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Plasma Creatinine Concentration (plasma + creatinine_concentration)
Selected AbstractsAngiotensin-I-converting enzyme insertion/deletion polymorphism and high urinary albumin concentration in French Type 2 diabetes patientsDIABETIC MEDICINE, Issue 8 2003S. Hadjadj Abstract Aims Family-based studies suggest a genetic basis for nephropathy in Type 2 diabetes. The angiotensin-I-converting enzyme (ACE) gene is a candidate gene for Type 1 diabetes nephropathy. We assessed the association between high urinary albumin concentration and ACE insertion/deletion (I/D) polymorphism, in French Type 2 diabetes patients. Methods We studied 3139 micro/macroalbuminuric French patients recruited in the DIABHYCAR Study, an ACE inhibition trial in Type 2 diabetes patients with renal and cardiovascular outcomes. The main inclusion criteria were age , 50 years, urinary albumin concentration , 20 mg/l assessed centrally during two consecutive screening visits, and plasma creatinine concentration , 150 µmol/l. These patients were compared with 605 normoalbuminuric (NA; urinary albumin concentration < 10 mg/l at first screening for the DIABHYCAR Study) French patients. ACE I/D genotype was determined by nested polymerase chain reaction. Results The ACE I/D polymorphism was in Hardy,Weinberg equilibrium. The distribution of genotypes did not differ significantly between micro/macroalbuminuric and NA patients: 552 and 115 II, 1468 and 282 ID, 1119 and 208 DD (P = 0.67). However, the ACE D allele was more frequent among normotensive micro/macroalbuminuric patients than among NA patients (P = 0.039). Conclusions The ACE I/D polymorphism was not associated with high urinary albumin concentration in French Type 2 diabetes patients. [source] Sodium Bicarbonate versus Sodium Chloride and Oral N-Acetylcysteine for the Prevention of Contrast-Induced Nephropathy in Advanced Chronic Kidney DiseaseJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 6 2009LINDA SHAVIT M.D. Introduction: Contrast-induced acute kidney injury (CI-AKI) is one of the leading causes of hospital-acquired acute kidney injury. Multiple clinical studies have proposed several preventive strategies. Aims: To examine the efficacy of sodium bicarbonate compared with sodium chloride and oral N-acetylcysteine (NAC) for preventive hydration after cardiac catheterization. Methods: We conducted a prospective, single-center trial. Patients with chronic kidney disease (CKD) stage III,IV undergoing cardiac catheterization were allocated to receive either an infusion of 0.9% sodium chloride and oral NAC or 154 mEq/L sodium bicarbonate. Main: Outcome measure CI-AKI, defined as an increase of 25% or 0.3 mg/dL or more in plasma creatinine within 2 days of contrast administration. Results: Ninety-three patients were allocated to one of the two groups: 42 patients in the saline plus NAC group and 51 patients in the bicarbonate group. There were no statistically significant differences between the groups in the most important clinical and procedural characteristics. Baseline plasma creatinine levels, estimated glomerular filtration rate, incidence of diabetes mellitus, hypertension, congestive heart failure, and contrast medium volume were similar. Mean plasma creatinine concentration was 1.76 ± 0.54 mg/dL in the saline and NAC group and 1.9 ± 1 mg/dL in the bicarbonate group (P = 0.23). The rate of CI-AKI was 9.8% in the bicarbonate group and 8.4% in the saline plus NAC group. No patient required renal replacement therapy. Conclusion: Hydration with sodium bicarbonate is not more effective than hydration with sodium chloride and oral NAC for prophylaxis of CI-AKI in patients with CKD stage III,IV undergoing cardiac catheterization. [source] Acid-base balance of cats with chronic renal failure: effect of deterioration in renal functionJOURNAL OF SMALL ANIMAL PRACTICE, Issue 6 2003J. Elliott In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52·6 per cent of animals with severe renal failure (plasma creatinine concentration > 400 umol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF. [source] Plasma Asymmetric Dimethylarginine, Symmetric Dimethylarginine, l -Arginine, and Nitrite/Nitrate Concentrations in Cats with Chronic Kidney Disease and HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008R.E. Jepson Background: Chronic kidney disease (CKD) and hypertension have been associated with decreased bioavailability of nitric oxide (NO) and endothelial dysfunction. Increased concentrations of the endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) are implicated. Hypothesis: Plasma ADMA concentration is increased in cats with CKD and systemic hypertension corresponding to a decrease in total plasma nitrate/nitrite (NOx) availability. Decrease in systolic blood pressure (SBP) and proteinuria during treatment of hypertension with amlodipine besylate may be associated with increased NOx availability. Animals: Sixty-nine client-owned normotensive and hypertensive cats with variable azotemia. Methods: Plasma ADMA, symmetric dimethylarginine (SDMA), and l -arginine were measured simultaneously by hydrophilic-interaction liquid chromatography-electrospray tandem mass spectrometry in cats from 6 groups: normotensive nonazotemic (n = 10), normotensive mildly azotemic (n = 10), hypertensive mildly azotemic with hypertensive retinopathy (n = 20), hypertensive mildly azotemic without hypertensive retinopathy (n = 10), normotensive moderately azotemic cats (n = 10), and hypertensive nonazotemic cats (n = 9). Plasma NOx concentrations were measured. Results: A moderate correlation between plasma creatinine and ADMA (n = 69, r= .608, P < .001), SDMA (n = 69, r= .741, P < .001), and NOx concentrations (n = 69, r= .589, P < .001) was observed. There was no association among plasma ADMA, SDMA, and NOx concentrations and SBP. Conclusions and Clinical Importance: Plasma ADMA and SDMA concentrations are increased in cats with CKD and correlate with plasma creatinine concentration. This may imply the presence of endothelial dysfunction in cats with CKD. Plasma ADMA concentrations were not associated with systemic hypertension. Treatment of systemic hypertension with amlodipine besylate did not affect plasma ADMA or NOx concentrations. [source] Liquid chromatography/mass spectrometry for metabonomics investigation of the biochemical effects induced by aristolochic acid in rats: the use of information-dependent acquisition for biomarker identificationRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 6 2008Wan Chan The toxic effects of oral administrations of nephrotoxic and carcinogenic aristolochic acid (AA) to male Sprague-Dawley rats were investigated by using high-performance liquid chromatography coupled with a quadrupole time-of-flight mass spectrometer. Analysis of the urine and plasma samples revealed distinct changes in the biochemical patterns in the AA-dosed rats. After peak finding and alignment, principal component analysis (PCA) and partial least-squares discriminant analysis (PLS-DA) were used for multivariate data analysis. Potential biomarkers were studied by high-resolution mass spectrometry (MS) and tandem mass spectrometry (MS/MS) analyses. The MS/MS spectra of all endogenous metabolites satisfying the pre-defined criteria were acquired in a single information-dependent acquisition (IDA) analysis, demonstrating that IDA was an efficient approach for structural elucidation in metabonomic studies. Citric acid and a glucuronide-containing metabolite were observed as potential biomarkers in rat urine. A significant increase in plasma creatinine concentration was also observed in the AA-dosed rats, which indicated that AA induced an adverse effect on the renal clearance function. Copyright © 2008 John Wiley & Sons, Ltd. [source] Point of care measurement of plasma creatinine in critically ill patients with acute kidney injuryANAESTHESIA, Issue 4 2009A. Udy Summary We report the utility of an enzymatic point of care system for estimation of plasma creatinine concentration in critically ill patients with acute kidney injury. Multiple measurements were obtained from a heterogenous population admitted to a multi-disciplinary intensive care unit. The acute kidney injury network guidelines were used to identify and stratify patients based on the creatinine concentration. Central laboratory values were used as comparators to assess the precision and bias of the system. Overall, point of care measurements correlated well with central pathology results (R2 = 0.991, p < 0.001), although there tended to be a small negative bias in patients with acute kidney injury (3 ,mol.l,1). The accuracy of point of care measurement is within clinically acceptable limits and given the much shorter turn around time can be used to identify and monitor patients with acute kidney injury in the critical care environment. [source] Acid-base balance of cats with chronic renal failure: effect of deterioration in renal functionJOURNAL OF SMALL ANIMAL PRACTICE, Issue 6 2003J. Elliott In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52·6 per cent of animals with severe renal failure (plasma creatinine concentration > 400 umol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF. [source] Assessment of acid-base status of cats with naturally occurring chronic renal failureJOURNAL OF SMALL ANIMAL PRACTICE, Issue 2 2003J. Elliott Metabolic acidosis is reported to be a common complication of feline chronic renal failure (CRF) but acid-base status of feline patients with this disease is rarely assessed by general practitioners. A cross-sectional study involving 59 cases of naturally occurring feline CRF was conducted to determine the prevalence of acid-base disturbances. Cases were categorised on the basis of their plasma creatinine concentrations as mild, moderate or severe. A group of 27 clinically healthy, age-matched cats was assessed for comparison. A low venous blood pH (<7·270) was found in 10 of the 19 severe cases (52·6 per cent), three of the 20 moderate cases (15 per cent) and none of the 20 mild cases. Acidaemia was associated with an increased anion gap contributed to by both low plasma bicarbonate and low chloride ion concentrations. Biochemical analysis of urine samples showed urine pH to decrease with increasing severity of renal failure. Urinary loss of bicarbonate was not associated with the occurrence of acidaemia and there was a tendency for urinary ammonium ion excretion to decrease as the severity of renal failure increased. Cats with naturally occurring CRF do not show plasma biochemical evidence of acid-base disturbances until the disease is advanced. [source] | ||||||||||