Home About us Contact
|
Home About us Contact | ||
|
|
||
Serum Urea Nitrogen (serum + urea_nitrogen)
Selected AbstractsNew enzymatic assay for serum urea nitrogen using urea amidolyaseJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 2 2003Shigeki Kimura Abstract We established an enzymatic assay for measurement of serum urea nitrogen using urea amidolyase (EC 3.5.1.45) from yeast species. The method is based on hydrolysis of urea by the enzyme. In this assay, we eliminated endogenous ammonium ion by use of glutamate dehydrogenase (EC 1.4.1.4). Then in the presence of urea amido-lyase, ATP, bicarbonate, magnesium, and potassium ions, ammonium ion was produced proportionally to urea concentration in serum. The concentra-tion of ammonium ion formed was determined by adding GLDH to produce NADP+ in the presence of 2-oxoglutarate and NADPH. We then monitored the change of absorbance at 340 nm. The inhibitory effect of calcium ion on this assay was eliminated by adding glyco-letherdiamine-N, N, N,, N,-tetraacetic acid to the reaction system. The with-in-assay coefficient of variations (CVs) of the present method were 1.80,3.76% (n = 10) at 2.8,19.0 mmol/L, respectively. The day-to-day CVs were 2.23,4.59%. Analytical recovery was 92,115%. The presence of ascorbic acid, bilirubin, hemoglobin, lipemic material, ammo-nium ion, or calcium ion did not affect this assay system. The correlation be-tween values obtained with the present method (y) and those by another enzy-matic method (x) was 0.997 (y = 1.02x , 0.10 mmol/L, Sy/x = 0.841, n = 100), with a mean difference of ,0.18 ± 0.86 mmol/L [(values by reference method , that of present method) ± SD] using the Bland-Altman technique. J. Clin. Lab. Anal. 17:52,56, 2003. © 2003 Wiley-Liss, Inc. [source] Protective role of ,-aminobutyric acid against chronic renal failure in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2006Sumiyo Sasaki The protective effect of ,-aminobutyric acid (GABA) against chronic renal failure (CRF) was investigated using a remnant kidney model with 5/6 nephrectomized rats. Nephrectomy led to renal dysfunction, which was evaluated via several parameters including serum urea nitrogen, creatinine (Cr) and Cr clearance. However, the administration of GABA ameliorated renal dysfunction, and a longer administration period of GABA increased its protective effect. In addition, nephrectomized control rats showed an elevation in the fractional excretion of sodium (FENa) with an increase in urinary sodium, while GABA led to a significant decline in FENa. Moreover, nephrectomy resulted in a decrease of serum albumin and an increase of urinary protein with a change in the urinary protein pattern, whereas the rats administered GABA showed improvement in these changes associated with CRF caused by nephrectomy. This suggests that GABA would inhibit the disease progression and have a protective role against CRF. As one of the risk factors for CRF progression, hypertension was also regulated by GABA. The results also indicate that GABA may play a protective role against CRF through improvement of the serum lipid profile, with reductions in triglyceride and total cholesterol. Furthermore, nephrectomy led to renal oxidative stress with a decrease in the activity of antioxidative enzymes and elevation of lipid peroxidation. The administration of GABA attenuated oxidative stress induced by nephrectomy through an increase in superoxide dismutase and catalase, and decrease in lipid peroxidation. The histopathological lesions, including glomerular, tubular and interstitial lesions, under nephrectomy were also improved by GABA with the inhibition of fibronectin expression. This study demonstrated that GABA attenuated renal dysfunction via regulation of blood pressure and lipid profile, and it also ameliorated the oxidative stress induced by nephrectomy, suggesting the promising potential of GABA in protecting against renal failure progression. [source] Protective effect of Hachimi-jio-gan against renal failure in a subtotal nephrectomy rat modelJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 12 2005Noriko Yamabe The protective effect of Hachimi-jio-gan extract against chronic renal failure in a subtotal nephrectomy rat model was investigated. The level of serum urea nitrogen by nephrectomy was increased over 15 weeks, but the administration of Hachimi-jio-gan at 50 and 200 mg led to the decrease. In addition, the levels of creatinine (Cr), urinary methylguanidine (MG) and MG/Cr were increased, whereas Cr clearance dramatically decreased in nephrectomized rats. However, oral administration of Hachimi-jio-gan extract prevented the elevation of these uremic toxins in serum and urine, and the production of hydroxyl radical. Moreover, nephrectomy led to a significant decline in superoxide dismutase (SOD) and catalase activities, but increased glutathione peroxidase activity compared with normal levels, indicating an abnormal antioxidative system. The increased activity of both SOD and catalase by the oral administration of Hachimi-jio-gan suggested that these enzymes are associated with the protective role of Hachimi-jio-gan extract against oxidative stress by nephrectomy. Moreover, the decrease in serum albumin in nephrectomized control rats was increased and proteinuria was ameliorated by the administration of Hachimi-jio-gan with improved glomerular hyalinosis, interstitial fibrosis and inflammation, suggesting the beneficial effect of Hachimi-jio-gan to prevent glomerular sclerosis and progressive renal fibrosis. This study suggests that Hachimi-jio-gan plays a protective role in the progression of chronic renal failure through the decline in uremic toxins, elevation of antioxidative enzyme activity such as SOD and catalase, and amelioration of histopathological lesions in the kidney. [source] Comparison of Glomerular Filtration Rate between Greyhounds and Non-Greyhound DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 3 2006Wm Tod Drost Greyhounds have significantly higher serum creatinine (SCr) concentration than do non-Greyhound dogs that may be attributable to differences in glomerular filtration rate (GFR). By means of plasma clearance of technetium Tc 99m diethylenetriaminepentaacetic acid, GFR was measured in 10 Greyhounds and 10 non-Greyhound dogs with normal findings of physical examination, CBC, serum biochemical analysis, and urinalysis. Dogs were fed the same diet for a minimum of 6 weeks before GFR data collection. Greyhounds had significantly higher mean ± SD GFR (3.0±0.1 vs 2.5±0.2 ml/min/kg; P= .01) and SCr concentration (1.8±0.1 vs 1.5±0.1 mg/dL; P= .03) than did non-Greyhound dogs, but the serum urea nitrogen (SUN) concentration was not significantly different (18±1 vs 18±2 mg/dL; P= .8). Therefore, the higher SCr concentration in Greyhounds is not attributable to decreased GFR, and may be associated with the high muscle mass in the breed. Healthy Greyhounds have higher GFR than do non-Greyhound dogs. [source] Hypercalcemia in Cats: A Retrospective Study of 71 Cases (1991,1997)JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2000Karine CM. A retrospective study was conducted to characterize the diseases, clinical findings, and clinicopathologic and ultrasonographic findings associated with hypercalcemia (serum calcium concentration >11 mg/dL) in 71 cats presented to North Carolina State University Veterinary Teaching Hospital. The 3 most common diagnoses were neoplasia (n = 21), renal failure (n = 18), and urolithiasis (n = 11). Primary hyperparathyroidism was diagnosed in 4 cats. Lymphoma and squamous cell carcinoma were the most frequently diagnosed tumors. Calcium oxalate uroliths were diagnosed in 8 of 11 cats with urolithiasis. Cats with neoplasia had a higher serum calcium concentration (13.5 ± 2.5 mg/dL) than cats with renal failure or urolithiasis and renal failure (11.5 ± 0.4 mg/dL; P <.03). Serum phosphorus concentration was higher in cats with renal failure than in cats with neoplasia (P < .004). Despite the fact that the majority of cats with uroliths were azotemic, their serum urea nitrogen and creatinine concentrations and urine specific gravity differed from that of cats with renal failure. Additional studies are warranted to determine the underlying disease mechanism in the cats we identified with hypercalcemia and urolithiasis. We also identified a small number of cats with diseases that are not commonly reported with hypercalcemia. Further studies are needed to determine whether an association exists between these diseases and hypercalcemia, as well as to characterize the underlying pathophysiologic mechanism for each disease process. [source] Exogenous bone marrow cells do not rescue non-irradiated mice from acute renal tubular damage caused by HgCl2, despite establishment of chimaerism and cell proliferation in bone marrow and spleenCELL PROLIFERATION, Issue 4 2008T.-C. Fang Objective: Various studies have shown that bone marrow stem cells can rescue mice from acute renal tubular damage under a conditioning advantage (irradiation or cisplatin treatment) favouring donor cell engraftment and regeneration; however, it is not known whether bone marrow cells (BMCs) can contribute to repair of acute tubular damage in the absence of a selection pressure for the donor cells. The aim of this study was to examine this possibility. Materials and methods: Ten-week-old female mice were assigned into control non-irradiated animals having only vehicle treatment, HgCl2 -treated non-irradiated mice, HgCl2 -treated non-irradiated mice infused with male BMCs 1 day after HgCl2, and vehicle-treated mice with male BMCs. Tritiated thymidine was given 1 h before animal killing. Results: Donor BMCs could not alleviate non-irradiated mice from acute tubular damage caused by HgCl2, deduced by no reduction in serum urea nitrogen combined with negligible cell engraftment. However, donor BMCs could home to the bone marrow and spleen and display proliferative activity. This is the first report to show that despite no preparative myeloablation of recipients, engrafted donor BMCs can synthesize DNA in the bone marrow and spleen. Conclusions: Exogenous BMCs do not rescue non-irradiated mice from acute renal tubular damage caused by HgCl2, despite establishment of chimerism and cell proliferation in bone marrow and spleen. [source] | ||||||||||