ABSTRACT
A multicentre evaluation of the new analyser, Hitachi 911, is reported for three different classes of homogeneous immunoassays (latex assays, immunoprecipitation assays, and CEDIA assays). The evaluation protocol follows ECCLS, IFCC and NCCLS guidelines. Using patient samples and commercial controls, within run and between run coefficients of variation were less than 3% in most cases, but as high as 9.7% for some CEDIA and latex assays. All the assays were linear, either in the reference or the therapeutic range of the analytes. No interference by haemolysis, lipaemia or icterus was observed. The methods were compared with other commercial methods. Coefficients of correlation were higher than 0.94 for all the methods. However, there were differences of slope and intercept for rheumatoid factor, apolipoprotein A-I and apolipoprotein B. On the Hitachi 911, all of the eight methods give precise and accurate results, and compare well with other established methods on immunoassay dedicated analysers. The discrepancies observed could be ascribed to current problems of immunoassay standardization.
Subject(s)
Chemistry, Clinical/instrumentation , Immunoassay/methods , Evaluation Studies as Topic , Humans , Reproducibility of ResultsABSTRACT
To assess whether calcium could be involved in the gentamicin-induced nephrotoxicity, we have studied the effect of the calcium channel blocker verapamil on renal function in rats intoxicated by gentamicin. Male Wistar rats were divided in three groups. In group I (n = 7) they were injected with gentamicin 100 mg/kg body wt/day s.c. for 5 days. In group II (n = 6), they received gentamicin and verapamil s.c. 2 mg/rat/day. In group III rats served as control. Plasma creatinine and creatinine clearance were daily measured. Rats treated with gentamicin showed a progressive increase in plasma creatinine and a drop in creatinine clearance. No differences between rats treated with gentamicin and those with gentamicin plus verapamil were observed. The urinary flow decreased after treatment with gentamicin, this decrease being more marked in rats treated with verapamil. No differences in daily urinary sodium and potassium excretion were found between intoxicated rats treated or not with verapamil. The present results show that, in rats, verapamil has no protective effect against the nephrotoxicity of gentamicin.
Subject(s)
Calcium/physiology , Gentamicins/adverse effects , Kidney Diseases/chemically induced , Verapamil/pharmacology , Animals , Kidney Diseases/physiopathology , Male , Rats , Rats, WistarABSTRACT
The present study was performed to measure the uptake of main renal cortical fuel substrates (glutamine and lactate) and the release of the main renal cortical products (ammonia and glucose) by cortical slices from gentamicin-treated rats. Experiments were done in 2 groups of female Wistar rats (250 g): In gentamicin group (n = 13), rats were injected s.c. with gentamicin-sulphate 100 mg/Kg body wt/day for 5 days. Control rats (n = 13) received isotonic saline. After anesthesia and blood sampling, renal cortical slices were obtained and incubated with L-glutamine and/or lactate at 1 or 5 mM concentration, containing L-glutamate and/or pyruvate at 0.1 or 0.5 mM. Creatinine clearance was reduced to a 50% in gentamicin-treated rats. In addition these animals showed a sharp increase in urinary excretion of N-acetyl-beta-D-glucosaminidase and alkaline phosphatase. Light microscopy examination revealed extensive cell necrosis and tubular obstruction of the proximal tubules in kidneys of rats injected with gentamicin. The renal cortical gentamicin concentration of rats injected with gentamicin was 310 +/- 43 mu/g, whereas it was undetectable in control rats. Cortical slices from gentamicin-treated rats, compared to control ones, showed a reduced production of ammonia and glucose, without differences in glutamine or lactate extraction. These alterations can be explained by both the increased rate of anabolic reactions to recover cell damage associated to renal failure, as well as by a direct effect of gentamicin on the rate of carboxylation reactions.