Podocytes, which are susceptible to injury by various stimuli and stress, are critical regulators of proteinuric kidney diseases, regardless of the primary disease and pathogenesis. We further confirmed a significant correlation between urinary CD147/basigin (Bsg) levels and proteinuria in patients with focal segmental glomerulosclerosis. However, the molecular mechanism of podocyte injury involving Bsg is not fully understood. Here, the involvement of Bsg in the pathogenesis of podocyte injury was elucidated. Healthy podocytes rarely express Bsg protein. In two independent mouse models, including adriamycin-induced nephropathy and N u -nitro-L-arginine methyl ester (L-name)-induced endothelial dysfunction, Bsg induction in injured podocytes caused podocyte effacement, which led to development of proteinuria. Bsg silencing in cultured podocytes exposed to transforming growth factor-b suppressed focal adhesion rearrangement and cellular motility via the activation of b 1 integrinefocal adhesion kinaseematrix metallopeptidase signaling. In addition, induction of vascular endothelial growth factor and endothelin-1, which are implicated in podocyte-to-endothelial cross-communication, was lower in the supernatants of cultured Bsg-silenced podocytes stimulated with transforming growth factor-b. In this setting, Bsg may be involved in a physiological positive feedback loop that accelerates podocyte cell motility and depolarization. The current study thus suggests that Bsg silencing via suppression of b 1 integrinefocal adhesion kinaseematrix metallopeptidase signaling may be an attractive therapeutic strategy for the maintenance of podocytes in patients with proteinuric kidney diseases.
Th17 cells play an important role in psoriasis. The differentiation of naïve CD4+ T cells into Th17 cells depends on glycolysis as the energy source. CD147/basigin, an integral transmembrane protein belonging to the immunoglobulin superfamily, regulates glycolysis in association with monocarboxylate transporters (MCTs)-1 and -4 in cancer cells and T cells. We examined whether CD147/basigin is involved in the pathogenesis of psoriasis in humans and psoriasis-model mice. The serum level of CD147 was increased in patients with psoriasis, and the expression of CD147 and MCT-1 was elevated in their dermal CD4+ RORγt+ T cells. In vitro, the potential of naïve CD4+ T cells to differentiate into Th17 cells was abrogated in CD147−/− T cells. Imiquimod (IMQ)-induced psoriatic dermatitis was significantly milder in CD147−/− mice and bone marrow chimeric mice lacking CD147 in the hematopoietic cells of myeloid lineage. These findings demonstrate that CD147 is essential for the development of psoriasis via the induction of Th17 cell differentiation.
Body Cell Mass (BCM) is a sum of all metabolically active cells of the body. Aim of the study was to compare BCM with other nutritional and inflammatory markers in patients with chronic kidney disease (CKD) stage 4-5 (NKF) without dialysis treatment and in hemodialysis patients(HD). We included 45 adult patients with CKD and eGFR o30 ml/min not treated with dialysis (26 male, age: 59,7 7 16,8) and 39 adults treated with HD three times a week, for more than three months (26 male, 5 diabetics, age: 59,8 716). Body composition was measured using multifrequency biopimpedance spectroscopy: Body Composition Monitor -FMC. We used BCM index (BCMI) defined as BCM divided by height to the power of 2. To measure hand grip strength (HGS) we used dynamometr Jamar. In statistics analysis we used Pearson correlations (SPSS v18). Predialysis group: BCMI: 7,1 7 1,6 kg/m 2 , Lean Tissue Index (LTI): 12,9 7 2,4 kg/m 2 , Fat Tissue Index (FTI): 14,7 7 5,4 kg/m 2 , BMI: 28,2 7 5 kg/m 2 , serum creatinine level (SCr): 3,9 7 2,1 mg/dl, eGFR: 18,3 77,0034 ml/min/1,73 m 2 , albumin (SA): 3,9 7 0,3 g/dl, prealbumin (PA): 32,8 78,8 mg/dl, CRP: 0,5 7 0,3 mg/dl. A positive correlation was found with BCMI and HGS (r ¼ 0,55; p ¼0,001), PA (r ¼ 0,41; p ¼0,004) and SCr (r ¼ 0,37; p ¼0,012). A negative correlation was found between BCMI and age (r ¼ -0,48; p¼0,006), CRP (r ¼ -0,33; p¼ 0,028). We do not observed correlation with BMI and SA. HD group: BCMI: 6,4 7 1,7 kg/m 2 , LTI: 12,1 7 2,3 kg/m 2 , FTI: 12 7 6 kg/m 2 , BMI: 24,8 7 4,8, SCr: 8,9 7 2,6 mg/dl, TP: 6,7 7 0,6 g/dl, SA: 3,9 7 0,47 g/dl, PA 33,8 7 11,4 g/dl, CRP: 1,1 7 1,4 mg/dl. A positive, significant correlation was found between BCMI and HGS (r ¼ 0,47; p¼ 0,003). A negative correlation was found with BCMI and age (r ¼ -0,55; p¼0,0005) and with CRP (r ¼ -0,31), but not statistically significant. We do not observed correlation between BCMI and BMI, SCr, TP, SA, PA, hemodialysis vintage, Kt/V. Assessment of body compartments is important tool in estimation nutritional status in patients with stage IV-V CKD and hemodialysis patients. Analysis of body composition in association with other markers worth to be studied, especially in larger groups of patients.
Arteriovenous fistula (AVF) after allograft biopsy occurs in 1.6-8.3% of kidney transplant patients and most cases remain asymptomatic. Here, we report a case of hemorrhagic shock in a kidney transplant recipient following bleeding from an AVF after graft biopsy. Immediate intensive care including angiographic embolization saved the patient and the allograft. A 62-year-old woman with end-stage renal disease caused by diabetic nephropathy underwent ABO-incompatible kidney transplantation. No complications occurred in the early postoperative period. However, serum creatinine levels did not decrease sufficiently and decreased graft diastolic blood flow was noted on ultrasound. Therefore, at 14 days after kidney transplantation, allograft biopsy was performed to elucidate the cause of allograft dysfunction. At 5 days after allograft biopsy, the patient developed hemorrhagic shock caused by bleeding from an AVF in the allograft. We immediately performed angiographic embolization, and her vital signs improved without deterioration in renal function. AVF can cause hemorrhagic shock, and angiographic embolization is effective for treating it.
Legionella pneumophila is a cause of community-acquired pneumonia that is reported to induce electrolyte disorders, including hyponatremia, hypokalemia, and hypophosphatemia. We herein report two Japanese men with Legionella pneumonia and hyponatremia and hypophosphatemia. These findings were associated with an elevation of urinary low-molecular-weight tubular protein, including urinary β2-microglobulin, N-acetyl-β-D-glucosaminidase, the fractional excretion of phosphate and uric acid, and the presence of glycosuria and panaminoaciduria, suggesting that their electrolyte disorders had been caused by Fanconi syndrome. In these two cases, hyponatremia was probably due to salt wasting. Electrolyte disorders caused by Legionella pneumonia are corrected by treatment of the primary disease and fluid administration.
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