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Biomedical subjects

E S Bear

Publications and source records attributed to E S Bear.

12 recordsLinked to original sources
PubMed1977

Immune complex disease associated with an infected ventriculojugular shunt: a curable form of glomerulonephritis.

A 22-year-old man with a ventriculojugular shunt had edema, hematuria, proteinuria, hypocomplementemia, azotemia, and S epidermidis bacteremia. Initial percutaneous renal biopsy showed a diffuse proliferative glomerulonephritis. Subendothelial and intramembranous deposits were seen on electron microscopy. Immunofluorescent studies were positive for IgG and C3. A repeat percutaneous renal biopsy six weeks after cessation of antibiotic therapy revealed a mild proliferative glomerulonephritis with some evidence of resolution. No deposits were seen on electron microscopy and immunofluorescent studies were negative. At elective shunt revision three months after cessation of therapy, culture of the jugular portion of the removed shunt revealed S epidermidis. Early recognition of immune complex glomerulonephritis occurring with an infected ventriculovascular shunt should permit early treatment (antibiotic therapy and removal of the infected foreign body) and a favorable outcome.

Adult↗
PubMed1976

Suicidal ingestion of isoniazid: an uncommon cause of metabolic acidosis and seizures.

Despite the widespread use of isoniazid, suicidal ingestion is rare. Two patients are presented who ingested 5 gm and 12 gm respectively, both having seizures within two hours and severe metabolic adisosis. They were treated successfully with intravenous administration of diazepam and bicarbonate, and forced diuresis. Both patients showed a mild rise in levels of serum glutamic oxaloacetic transaminase and lactic acid dehydrogenase. Physicians should be alerted to the possibility of isoniazid ingestion in patients with an unexplained severe metabolic acidosis and seizures.

Acidosis↗
PubMed1975

Factors influencing sodium and water excretion in uremic man.

Urinary excretion of sodium and water was investigated in patients with chronic end-stage renal disease before and after three different experimental manipulations: reduction in urea solute load by dialysis while extracellular fluid volume (ECFV) was maintained, dialysis without alteration in urea solute load or ECFV and reduction in ECFV without alteration in urea solute load. Sodium and water excretion significantly declined in association with a reduction in both urea solute load and ECFV, but not during a dialysis when reduction on both of these indexes was prevented. The excretory changes occurred in the absence of any alteration in creatinine clearance. The studies suggest that both solute load and the degree of extracellular fluid volume expansion contribute independently to the rate of sodium and water excretion in chronic renal disease. It is concluded that in any given patient the overall excretion of sodium and water is directly influenced by a number of factors including the solute load, the degree of ECFV and the glomerular filtration rate.

Adult↗