Variation of Peripheral Th17/Treg Imbalance in Patients with Idiopathic Membranous Nephropathy after Cyclosporin A Treatment: A Prognostic Marker of Idiopathic Membranous Nephropathy
Journal Title: Nephrology – Open Journal - Year 2017, Vol 3, Issue 1
Abstract
Despite impressive improvements in the 1-year graft survival for kidney transplantation, which has risen from 60% to 95% over the last few decades, little progress has been made in long-term graft survival. Half of the grafted and functional kidneys are lost within 10-12 years after transplantation because of premature recipient mortality; cardiovascular disease being a leading cause of both death and graft loss in this population. Many dialysis patients have acquired into end-stage kidney diseases because of diabetes, but among those non-diabetic patients, the majority suffer from a constellation of cardiovascular risk factors, including overweight, hypertension, dyslipidemia, and insulin resistance. After kidney transplantation, recipients often experience about 10-15% of weight gain,1 owing to increased appetite by steroids, as well as the loss of uremia and dietary restrictions from the dialysis period. Additionally, many recipients experience difficulties with exercise due to comorbid conditions like sarcopenia, amputations, or heart failure. All these circumstances make a perfect breeding ground for the development of diabetes after transplantation, or post-transplant diabetes (PTDM). PTDM develops from the interplay of transplant-specific factors such as immunosuppressive drugs on top of all these traditional risk factors.2 PTDM is a relatively common complication after kidney transplantation that influences graft and patient survival, and is defined as a type of diabetes that occurs after a transplant procedure in patients who did not present any remarkable feature of diabetes before the transplantation. The timing for diagnosis has not been clearly established but most PTDM happen during the first three months after transplantation,3 which is the period with the greatest exposure to the immunosuppressive cocktail. Therefore, the disease seems to develop because of the effect of immunosuppressive drugs in both insulin sensitivity (in peripheral tissues) and insulin secretion (by pancreatic beta-cells). However, minimising or withdrawing immune suppression is often unwanted because of the fear of rejection, and it remains difficult to lose weight after transplantation. Since no established therapy exists to prevent or revert PTDM, understanding the mechanisms involved in the effects of the immunosuppressive therapies in pancreatic beta-cells will be essential to improve preventive and therapeutic strategies for transplant recipients.
Authors and Affiliations
JianBin Zhang
Keywords
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- EP ID EP558293
- DOI 10.17140/NPOJ-3-117
- Views 105
- Downloads 0
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