PubMed · 5909858
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1966-04-23. Kidneys from cadavers.. https://pubmed.ncbi.nlm.nih.gov/5909858/
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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.
BACKGROUND: Previous studies suggested that RheothRx (poloxamer 188) reduces infarct size and improves left ventricular (LV) function in acute myocardial infarction (AMI). We therefore evaluated the effects of various doses of RheothRx in 2948 patients presenting with AMI. METHODS AND RESULTS: Patients were randomized to a control group (n = 963) or to receive RheothRx. Patients receiving RheothRx were allocated to receive a 1-hour bolus only (regimen A, n = 844), an additional 11-hour infusion at a low dose (target serum concentration of 0.5 mg/mL) (regimen Y, n = 490), or an additional 23-hour infusion at a low dose (regimen B, n = 483). Three higher doses (1-hour bolus+low-dose infusion for 47 hours, 1-hour bolus+high dose, target serum concentration of 1.0 mg/ml for 24 hours, or 1-hour bolus+high dose for 48 hours) were discontinued because of high rates of renal dysfunction (8.8%). Renal dysfunction was also observed at lower doses (regimen A, 3.1%; Y, 2.7%; and B, 4.1%) compared with the control patients (1.0%). There was no significant difference in the composite outcome of death, cardiogenic shock, or reinfarction at 35 days (all RheothRx, 13.6%; control, 12.7%). There was a higher incidence of sinus tachycardia (24.7% versus 21.6%, P = .02), atrial flutter (3.0% versus 1.3%, P = .019), atrial fibrillation (10.2% versus 7.3%, P = .082), pericarditis (6.6% versus 4.7%, P = .055), and clinical (21.9% versus 17.9%, P = .005) and radiological (15.3% versus 12.3%, P = .12) evidence of heart failure. This was associated with a lower LV ejection fraction (n = 1053) in treated patients (by = -0.02, P = .026), but there was little difference (P = .34) in infarct size (n = 1088). CONCLUSIONS: In this study of nearly 3000 patients, RheothRx had no effect on mortality, reinfarction, or cardiogenic shock and an adverse effect on renal function, LV ejection fraction, and various clinical manifestations of LV dysfunction or heart failure.
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