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Correlation between MELD and UNa/K ratio in predicting renal dysfunction in cirrhotic patients

Introduction Renal dysfunction is broadly defined as decline in renal perfusion associated with decrease glomerular filtration rate (GFR) < 60ml/min/1.73 m 2 and sodium excretion less than 10 mEq/day.[ 1 ] It is one of the dreaded complications of cirrhosis [2,3] and is a clinical consequence of peripheral arterial vasodilatation and hyperdynamic circulation caused by portal hypertension.[ 4 ] The incidence of renal dysfunction in cirrhosis is approximately 8% with ascites but the prevalence increases with advancement of the disease.[ 3 ] Model of End

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Neutrophil Gelatinase-Associated Lipocalin as a Marker for Renal Dysfunction Detection in Critically Ill Patients with Increased Intraabdominal Pressure

R eferences 1. Bradley SE, Bradley GP. The effect of increased intraabdominal pressure on renal function in man. J Clin Invest. 1947;26:1010-1022. 2. Mohmand H, Goldfarb S. Renal dysfunction associated with intraabdominal hypertension and the abdominal compartment syndrome. J Am Soc Nephrol. 2011;22:615-621. 3. Malbrain ML, Chiumello D, Pelosi P. Prevalence of intraabdominal hypertension in critically ill patients: a multicentre epidemiological study. Intensive Care Med. 2004;30(5):822-9. 4. Vidal MG, Ruiz Weisser J, Gonzalez F, et al

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A pilot study to assess kidney functions and toxic dimethyl-arginines as risk biomarkers in women with low vitamin D levels

eliminated by renal excretion. Moreover, SDMA has an indirect (or weak) effect on NOS activity by restricting the availability of arginine to NOS and competing for the transportation of arginine ( 10 , 12 , 14 ). SDMA is considered as an early marker of renal dysfunction. Fliser et al. ( 15 ) reported a close correlation among SDMA, creatinine, and glamor filtration rate (GFR), and suggested that the SDMA level is equal to the serum creatinine level. However, it has been assumed that both ADMA and SDMA may interfere with the physiological defense mechanism in patients

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Beta-Trace Protein as a Marker of Renal Dysfunction in Patients with Chronic Kidney Disease: Comparison with Other Renal Markers

Beta-Trace Protein as a Marker of Renal Dysfunction in Patients with Chronic Kidney Disease: Comparison with Other Renal Markers

Beta-trace protein (BTP), also known as prostaglandin D synthase, is a low-molecular-mass protein which belongs to the lipocalin protein family. It was found to be increased in the serum of patients with renal diseases. The aim of this study was to compare the clinical usefulness of serum levels of beta-trace protein for the detection of renal dysfunction in patients with chronic kidney disease (CKD) with levels of other renal markers: creatinine, cystatin C and β2-microglobulin (B2M). The study included 134 patients with a wide range of renal dysfunction that encompassed all five CKD stages. Obtained data showed that beta-trace protein highly correlated (Spearman test) with creatinine (r = 0.890), cystatin C (r = 0.904) and B2M (r = 0.933) and its levels in serum significantly increased from CKD stage 1 to 5. Furthermore, the values of glomerular filtration rate (GFR) estimated from a BTP-based formula significantly correlated with GFR calculated from creatinine-based and cystatin C-based formulas. ROC analyses showed that BTP had similar diagnostic accuracy for detection of reduced renal function in CKD stages as other renal markers, for estimated GFRs of < 30, < 60 and < 90 mL/min/1.73 m2. The areas under the ROC curves (AUC) for BTP, for these GFR limits, were from 0.983 to 0.917 and they were not significantly different from AUCs for other renal markers. The results of this study showed that BTP may be a useful and reliable serum marker for identifying the magnitude of renal dysfunction in patients with CKD and may have its place beside serum cystatin C and creatinine as an alternative endogenous GFR marker.

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Original article. Mitigation of diazinon-induced cardiovascular and renal dysfunction by gallic acid

study in Brownsville, Texas. Int J Environ Res Public Health 11: 10165-10181. Shah MD, Iqbal M. (2010). Diazinon-induced oxidative stress and renal dysfunction in rats. Food Chem Toxicol 48: 3345-3353. Shinha KA. (1972). Colorimetric assay of Catalase. Anal Biochem 47: 389-394. Stonys A, Kuzminskis V, Seputyte A, Astasauskaite S, Jeseviciūte. (2007). [Acute renal failure in patients with alcoholic surrogate intoxication]. Medicina (Kaunas) Suppl 1: 36-39. Subramanian V, Venkatesan B, Tumala A, Vellaichamy

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Risk Factors Associated with Acute Coronary Syndrome after Successful Percutaneous Coronary Intervention

infarction treated with thrombolysis. GISSI-2 Investigators. Gruppo Italiano per lo Studio della, Sopravvivena nell’Infarto Miocardico. J Hypertens. 1996;14:743–750. 4. Hadadi L, Somkereki C, Dobreanu D. Renal dysfunction at hospital admission, high complexity of coronary artery disease and short term prognosis in acute ST-segment elevation myocardial infarction. Rev Romana Med Lab. 2012;20:363-369. 5. Washam JB, Herzog CA, Beitelshees AL, et al – Pharmacotherapy in chronic kidney disease patients presenting with acute coronary syndrome: a scientific statement

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Common Carotid Artery Thickness in Chronic Kidney Disease

. Atherosclerosis. 2003;171(2): 295-302. 17. Rossi M, et al. Ultrasonic tissue characterization of the carotid artery in chronic renal failure patients. Nephron. 2002; 91 (2): 270-275. 18. Fathi R, et al. The effect of long-term aggressive lipid lowering on ischemic and atherosclerotic burden in patients with chronic kidney disease. Am J Kidney Dis. 2004; 43(1): 45-52. 19. Leoncini G, et al. Mild renal dysfunction and subclinical cardiovascular damage in primary hypertension. Hypertension. 2003;42(1): 14-18. 20

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Pathogenesis and Assessment of Renal Function in Patients With Liver Cirrhosis

proposal for a revised classification system of renal dysfunction in patients with cirrhosis. Gut 2011;60:702-9. 11. Moreau R, Lebrec D. Diagnosis and treatment of acute renal failure in patients with cirrhosis. Best Pract Res Clin Gastroenterol 2007;1:111-23. 12. Martin-Llahi M, Guevara M, Torre A, et al. Prognostic importance of the cause of renal failure in patients with cirrhosis. Gastroenterology 2011;140:488-96. 13. Tandon P, Garsia-Tsao G. Renal dysfunction is the most important independent predictor of mortality in

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New Insights in the Pathogenesis of Cisplatin-Induced Nephrotoxicity

.1152/ajprenal.00401.2004 74. Ramesh G, Reeves WB. Cisplatin increases TNF-alpha mRNA stability in kidney proximal tubule cells. Ren Fail. 2006;28(7):583-92. doi: 10.1080/08860220600843839 75. Ramesh G, Zhang B, Uematsu S, Akira S, Reeves WB. Endotoxin and cisplatin synergistically induce renal dysfunction and cytokine production in mice. Am J Physiol Renal Physiol. 2007 Jul;293(1):F325-32. doi: 10.1152/ajprenal.00158.2007 76. Zhang B, Ramesh G, Norbury CC, Reeves WB. Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-alpha produced by

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Predisposing factors for chemotherapy-induced nephrotoxicity in patients with advanced esophageal cancer who received combination chemotherapy with docetaxel, cisplatin, and 5-fluorouracil

our study, renal dysfunction was therefore defined as a Ccr of less than 60 mL/min, and the patients were classified into 2 groups: patients with nephrotoxicity and patients without nephrotoxicity. To accurately predict the development of nephrotoxicity, we analyzed the data for the course of treatment in which nephrotoxicity developed in patients with nephrotoxicity and the data during the final course of chemotherapy in patients without nephrotoxicity. Statistical analysis Univariate analysis was performed to determine explanatory variables. Categorical data

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