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Biomedical subjects

M H Gault

Publications and source records attributed to M H Gault.

At least 109 records · Page 6Linked to original sources
PubMed1976

Toxic nephropathy after low-dose methoxyflurane anesthesia: drug interaction with secobarbital?

Vasopressin-resistant nonoliguric renal insufficiency developed in a 57-year-old man after 2 1/2 hours of low-dose methoxyflurane anesthesia. Secobarbital, 100 mg daily, had been taken for 1 month before. Of 13 patients in whom the influence of methoxyflurane on renal function was being studied, he was the only one to have taken a drug that induces microsomal enzymes. Blood values of methoxyflurane in this patient were lower than group means on all five occasions during anesthesia. Postoperatively his serum inorganic fluoride value reached 114 mumol/l -- more than two standard deviations greater than the group mean. Peak values for serum urea nitrogen, creatinine and uric acid and postvasopressin urine osmolality, and the lowest creatinine clearance in this patient also differed by more than 2 SD from the group mean, and the peak amount of oxalate excreted in his urine was double the group mean. Pretreatment with the barbiturate appears to have altered methoxyflurane metabolism and led to toxic concentrations of metabolites in the blood.

Drug Interactions↗
PubMed1976

Extraction of digoxin and its metabolites from urine and their separation by Sephadex LH-20 column chromatography.

The efficiency with which serveral solvent systems extract digoxin and its metabolites from urine has been studied and column chromatography using Sephadex LH-20 has been used to separate digoxin and its metabolites. These procedures have been evaluated and used to study the excretion of 3H-digoxin-12alpha and its metabolites in urines collected serially in 7 patients and in bile in one. The percentage of the radioactivity excreted as metabolites in urine and bile was found to reach a peak within the first day and then to gradualy decline to minimal amounts in patients with advanced renal failure as well as those with good renal function. The maximum percentage measured as metabolites in 4 patients with the most advanced renal failure was 10%.

Bile↗
PubMed1976

Glomerular injury in patients with neoplasia.

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.

Adolescent↗
PubMed1976

Prediction of creatinine clearance from serum creatinine.

A formula has been developed to predict creatinine clearance (Ccr) from serum creatinine (Scr) in adult males: (see article)(15% less in females). Derivation included the relationship found between age and 24-hour creatinine excretion/kg in 249 patients aged 18-92. Values for Ccr were predicted by this formula and four other methods and the results compared with the means of two 24-hour Ccr's measured in 236 patients. The above formula gave a correlation coefficient between predicted and mean measured Ccr's of 0.83; on average, the difference predicted and mean measured values was no greater than that between paired clearances. Factors for age and body weight must be included for reasonable prediction.

Adolescent↗
PubMed1975

Letter: The clinical course of patients with analgesic nephropathy.

Thirty-four patients with analgesic nephropathy were followed at intervals of 1 to 3 months with measurements of creatinine clearance and serum concentration of acetylsalicylic acid (ASA) for a total of 105 patient-years. Diagnostic criteria included total consumption of at least 2 kg of phenacetin and 3 kg of ASA, compatible tissue abnormality on biopsy and evidence of papillary necrosis on an intravenous pyelogram. Nephropathy was induced by the same compound analgesic containing ASA, pehnacetin, caffeine and codeine (APC&C) in 30. Phenacetin was removed from this preparation in 1970 and replaced by an approximately equal amount of ASA (ACC). Creatinine clearance remained unchanged or improved in 11 of 15 patients who stopped taking analgesics containing phenacetin or ASA and in 10 of 11 of those who continued to take the ACC preparation. In contrast, renal function deteriorated in seven of eight patients who continued to abuse APC&C analgesics. The results suggest that phenacetin is necessary for the major nephrotoxic effect of this APC&C combination, but that ASA is not absolved of some nephrotoxicity.

Analgesics↗
PubMed1975

Solitary intrarenal cyst: correctable cause of hypertension.

A patient with hypertension was found to have a solitary renal cyst in his right kidney. Peripheral plasma renin activity was elevated following furosemide challenge, and there was increased renal vein renin activity on the affected side with suppression of renin secretion from the contralateral kidney. Percutaneous aspiration of the cyst and injection of a sclerosing contrast medium was associated with a sustained decrease in blood pressure.

Contrast Media↗
PubMed1973

Peritoneal dialysis solutions.

Certain preventable complications in the treatment of renal failure, in part related to the composition of commercially prepared peritoneal dialysis solutions, continue to occur.Solutions are advocated which would contain sodium 132, calcium 3.5, magnesium 1.5, chloride 102 and lactate or acetate 35 mEq./1., and dextrose 1.5% or about 4.25%. Elimination of 7% dextrose solutions and a reduction of the sodium and lactate concentrations should reduce complications due to hypovolemia, hyperglycemia, hypernatremia and alkalosis. Reduction in the number of solutions should simplify the procedure and perhaps reduce costs. It is anticipated that some of the changes discussed will soon be introduced by industry.

Acetates↗
PubMed1973

Hepatitis with Australia antigenemia following renal transplantation.

Over a seven-year period 18 of 125 patients who underwent renal transplantation developed hepatitis. Acute hepatic necrosis occurred in two, chronic aggressive hepatitis progressing to posthepatitic cirrhosis in eight, chronic persistent hepatitis in five, acute hepatitis with recovery in two and cholestatic hepatitis in one. Hepatic failure was the cause of death in four and a major contributing factor in three. Fifteen of the 18 were of blood Group A. After renal transplantation Australia antigen (Au) was present in the blood of 12 of the 15 patients with hepatitis who were tested and in one of 38 patients without clinical evidence of liver disease. Once present, Au persisted in all patients but one. Particles measuring 210 to 250 A, characteristic of Au, were seen in liver cells by electronmicroscopy in nine of the 10 patients examined who had hepatitis with Australia antigenemia, but they were not seen in the two patients studied with Au-negative hepatitis.

Acute Disease↗
PubMed1972

Evidence for the nephrotoxicity of analgesics.

Analgesic nephropathy in man is a definite but complex and probably multifactorial disorder, which largely follows long-term abuse of mixed analgesics. In North America the disorder has been almost entirely associated with heavy ingestion of the combination acetylsalicylic acid (ASA), phenacetin and caffeine. There is less clinical and experimental evidence for the nephrotoxicity of single analgesics; however, evidence for the nephrotoxicity of ASA alone is greater than that for phenacetin. In view of the evidence for nephrotoxicity of most mild analgesics, removal of phenacetin from the market would be unlikely to eliminate the problem of analgesic nephropathy.

Analgesics↗