PubMed · 4420789
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M A Ghoneim, A Ashamallah. 1974. Further experience with the rectosigmoid bladder.. https://doi.org/10.1111/j.1464-410x.1974.tb03849.x
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Early transplant dysfunction and failure because of immunological and nonimmunological factors still presents a significant clinical problem for transplant recipients. A critical unmet need is the noninvasive detection and prediction of immune injury such that acute injury can be reversed by proactive immunosuppression titration. In this study, we used iTRAQ -based proteomic discovery and targeted ELISA validation to discover and validate candidate urine protein biomarkers from 262 renal allograft recipients with biopsy-confirmed allograft injury. Urine samples were randomly split into a training set of 108 patients and an independent validation set of 154 patients, which comprised the clinical biopsy-confirmed phenotypes of acute rejection (AR) (n = 74), stable graft (STA) (n = 74), chronic allograft injury (CAI) (n = 58), BK virus nephritis (BKVN) (n = 38), nephrotic syndrome (NS) (n = 8), and healthy, normal control (HC) (n = 10). A total of 389 proteins were measured that displayed differential abundances across urine specimens of the injury types (p < 0.05) with a significant finding that SUMO2 (small ubiquitin-related modifier 2) was identified as a "hub" protein for graft injury irrespective of causation. Sixty-nine urine proteins had differences in abundance (p < 0.01) in AR compared with stable graft, of which 12 proteins were up-regulated in AR with a mean fold increase of 2.8. Nine urine proteins were highly specific for AR because of their significant differences (p < 0.01; fold increase >1.5) from all other transplant categories (HLA class II protein HLA-DRB1, KRT14, HIST1H4B, FGG, ACTB, FGB, FGA, KRT7, DPP4). Increased levels of three of these proteins, fibrinogen beta (FGB; p = 0.04), fibrinogen gamma (FGG; p = 0.03), and HLA DRB1 (p = 0.003) were validated by ELISA in AR using an independent sample set. The fibrinogen proteins further segregated AR from BK virus nephritis (FGB p = 0.03, FGG p = 0.02), a finding that supports the utility of monitoring these urinary proteins for the specific and sensitive noninvasive diagnosis of acute renal allograft rejection.
Serum and dialysate boron levels in 17 patients with long term hemodialysis (HD) were determined by inductively coupled plasma emission spectrometry (ICPES). Serum boron level was compared with the value of age matched 467 healthy controls and the relationship between serum and dialysate boron level was analyzed. The results showed that serum boron level was significantly higher at the beginning of HD, and lower at the completion of HD in comparison with controls. Although the dialysate was contaminated with trace boron, HD resulted in an excessive decrease of serum boron, rather than boron exposure from the dialysate. Boron hemodialyzability was almost proportional to the gradient of the boron level at the beginning of HD and it could be controlled by the adjustment of the gradient. In conclusion, the serum boron level was very much disturbed in long term HD patients. If boron excess in serum at the beginning of HD, or deficiency at the completion of HD may contribute to the complications of HD patients, fine adjustment and close surveillance of the gradient should be taken into account.
Cyclosporin A (CsA) is a potent inhibitor of the Ca(2+)-dependent "pore" in isolated mitochondrial from diverse sources. Cisplatin-induced acute renal failure has been associated with morphological and functional alterations in renal cortex mitochondrial (RCM). This study was undertaken to examine the probable involvement of Ca(2+)-dependent permeabilization of RCM in cisplatin nephrotoxicity. RCM from rats injected with cisplatin (5 mg/kg body wt) 4 days earlier showed a significantly reduced capacity of retaining matrix Ca2+ and membrane potential in the presence of 15 nmol Ca2+/mg protein and 0.1 mM Pi (inorganic phosphate), compared to controls (those of rats that received carrier alone). These indices of mitochondrial dysfunction were restored to control levels when 1 microM CsA was added to assay media of RCM obtained from cisplatin-treated rats. Renal insufficiency induced by cisplatin assessed by serum creatinine and urea levels was significantly alleviated in rats 4 days after i.p. injections of cisplatin (5 mg/kg body wt) and CsA (50 micrograms/kg body wt), compared to those injected with cisplatin alone. Our findings support an involvement of Ca(2+)-mediated RCM damage in the mechanism of cisplatin nephrotoxicity, and suggest that suitable antagonists of Ca(2+)-dependent "pore" formation may improve renal tolerance to cisplatin.