role of Ischemia reperfusion damage on renal transplant, what are the new treatments?

Ischemia reperfusion damage usually occurs after renal transplantation. These injuries can stimulate the innate immune system, trigger an inflammatory response and ultimately activate the adaptive immune system. These events may result in rejection, graft fibrosis and chronicallograft nephropathy. Different mechanisms contribute to innate immune system activation following ischemia reperfusion injury in renal transplants. Some of these mechanisms are known and described by investigators while the remaining are still unknown. To clarify the precise mechanisms underlying the innate immune system activation and rejection progression helps us to plan therapeutic protocols to reduce immunologic responses to ischemic events and to improve the graft function and outcome. In this review, we will discuss how innate and adaptive immune systems are activated during an ischemic insult and thereafter discuss related therapeutic interventions to block the activating pathways

Pulmonary hypertension and predisposing factors in patients receiving hemodialysis

The aim of this study was to evaluate the frequency of unexplained pulmonary hypertension [PHT] among patients on hemodialysis at 2 centers and to evaluate possible predisposing factors. In this cross-sectional study, PHT was screened by Doppler echocardiography on the day after dialysis in 62 patients with end-stage renal disease receiving maintenance hemodialysis via arteriovenous access. Pulmonary hypertension was defined as a systolic pulmonary arterial pressure [PAP] higher than 35 mm Hg, and the systolic PAP was calculated using the modified Bernoulli equation. Clinical variables were compared between patients with and without PHT. A PAP higher than 35 mm Hg was found in 32 patients [49.3%] receiving hemodialysis, with a mean systolic PAP of 39.58 +/- 13.27 mm Hg. Blood hemoglobin level was significantly lower in the patients with PHT than those without PHT [9.8 +/- 1.97 g/dL versus 11.07 +/- 1.86 g/dL; P = .01]. In addition, serum levels of albumin was lower in these patients [3.38 +/- 0.32 g/dL versus 3.75 +/- 0.44 g/dL; P = .02]. This study demonstrates a surprisingly high prevalence of PHT among patients with end-stage renal disease receiving hemodialysis. We concluded that the best approach to this unrecognized complication that is associated with reduced survival is keeping it in mind and looking for it in the management of patients on dialysis