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PurposeTraditionally, the surgical repair of umbilical hernia in cirrhotic patients with ascites is avoided because of a significant recurrence rate and perioperative morbidity/mortality. However, recent reports recommend early elective surgery in these patients because surgery-related complications can be reduced with minimally invasive surgery and development of perioperative patient care. The current study was conducted to analyze safety and feasibility of umbilical hernia repairs performed in a single institute.MethodsA single center retrospective analysis of patients' data was conducted. Eighteen patients with umbilical hernia accompanied by liver cirrhosis underwent hernia repair in the period between 2005 and 2012. The charts of these patients were reviewed and demographic data, postoperative complications, and recurrence were recorded.ResultsEleven males and seven females with a mean age of 62.9 years were analyzed. Two of the patients were classified as Child's class A, 11 as Child's class B, and five as Child's class C. Four patients underwent emergency surgery because of perforations in the hernia sac in two cases and incarcerated hernias in the other two cases. Of the 18 patients who underwent surgery, four (22%) experienced a recurrence, three (17%) developed edema at the surgical sites, one (5%) experienced hepatic coma, and one (5%) showed postoperative variceal hemorrhage. All of these events occurred after emergency surgery.ConclusionIn contrast to traditional concepts, early and elective repair of umbilical hernia can be performed easily and safely in cirrhotic patients.

The establishment of a trauma center and the implementation of a new protocol that included EPP were effective in the treatment of patients with hemodynamically unstable pelvic fractures.

Mitochondrial injury plays important roles in the pathogenesis of various kidney diseases. However, mitochondrial injury in IgA nephropathy (IgAN) remains largely unexplored. Here, we examined the associations among mitochondrial injury, IgAN, and treatment outcomes. We prospectively enrolled patients with IgAN and age-/sex-matched healthy volunteers (HVs) as controls (n = 31 each). Urinary copy numbers of the mitochondrial DNA (mtDNA) genes cytochrome-c oxidase-3 (COX3) and nicotinamide adenine dinucleotide dehydrogenase subunit-1 (ND1) were measured. Urinary mtDNA levels were elevated in the IgAN group compared with that in HVs (p < 0.001). Urinary ND1 levels were significantly higher in the low proteinuria group than in the high proteinuria group (p = 0.027). Changes in urinary levels of ND1 and COX3 were positively correlated with changes in proteinuria (p = 0.038 and 0.024, respectively) and inversely correlated with changes in the estimated glomerular filtration rate (p = 0.033 and 0.017, respectively) after medical treatment. Mitochondrial injury played important roles in IgAN pathogenesis and may be involved in early-stage glomerular inflammation, prior to pathological changes and increased proteinuria. The correlation between changes in urinary mtDNA and proteinuria suggest that these factors may be promising biomarkers for treatment outcomes in IgAN.