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Biomedical subjects

S A Kleit

Publications and source records attributed to S A Kleit.

At least 37 records · Page 2Linked to original sources
PubMed1976

Nephrotoxicity of cephalosporin-gentamicin combinations in rats.

TO STUDY THE POSSIBILITY THAT CEPHALOSPORINS AUGMENT THE NEPHROTOXICITY OF GENTAMICIN, GROUPS OF RATS WERE GIVEN FOUR HOURLY SUBCUTANEOUS DOSES OF: gentamicin (5 mg/kg), gentamicin plus cephalothin (100 mg/kg), gentamicin plus cefazolin (20 mg/kg), gentamicin plus cefazolin (50 mg/kg), gentamicin plus cephaloridine (50 mg/kg), or saline diluent for 15 days. Periodic measurements were made of urine volume, urine osmolality, urine protein excretion and lysosomal enzymuria, as well as blood urea nitrogen, creatinine clearance, and drug concentrations in renal cortex and medulla. Tissue was examined by light and electron microscopy. Enzymuria and proteinuria increased early in the course of all treatment groups, whereas urine osmolality declined. No distinct patterns of these variables were discernable among the groups. Gentamicin alone, gentamicin plus cephalothin, and gentamicin plus cefazolin (20 mg/kg) caused the same significant fall in glomerular filtrate rate from control values by day 15 (P < 0.05). Gentamicin plus cefazolin (50 mg/kg) and gentamicin plus cephaloridine failed to cause a decline in glomerular filtration rate compared with controls (P > 0.05). Gentamicin concentrations in renal cortex were 5 to 10 times higher than those in medulla in all groups. Cephaloridine and cefazolin (50 mg/kg) also displayed a gradient pattern in renal cortex, whereas cephalothin and cefazolin (20 mg/kg) did not. Cytosegrosomes with myeloid figures were characteristic ultra-structural changes seen in all groups; however, they tended to be smaller with less numerous myeloid bodies in the groups receiving gentamicin plus cephalothin, cefazolin (50 mg/kg), or cephaloridine. Cephalosporins did not augment gentamicin toxicity. High doses of cefazolin and cephaloridine protected kidneys from gentamicin nephrotoxicity. The protection may involve intracellular drug interaction within the renal cortex.

Animals↗
PubMed1976

The influence of selective thrombocytopenia on nephrotoxic nephritis.

Anticoagulation with agents that interfere with fibrin formation inhibit the development of the autologous phase of nephrotoxic nephritis (NTN). Platelet participation in the nephritic process has been suggested but not proved, therefore, the influence of selective thrombocytopenia on the autologous phase in rabbits was evaluated. NTN was produced with goat antirabbit glomerular basement membrane antiserum. Thrombocytopenia was induced with goat antirabbit platelet antiserum 24 hours prior to the onset of nephritis. Platelet accumulation within the nephritic kidney was quantitated using chromium labeled platelets. Thrombocytopenia has no inhibitory effect on the development of the autologous phase of NTN in rabbits. There was no platelet accumulation within the nephritic kidney in the presence of thrombocytopenia. Pharmacologic inhibition of platelet aggregation may be of no benefit in glomerulonephritis produced by a fixed antigen-antibody reaction within the glomerular capillary wall.

Animals↗
PubMed1975

Thrombosis of the renal veins and vena cava. Occurrence in morbid obesity.

Renal vein thrombosis caused the nephrotic syndrome in a patient with morbid obesity. Pulmonary embolism occurred initially, but not after anticoagulants were administered. Surviving for three years, the patient died of profound uremia and hyperosmolar coma. At autopsy, membranous glomerular changes were found. Conclusive exclusion of renal vein thrombosis in the morbidly obese patient with nephrotic syndrome appears advisable.

Autopsy↗
PubMed1975

Iodine absorption in burn patients treated topically with povidone-iodine.

Providone-iodine is used as a topical antimicrobial in burn patients. Although absorption of iodine has been thought to be negligible, several patients have recently been noted with substantial elevations of serum free iodide. Unexplained abnormalities occurred in several of these patients, renal failure, metabolic acidosis, and elevation of serum glutamic oxaloacetic transaminase. It is conceivable that the large iodide loads noted were at least in part responsible for these abnormalities.

Acid-Base Equilibrium↗
PubMed1975

Enzymuria in gentamicin-induced kidney damage.

To assess their potential value as early indicators of gentamicin-induced kidney damage, lysosomal hydrolases were measured in the 24-h urines of rats receiving 30 or 60 mg of gentamicin per kg per day for 15 days. Proteinuria, urine osmolality, blood urea nitrogen, and creatinine clearance were also measured. Kidney tissue was examined by both light and electron microscopy. Beta-galactosidase, beta-n-acetyl-hexosaminidase, and alpha-fucosidase were sensitive indicators and were significantly elevated above control values by day 3 at both doses (P < 0.01). Proteinuria, urine osmolality, and tests reflecting glomerular filtration rate were later indicators of nephron damage. Changes by light microscopy were detected on day 5. Necrosis was most prominent in the proximal convoluted tubules on day 10. Electron microscopy revealed numerous cytosomes with myeloid bodies within the proximal tubular epithelium on day 5. Lysosomal enzymuria appears to be an early manifestation of gentamicin nephrotoxicity and may possibly be related to the lysosomal abnormalities seen on electron microscopy.

Animals↗
PubMed1975

Acute renal failure following trauma.

Acute renal failure is often fatal, but usually this complication following trauma is avoidable. Of fifteen patients with acute tubular necrosis associated with severe trauma, thirteen survived. This is a marked improvement in survival rate compared with the rates previously published. We credit the improvement to aggressive medical and surgical treatment by a team of orthopaedic surgeons, nephrologists, and surgeons.

Acute Kidney Injury↗
PubMed1975

Acute renal failure following operation for aortic aneurysm.

Thirty-eight patients with acute renal failure following operation for aortic aneurysm were analyzed retrospectively in search of predictors of survival. Of 14 potential predictor variablesonsidered, none taken singly were significant; however, the combination of age, operative interruption of renal blood flow and prior renal dysfunction served as a significant predictor, p less than 0.05. Low survival rates occurred if the patient was over 70 years of age, if renal blood flow required interruption or if preoperative renal impairment was present. High survival rates occured in patients less than 70 years of age who had no interruption of renal blood flow and who had normal preoperative renal function. Although the total mortality rate of these patients with acute renal failure was 61 per cent, only one of 12 patients with favorable prognostic indicators died. Acute renal failure following aortic aneurysm repair has no worse prognosis that that stated in the literature for acute renal failure following other surgical procedures. A virorous therapeutic approach should be maintained despite the advent of complications.

Acute Kidney Injury↗
PubMed1975

Experimental aminoglycoside nephrotoxicity.

The nephrotoxicities of gentamicin and three other experimental aminoglycosides were compared at a single 60 mg. per kilogram per day dose in rats. Renal function, lysosomal enzymuria, and antibiotic concentrations in plasma, urine, and renal tissue were measured at regular intervals throughout the course of treatment. Kidney tissue was examined by light and electron microscopy in animals killed at intervals throughout the period of antibiotic administration. Proteinuria and enzymuria were early indicators of nephron dysfunction, whereas endogenous creatinine clearance declined later in the course of treatment. All animals were killed 24 hours after a previous antibiotic injection and displayed sustained renal tissue antibiotic concentrations which were 5 to 10 times higher than those in serum or urine. When assayed separately, renal cortical tissue had a fivefold greater antibiotic concentration than renal medulla. Light microscopy displayed necrosis of the pars convoluta of the proximal tubule. Electron microscopy revealed appearance of cytosegrosomes with myeloid bodies. It is possible that impaired cytoplasmic degradation of sequestered organelle membranes, resulting from aminoglycoside accumulation, is responsible for the myeloid body formation and subsequent tubular necrosis.

Aminoglycosides↗
PubMed1974

Comparison of the distribution of tobramycin and gentamicin in body fluids of dogs.

Tobramycin serum, thoracic lymph, renal lymph, and urine concentrations were measured in mongrel dogs after intravenously administered 5, 10, and 20 mg/kg doses. These were compared with intravenous gentamicin delivered at 5 and 20 mg/kg. Both drugs achieved similar concentrations in serum and thoracic lymph. At 20 mg/kg, tobramycin showed consistently higher renal lymph and urine concentrations than gentamicin. At 5 mg of tobramycin per kg, renal lymph and urine concentrations were higher than with gentamicin only within the 1st h after administration. Thereafter the difference was no longer significant. These data suggest that on the basis of distribution in the body fluids of dogs, tobramycin is a reasonable alternative to gentamicin.

Animals↗