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Conclusions: It was found that endotoxemia was probably common in PD patients, and the degree of circulating endotoxemia might be related to the severity of systemic inflammation and features of atherosclerosis. This result suggests that endotoxemia may have a contributory role to the systemic inflammatory state and accelerated atherosclerosis in PD patients.

As compared to conventional PD solution, the use of balance, a neutral pH, low GDP solution resulted in a superior profile of PDE mesothelial cell marker and a lower degree of systemic inflammation, and the difference was maintained for 1 year. It remains to be determined whether these effects could result in better long-term clinical outcome.

The results suggested that serum miR-146a and miR-155 participate in the pathophysiology of SLE and might be used as biomarkers of SLE.

Enterobacteriaceae peritonitis is a serious complication in peritoneal dialysis (PD), but the clinical course of PD-related Enterobacteriaceae peritonitis remains unclear. We reviewed all Enterobacteriaceae peritonitis in our dialysis unit from 1995 to 2004. During this period, there were 1748 episodes of peritonitis recorded; 210 episodes (12.0%) in 123 patients were caused by Enterobacteriaceae. The most common species was Escherichia coli, accounting for 111 episodes. The primary response rate was 84.8% and complete cure rate was 58.1%. The presence of exit site infection was associated with a lower complete cure rate (43.2 versus 61.3%, P = 0.034). A total of 82 episodes (39.0%) did not respond to single antibiotic treatment despite sensitivity in vitro, and a second antibiotic was added. Patients treated with two antibiotics had a marginally lower risk of relapse and recurrence than those with one antibiotic (21.4 versus 36.1%, P = 0.051). The episodes that had recent antibiotic therapy had a marginally lower complete cure rate (49.3 versus 62.8%, P = 0.06). There was a gradual increase in the prevalence of resistance to several commonly used antibiotics over the years. Recent antibiotic therapy was associated with resistance to cefotaxime, ceftazidime, cefoperazone/sulbactam, and piperacillin/tazobactam. We conclude that Enterobacteriaceae peritonitis is a serious complication of PD. Recent antibiotic therapy is the major risk factor of antibiotic resistance. Exit site infection, and probably recent antibiotic therapy, is associated with poor therapeutic response. Contrary to the current recommendation, treatment with two antibiotics may reduce the risk of relapse and recurrence.

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Background: MicroRNAs (miRNAs) play important roles in the progression of renal fibrosis. We studied the urinary levels of miR-21, miR-29 family and miR-93, which are downstream mediators of the transforming growth factor-β₁ (TGF-β₁), in patients with immunoglobulin A (IgA) nephropathy. Methods: We studied the urinary miRNA levels of 43 IgA nephropathy patients and 13 healthy controls. Results: The IgA nephropathy group had significantly lower urinary miR-29b and miR-29c, but higher miR-93 levels than controls. Proteinuria significantly correlated with urinary levels of miR-29b (r = –0.388, p = 0.003) and miR-29c (r = –0.409, p = 0.002). Glomerular filtration rate significantly correlated with urinary levels of miR-21 (r = 0.338, p = 0.028), miR-29b (r = 0.333, p = 0.031) and miR-29c (r = 0.304, p = 0.050). Urinary miR-93 level significantly correlated with glomerular scarring (r = –0.392, p = 0.010). Urinary miRNA level of SMAD3, but not TGF-β₁, correlated with urinary miR-21 (r = 0.624, p < 0.001), miR-29b (r = 0.566, p < 0.001), miR-29c (r = 0.619, p < 0.001) and miR-93 (r = 0.332, p = 0.032). Conclusions: Urinary miR-29b and miR-29c levels correlated with proteinuria and renal function, while urinary miR-93 level correlated with glomerular scarring. More importantly, urinary levels of these miRNA targets significantly correlated with urinary SMAD3 level. Our results suggest that these miRNA targets are regulated by the TGF-β₁/SMAD3 pathway and they may play important roles in the development of progressive renal fibrosis in IgA nephropathy.