IL-10 (rs1800896) AG+GG than AA genotype (1.28 ± 2.14 vs. 0.33 ± 0.90, p < 0.001). Conclusions: Gene polymorphisms of IL-10 and TNF-α are associated with CIN risk and long-term renal outcome after PCI. More prospective studies are needed to confirm our results.

Background/Aims: Pentoxifylline (PTX) has been shown to inhibit renal inflammation in a rat model of crescentic glomerulonephritis. The present study investigated the role of PTX in renal fibrosis in rats with crescentic glomerulonephritis. Methods: A rat model of accelerated anti-glomerular basement membrane glomerulonephritis was induced and treated with PTX or vehicle control for 3, 7, 14 and 28 days. The therapeutic effect and mechanism of PTX on renal fibrosis were examined by Northern blot and immunohistochemistry. Results: Diseased rats treated with vehicle control developed a severe crescentic glomerulonephritis with progressive renal fibrosis identified by a marked accumulation of α-SMA+ myofibroblasts and collagen matrix. This was associated with tubular epithelial-myofibroblast transition as evident by de novo expression of α-SMA and a loss of E-cadherin on damaged tubular epithelial cells. Further studies revealed that severe renal fibrosis was associated with upregulation of renal TGF-β1 and activation of TGF-β/Smad signaling, which was blocked by treatment with PTX. Conclusions: PTX may be an anti-fibrosis agent capable of inhibiting renal fibrosis in a rat model of crescentic glomerulonephritis. Blockade of TGF-β1 expression and Smad2/3 activation may be a mechanism by which PTX inhibits renal fibrosis.

Central vein stenosis is an indolent and underestimated complication of permanent pacemaker placement. It leads to serious problems in hemodialysis patients when arteriovenous (AV) fistulae/grafts were created at the ipsilateral arm. We, herein, reported 3 cases of AV access failure resulting from permanent pacemaker-related central vein stenosis. The pathogenesis, clinical manifestations, radiological findings, and therapeutic solution on this issue are discussed. It is mandatory to place the AV fistula/graft and permanent pacemaker wire on the opposite side for prevention of the high risk of AV access failure.

Spiral computed tomographic angiography (CTA), a new noninvasive imaging technique, was used to study 10 arteriovenous fistulas (AVF) in 9 hemodialysis patients. Digital subtraction angiography (DSA) was also performed as a gold standard for comparison. AVF stenosis was graded by a four-point scale: grade 0, well patency of supplying artery, anastomosis and drainage vein; grade 1

Background and Aims: Mesenteric ischemia is an uncommon disorder associated with an extremely high mortality rate. Only limited studies have evaluated this lethal disease among patients with end-stage renal disease (ESRD). The objective of this study was to evaluate the risks of mesenteric ischemia among ESRD patients and compare the incidence between two dialysis modalities. Methods: Records of all ESRD patients older than 20 years of age from 1998 to 2007 and a control group consisting of 1 million records were retrieved from the Taiwan National Health Insurance Research Database. Hospitalizations for mesenteric ischemic events were retrieved using ICD-9-CM diagnosis codes and ICD-9-CM operation codes from inpatient claims. Results: Among 55,807 incident ESRD patients who received hemodialysis or peritoneal dialysis, there were 458 mesenteric ischemic events, corresponding to an incidence rate of 2.7 per 1,000 patient-years. Multivariate Cox regression analysis indicated that the independent risk factors were old age (HR 1.42 per 10 years), diabetes (HR 2.85), peripheral vascular disease (HR 2.66), atrial fibrillation (HR 2.15), heart failure (HR 1.65), chronic pulmonary disease (HR 1.41), neoplasm (HR 1.54), peptic ulcer disease (HR 1.86), and peritoneal dialysis (HR 1.51, all p < 0.05). There was no effect of dialysis modality on the mesenteric ischemia mortality rate. Conclusion: The risk of mesenteric ischemia for ESRD patients was 44.1 (95% confidence interval 13.4–106.2, p < 0.001) times higher than that of the general population. Compared to hemodialysis, peritoneal dialysis was associated with a higher risk of mesenteric ischemia.

Patients with gouty arthritis were examined at Veterans General Hospital to evaluate whether their renal function is impaired and to define the factor(s), if any, of renal function deterioration. A total of 152 cases were included in the study, and the patients were divided into two groups. One group (n = 80) exhibited pure gout without any associated medical problems or preexisting renal disorders. The second group (n = 72) included patients with gout and hypertension. The group with pure gout was further stratified into patients with tophi (n = 21) and those without (n = 59). Seventy-two sex- and age-matched normal adults served as the control group. We found (1) that the renal function was impaired in the pure-gout group when compared with sex- and age-matched normal individuals (serum creatinine 1.56 +/- 0.64 vs. 0.90 +/- 0.16 mg/dl, p = 0.0001; creatinine clearance 59.91 +/- 30.90 vs. 97.10 +/- 27.19 ml/min, p = 0.0001); (2) that the renal function was significantly more aggravated in patients with clinically visible tophi than in those without (gout with tophi vs. gout without tophi: serum creatinine 1.89 +/- 0.90 vs. 1.44 +/- 0.48 mg/dl, p = 0.040; creatinine clearance 47.27 +/- 31.90 vs. 64.40 +/- 29.53 ml/min, p = 0.030), and (3) that a further significant decline of the renal function was noted in gouty patients with an associated medical illness, i.e., hypertension (gout with hypertension vs. pure gout: serum creatinine 2.10 +/- 0.97 vs. 1.56 +/- 0.64 mg/dl, p = 0.0001; creatinine clearance 45.06 +/- 24.69 vs. 59.91 +/- 30.90 ml/min, p = 0.0029).(ABSTRACT TRUNCATED AT 250 WORDS)