PubMed · 3581124
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R W Frater. 1987. Emergency valvular surgery.. https://pubmed.ncbi.nlm.nih.gov/3581124/
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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: Transarterial chemoembolization is effective for hepatocellular carcinoma. Acute renal failure may occur after transarterial chemoembolization because of radiocontrast agent, but its clinical aspects are unknown. AIM: To investigate the incidence, risk factors and outcome of acute renal failure, defined as increase of serum creatinine > 1.5 mg/dL, after transarterial chemoembolization. METHODS: A total of 235 hepatocellular carcinoma patients with 843 transarterial chemoembolization treatment sessions were analysed. RESULTS: Acute renal failure developed in 56 (23.8%) patients and the estimated risk of developing acute renal failure was 6.6% in each treatment session. Comparison between the episodes of transarterial chemoembolization with and without acute renal failure by using the generalized estimating equation disclosed that Child-Pugh class B (odds ratio: 2.6, P = 0.007) and treatment session (odds ratio: 1.3; P < 0.0001) were independent risk factors of acute renal failure. Twenty-seven patients had prolonged renal function impairment. Multivariate analysis by generalized estimating equation showed that Child-Pugh class B (odds ratio: 4.3, P = 0.0004) and diabetes mellitus (odds ratio: 5.2, P < 0.0001) were linked with prolonged acute renal failure, which independently predicted a decreased survival (relative risk: 2.3, P = 0.002). CONCLUSIONS: Acute renal failure after transarterial chemoembolization appears to be dose-related and is associated with the severity of cirrhosis. Patients with diabetes mellitus or Child-Pugh class B more frequently develop prolonged acute renal failure, which in turn is a poor prognostic predictor.
Tumor lysis syndrome is an oncologic emergency that is characterized by severe electrolyte abnormalities and, frequently, by acute renal failure. The syndrome typically occurs in patients with lymphoproliferative malignancies, most often after initiation of treatment. The pathophysiology involves massive tumor cell lysis resulting in the release of large amounts of potassium, phosphate, and uric acid. Deposition of uric acid and calcium phosphate crystals in the renal tubules may lead to acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. The kidney normally excretes these products, and consequently preexisting renal failure exacerbates the metabolic derangements of tumor lysis syndrome. Standard treatment aims to clear high plasma levels of potassium, uric acid, and phosphorus; correct acidosis; and prevent acute renal failure by way of aggressive intravenous hydration; lowering serum potassium levels; use of allopurinol; urinary alkalinization; or renal replacement therapy (if necessary). Allopurinol is the standard of care for treating hyperuricemia of malignancy, but is associated with drawbacks. Recombinant urate oxidase (rasburicase), which recently became available in the United States, provides a safe and effective alternative to allopurinol for lowering uric acid levels and preventing uric acid nephropathy.