It is acquired distinct entity described a reduced number of thrombocytes in ADPKD patients in comparison with matched control subjects

In addition to an increased platelet volume, suggesting that there is enhanced platelet consumption in ADPKD. Our regression analysis showed that the TKV growth rate was significantly influenced by the thrombocyte count, suggesting that platelets might be implicated in the pathogenesis of cyst growth. Further studies need to be performed to define the pathogenic role of thrombocytes in ADPKD. In conclusion, we describe the clinical characteristics and the factors that predict disease progression in a large cohort of Chinese patients with ADPKD. Among the progression factors we found that log10-transformed TKV and protein/creatinine ratio significantly predicted eGFR loss and were associated with TKV growth. Furthermore we identified the decreased thrombocyte count as a novel parameter which is associated with more advanced renal impairment, higher TKV and higher TKV growth. Fractures caused by osteoporosis constitute a major health concern and result in a huge economic burden on health care systems. In Sweden, the lifetime risk of any osteoporotic fracture is 47% and 24% in women and men, respectively. In USA, the risk has been reported to be 40% and 13% in white women and men, respectively and fractures are associated with significant mortality and morbidity. Cortical bone is the major contributor to non-vertebral fracture risk and comprises more than 80% of the skeleton. The skeleton is remodeled by bone forming osteoblasts and bone resorbing osteoclasts. Macrophage colony stimulating factor increases proliferation and survival of OCLs precursor cells as well as up-regulates expression of receptor activator of nuclear factor-kB in OCL. This allows RANK ligand to bind and start the signaling cascade that leads to OCL formation. The effect of RANKL can be inhibited by Osteoprotegerin, which is a decoy receptor for RANKL. The association between inflammation and bone loss is well established. In autoimmune diseases, osteoclastic bone resorption is driven by inflammatory cytokines produced by immune cells e.g. high throughput screening inhibitor activated T cells. In addition, low-grade systemic inflammation, indicated by moderately elevated serum levels of high sensitivity C-reactive protein, associates with low bone mineral density, elevated bone resorption and increased fracture risk. The estrogen deficiency that occurs after menopause results in increased formation and prolonged survival of OCLs. This is suggested to be due to a number of factors including loss of the immunosuppressive effects of estrogen, resulting in increased production of cytokines promoting osteoclastogenesis, and direct effects of estrogen on OCLs. In line with these data, blockade of the inflammatory cytokines TNFa and IL-1 leads to a decrease in bone resorption markers in early postmenopausal women. In recent years, the importance of the gut microbiota for both health and disease has been intensively studied. The GM constitutes of trillions of bacteria which collectively contain 150- fold more genes than our human genome.

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