One of the major adverse reactions to gentamicin sulfate administration is nephrotoxicity. Factors potentiating or modifying this toxicity have not been studied. The purpose of this investigation is to examine through use of an experimental animal model the effect on gentamicin nephrotoxicity of metabolic acidosis, a common physiological alteration frequently observed in clinical practice.Methods. Male Sprague-Dawley rats weighing 220-240 g were fed Purina Rat Chow and weighed daily. Animals were divided into 2 groups. In group one, 23 rats were given tap water ad libitum, 18 of which were injected im with gentamicin sulfate 20 mg/kg body wt daily for 16 days. The remaining 5 animals were given 40 mg/kg body wt daily for 12 days. In group 2, metabolic acidosis was induced in 27 rats by substituting 1% NH,Cl solution for drinking water throughout the experiment. Gentamicin sulfate 20 mg/kg body wt was administered im daily for 18 of these rats beginning 24 hr after acid loading; 9 rats were given an equivalent volume of normal saline for 16 days.Two milliliters of blood were sampled from the tail vein on days 6, 12 and 16. Serum urea nitrogen (SUN) was determined by a Technicon Autoanalyzer. Serum CO, content was measured by a Natelson Microgasameter Model 600.The animals in each series were sacrificed following completion of the experiment. 1Supported by a Grant from the Kidney Foundation of Michigan. 2 Theodore W. Kurtz is a trainee of the Cardiovascular Research Program.Kidneys were excised and submitted for macroscopic and microscopic examination. Tissues were stained with hematoxylin-eosin for histological examinations.Renal cortical uptakes of paraaminohippurate (PAH) and tetraethylammonium bromide (TEA) were also evaluated in vitro as measures of renal function (1) in the following groups of male Sprague-Dawley rats, weighing 160-170 g at the beginning of the experiment. Group I: Twelve rats were given tap water ad libitum, 6 of which were injected im with gentamicin sulfate 20 mg/kg body wt daily for 16 days. The other 6 rats were injected with an equivalent volume of saline for the same duration of time. Group 11: Twelve rats were made acidotic as previously described. Gentamicin sulfate 20 mg/kg body wt was given im to 6 rats for 16 days; another 6 rats were given saline im as controls. All animals were sacrificed on the 16th day, kidneys removed and immediately immersed in ice cold saline for PAH and TEA uptake studies.Renal cortical slices 0.3-0.4 mm thick and weighing approximately 70-90 mg were prepared with a Stadie-Riggs microtome. Incubation of slices at pH 7.40 in 3.0 ml Cross and Taggert's solution (2), containing 2 X A4 each of 3H-paraaminohippurate and 14C-tetraethylammonium bromide was performed on a Dubnoff metabolic shaker at 25", shaking at 100 cycles/ min with 100% oxygen as the gas phase for 90 min.After incubation slices were suspended in 10% trichloroacetic acid, homogenized, and centrifuged. One ml supernatant was placed 894
A double-blind cross-over study was conducted on 21 patients on maintenance hemodialysis to determine if changes in serum erythropoietin level, packed cell volume, red cell mass, hemoglobin concentration and 2,3-diphosphoglycerate content of red cells follow administration of nandrolone decanoate. There was a rise in mean serum erythropoietin level, packed cell volume, red cell mass and hemoglobin concentration. No alteration in mean 2,3-diphosphoglycerate content of red blood cells was found.
The dialysis dementia syndrome was observed in eight of 21 patients dialyzed in a small center during a 22-month period in which dialysate contained aluminum levels of 618 microgram/liter. This incidence of 38% was significantly higher than the zero incidence of four prior years when no aluminum was added to city water (p less than 0.05) and also when compared to the zero incidence in the 2.5 years subsequent to deionization of dialysis water which lowered its aluminum content to less than 1 microgram/liter (p less than 0.0002). Since other factors were not altered, we conclude that aluminum intoxication from the dialysate was the cause for the outbreak of this progressive encephalopathy.
An infusion of 180 mEq sodium acetate was given to nine dialysis patients and eight normal volunteers simulating the transfer of acetate that occurs during 30 min of rapid hemodialysis. While serum acetate concentrations had almost normalized 15 min after the end of infusion, there was no increase in serum cholesterol and triglyceride concentrations. In this short-term study, acetate does not appear to be a major contributing factor for the hyperlipidemia of dialysis patients.
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