PubMed · 14233741
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M L SELZER, L B INDERBITZIN. 1964. RENAL FUNCTION AFTER EST.. https://doi.org/10.1176/ajp.121.3.266
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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.
Renal ischemia-reperfusion (I/R) is an important etiopathological mechanism of acute renal failure (ARF). Despite improvements in the treatment of ARF, it is associated with significant morbidity and mortality. I/R injury also occurs during renal transplantation and leads to reduced allograft survival. Sex differences have been found in I/R injury in many different organs including the kidney. Women have half the mortality of men in ARF. In animal models also, females are protected against renal I/R injury. The mechanisms by which sex affects the outcome to renal I/R injury are being actively investigated. This review will examine the evidence for gender differences in renal I/R injury and discuss the probable mechanisms by which sex affects the renal response to I/R injury.
Seven patients aged 13 to 17.5 years developed acute renal failure after treatment with a variety of non-steroidal anti-inflammatory drugs (NSAID): naproxen, diclofenac, ibuprofen, dipyrone and paracetamol. Six of the patients used more than one kind of NSAID. None of the patients had previous history of renal disease or concomitant treatment with other drugs. The time interval between NSAID administration to the emergence of symptoms ranged from 1 to 4 days. The most common presenting symptoms were flank pain (4 patients), abdominal pain (3 patients) and vomiting (3 patients). All patients had normal urine output. Microscopic hematuria and proteinuria were found in 5 patients and leukocyturia in 2. Serum creatinine ranged from 1.3 to 8.3 mg% at presentation. Kidney biopsy was performed in 3 patients and showed findings consistent with mild interstitial inflammation in 1 patient, and normal renal tissue in 2. All patients were treated with intravenous fluids, 1 received corticosteroids. Renal function completely normalized in all patients within 7 to 16 days.