Excessive salt intake increases peritoneal solute transport rate via local tonicity-responsive enhancer binding protein in subtotal nephrectomized mice.

BACKGROUND: High peritoneal transport is associated with high mortality and technical failure in peritoneal dialysis (PD). Baseline peritoneal solute transport rate (PSTR) as measured by the peritoneal equilibration test (PET) within 6 months after PD initiation varies between patients. Sodium is reported to be stored in the skin or muscle of dialysis patients. This study investigated whether excessive salt intake in uremic mice caused peritoneal alterations without exposure to PD fluid. METHODS: Sham-operated (Sham) and subtotal nephrectomized (Nx) mice were randomly given tap water or 1% sodium chloride (NaCl)-containing water for 8 weeks. PET was then performed to evaluate peritoneal function. Human mesothelial cell line Met-5A was used for in vitro studies. RESULTS: We observed higher PSTR in Nx mice with 1% NaCl-containing drinking water (Nx + salt) compared with those with tap water (Nx + water), along with enhanced angiogenesis and inflammation in the peritoneum. Blockade of interleukin (IL)-6 signaling rescued peritoneal transport function in Nx + salt mice. In cultured Met-5A, additional NaCl in the medium upregulated IL-6 as well as vascular endothelial growth factor-A, associated with increased expression and nuclear translocation of tonicity-responsive enhancer binding protein (TonEBP). Knockdown of TonEBP lowered the induction caused by high tonicity. Peritoneal TonEBP expression was higher in Nx + salt mice, while removal of high-salt diet lowered TonEBP level and improved peritoneal transport function. CONCLUSIONS: Excessive dietary salt intake caused peritoneal membrane functional and structural changes under uremic status. TonEBP regulated hypertonicity-related inflammatory changes and might play a crucial role in high baseline peritoneal transport.

Balloon tamponade during cesarean section is useful for severe post-partum hemorrhage due to placenta previa.

AIM: Severe post-partum hemorrhage during cesarean section due to placenta previa is still one of the leading causes of maternal mortality. The aim of this study was to evaluate the efficiency of intrauterine tamponade with a Sengstaken-Blakemore tube (SB-tube) for the treatment of severe post-partum hemorrhage in cases of placenta previa. MATERIAL AND METHODS: Data were collected from our departmental clinical records on all patients who underwent caesarian section due to placenta previa between 2007 and 2009. RESULTS: During the period analyzed, 37 patients underwent caesarian section due to placenta previa/low-lying placenta. Four (11%) underwent hysterectomy due to placenta accreta and 33 (89%) were treated conservatively. Of the 33 patients with conserved uterus, 10 (28%) patients required a SB-tube during the cesarean section because of continuous post-partum hemorrhage despite appropriate medical treatment. The median bleeding during the operation was 2030±860mL in the patients who used SB-tube. None of them presented severe complications related to these procedures or required any further invasive surgery. CONCLUSION: Intrauterine balloon-tamponade could successfully control severe hemorrhage from a lower uterine segment of a patient with placenta previa. This technique is simple to use, scarcely invasive, and available at a low cost to all maternity wards, and should be considered as one of the first management options to reduce the risk of undesirable hysterectomy.

Augmentation of 11beta-hydroxysteroid dehydrogenase type 1 in LPS-activated J774.1 macrophages--role of 11beta-HSD1 in pro-inflammatory properties in macrophages.

Macrophage infiltration in obese adipose tissue provokes local inflammation and insulin resistance. Evidence has accumulated that activation of 11beta-HSD1 in adipocytes is critically involved in dysfunction of adipose tissue. However, the potential role of 11beta-HSD1 in macrophages still remains unclear. We here demonstrate that a murine macrophage cell line, J774.1 cells expressed 11beta-HSD1 mRNA and reductase activity, both of which were augmented by lipopolysaccharide (LPS)-induced cell activation. Three kinds of pharmacological inhibition of 11beta-HSD1 in LPS-treated macrophages significantly suppressed the expression and secretion of interleukin 1beta, tumor necrosis factor alpha or monocyte chemoattractant protein 1, thereby highlighting a novel role of 11beta-HSD1 in pro-inflammatory properties of activated macrophages.