ABSTRACT
The influence of magnesium (Mg) deficiency on the concentration of calcium (Ca) in the aorta, heart, and kidney was evaluated in uremic rats. A total of 32 rats were randomly assigned to two groups: one group made uremic by the 5/6 nephrectomy method, and the other serving as sham-operated controls. Both groups were randomly assigned to two subgroups: one group given a Mg-deficient diet and the other fed a Mg-supplemented diet. After 12 weeks on the regimen, all animals were sacrificed. In Mg-supplemented uremic rats, the concentration of Ca in the aorta was higher than in Mg-supplemented control rats. The concentration of Ca in the aorta was further increased in Mg-deficient uremic rats. The concentrations of Ca in the heart and the kidney were also increased in Mg-deficient uremic rats, as compared with Mg-supplemented uremic rats. The concentration of Mg was decreased in the aorta and increased in the kidney of Mg-deficient rats. There was no significant influence of Mg deficiency on the concentration of phosphate in tissue. Results suggest that Mg deficiency in uremia may increase aortic calcification.
Subject(s)
Calcinosis/etiology , Calcium/analysis , Magnesium Deficiency/complications , Magnesium/analysis , Phosphates/analysis , Animals , Calcinosis/physiopathology , Calcium/blood , Culture Techniques , Diet , Disease Models, Animal , Magnesium/blood , Male , Phosphates/blood , Random Allocation , Rats , Rats, Sprague-Dawley , Reference Values , UremiaABSTRACT
The concentration of calcium was measured in the aorta, heart, and kidney of uremic rats treated with 100 ng/kg/day 1,25-dihydroxyvitamin D3 (1,25 D3) or 60 mg/kg/day diltiazem for 12 weeks. The concentration of calcium was increased in the aorta, heart, and kidney of uremic rats, and was further increased by administration of 1,25 D3. The 1,25 D3-induced increase in calcium in the aorta was inhibited by diltiazem, but this effect was not accompanied by a decrease in serum calcium x phosphate products. Diltiazem had no effect on the 1,25 D3-induced increase of calcium in the heart and kidney. Thus, in uremia 1,25 D3 may promote the calcification of the aorta; calcium antagonists may protect against calcification without a reduction in serum calcium x phosphate products.
Subject(s)
Aorta/metabolism , Calcitriol/pharmacology , Calcium Channel Blockers/pharmacology , Calcium/metabolism , Diltiazem/pharmacology , Kidney/metabolism , Myocardium/metabolism , Uremia/drug therapy , Animals , Aorta/drug effects , Aorta/pathology , Calcinosis , Calcitriol/administration & dosage , Calcium Channel Blockers/administration & dosage , Diltiazem/administration & dosage , Disease Models, Animal , Heart/drug effects , Kidney/drug effects , Kidney/pathology , Male , Myocardium/pathology , Phosphates/metabolism , Rats , Rats, Sprague-Dawley , Uremia/metabolismABSTRACT
The adsorption of the anticoagulant nafamostat mesilate (FUT-175) by five different hemodialysis membranes was studied in vivo and in vitro. In vivo, FUT-175 was adsorbed strongly by a polyacrylonitrile (AN69) membrane and slightly by another polyacrylonitrile (J-PAN) membrane but not by Cuprophan (CU), hemophan (HE), or polymethylmethacrylate (PMMA) membranes during hemodialysis performed in 4 patients in whom FUT-175 was used as an anticoagulant. Only during hemodialysis using the AN69 membrane did FUT-175 not induce a significant prolongation of celite-activated coagulation time. In vitro studies showed that FUT-175 was adsorbed by the AN69, J-PAN, and PMMA membranes but not by the CU and HE membranes. Methylene blue, a dye that possesses a cationic portion in its chemical structure, stained AN69, J-PAN, and PMMA membranes. Since FUT-175 also possesses a cationic portion, we conclude that FUT-175 is adsorbed by negatively charged membranes via an ionic bond and is unsuited for use as an anticoagulant in hemodialysis using an AN69 membrane because of that membrane's marked capacity to adsorb FUT-175.
Subject(s)
Antithrombins , Guanidines , Membranes, Artificial , Renal Dialysis , Adsorption , Benzamidines , Guanidines/chemistry , Humans , Renal Dialysis/instrumentationABSTRACT
We studied the pharmacokinetics of aztreonam (AZT) in 6 patients with renal insufficiencies during nonhemodialysis and hemodialysis. After intravenous injection of 1 g AZT, it was found that serum AZT concentrations during hemodialysis were different from those during nonhemodialysis and serum half-lives (T 1/2 beta) were 3.44 hours and 16.97 hours, respectively. AZT clearance changed from 0.762 L/hr during hemodialysis to 3.360 L/hr during nonhemodialysis. These findings suggest that hemodialysis patients should receive the standard dose of AZT as a loading dose, followed by one-half the loading dose per day and receive a supplemental dose equal to half their usual maintenance dose after each dialysis session.