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Biomedical subjects

E Bourke

Publications and source records attributed to E Bourke.

At least 55 records · Page 3Linked to original sources
PubMed1982

Fenoprofen nephropathy: lipoid nephrosis and interstitial nephritis. A possible T-lymphocyte disorder.

Five patients are presented, each of whom had an acute idiosyncratic reaction to fenoprofen calcium (Nalfon) characterized by acute renal failure and marked proteinuria. Renal pathology was similar in all patients. Light microscopy revealed marked lymphocytic inflammatory infiltrates and normal glomeruli. Immunofluorescent staining was minimal or absent. Electron microscopy showed fusion of podocytes in otherwise normal glomeruli. Two patients were studied using T-cell and B-cell specific fluorescent staining, which revealed that the interstitial infiltrates were composed exclusively of T-lymphocytes. This finding is considered in relation to prior experimental and theoretic work. It is suggested that the various clinical and pathologic findings in fenoprofen nephropathy are all manifestations of a disordered cell-mediated immunity.

Acute Kidney Injury↗
PubMed1982

Management of chronic peritoneal catheter malfunction.

This paper presents a modification of Tenckhoff's insertion procedure for chronic peritoneal dialysis catheters and reviews the results of a technique of management of catheter malfunction by manipulation which obviates the need for catheter replacement. 43 catheters in 33 patients were observed for no less than 1 year. Catheters which malfunctioned within 3 weeks benefited only marginally from manipulation. In those catheters which functioned for more than 3 weeks, manipulation extended mean survival time by 103% (8.5-17.3 months) and overall survival did not differ statistically from catheters not requiring manipulation. The technique is safe and simple and contributes to the effective management of patients undergoing chronic peritoneal dialysis.

Adult↗
PubMed1981

Bartter's syndrome - a dilemma of cause and effect.

Six interrelated abnormalities of Bartter's syndrome are analyzed-juxtaglomerular hyperplasia, angiotensin resistance, altered kallikrein-kinin system, hyperprostaglandinuria, hypokalemia, and chloride-losing nephropathy. Arguments are advanced that any one of these could be the proximate cause and result in all the others. By the same token, each abnormality could be a consequence of any of the others and, furthermore, modulate the others by negative or positive feedback. Despite many recent insights, available data do not permit a definitive conclusion as to the locus of the primary abnormality. Rather, the syndrome presents as a remarkable biological counterpart to an electronic integrated circuit. The altered physiology of Bartter's syndrome is reviewed and the pathogenesis of the syndrome analyzed in the light of recent literature.

Angiotensin II↗
PubMed1981

Bartter's syndrome: physiological and pharmacological studies.

Six siblings with Bartter's syndrome were studied. Increased urinary immunoreactive prostaglandin E (iPgE) was corrected by administration of the prostaglandin synthetase inhibitors, indomethacin, ibuprofen and meclofenamate. In addition, plasma potassium rose, plasma renin activity and angiotensin resistance decreased, and the exaggerated natriuresis following saline loading was abolished. Increased urinary iPgE also became normal following the phospholipase inhibitor, mepacrine, but the other abnormalities remained unaltered. The kallikrein inhibitor, aprotinin, did not alter urinary iPgE, plasma potassium or electrolyte balance. During hypotonic saline infusion, proximal tubular potassium or electrolyte balance. During hypotonic saline infusion, proximal tubular sodium reabsorption was normal or increased. Free water clearance and the percentage of distally delivered sodium which was reabsorbed were, however, significantly decreased. The results suggest that neither the increased renal PgE production nor the hyperbradykininemia seen in Bartter's syndrome play a major role in its pathogenesis, or manifestations, and that the effects of the prostaglandin synthetase inhibitors on the syndrome are non-specific. The results and relevant literature are analysed in an attempt to identify the initial defect in the interrelated sequence of events. The data are compatible with an intrarenal defect in sodium transport, leading to increased sodium delivery to the distal tubule, with secondary hyperreninemia, hypokalemia and elevated iPgE excretion.

Adult↗
PubMed1980

Complement deficiency and nephritis. A report of a family.

A family is described in which three children had homozygous deficiency of C3 and in which both parents and two other children were heterozygous for the C3 null gene. One child with heterozygous C3 deficiency was found to have membranoproliferative glomerulonephritis; proteinuria and/or microscopical haematuria was present in all three homozygous C3-deficient children. All children with homozygous or heterozygous C3 deficiency were, to a varying degree, susceptible to infection. The only child of the family with normal complement had no increased risk of infection and no renal disease. This family study provides further support for the proposal that C3 deficiency predisposes to nephritis.

Adolescent↗
PubMed1980

Effect of megadoses of ascorbic acid on serum and urinary oxalate.

Serum and urinary oxalate was determined in 9 normal subjects, ingesting 8 g of ascorbic acid daily. Serum oxalate levels increased to 310% of control values during supplementation. Plasma ascrobate levels reached a mean value of 3.6 mg% far exceeding the previously reported plateau level of 1.8 mg%. Urinary oxalate gradually increased during ascorbate intake and 7 days post cessation of ascorbate, rose unexpectedly for all subjects into the hyperoxaluric range.

Administration, Oral↗
PubMed1979

Effects of fluorocitrate on renal ammoniagenesis and glutamine metabolism in the intact dog kidney.

Renal glutamine metabolism was studied in vivo following infusions of fluorocitrate into chronically acidotic and alkalotic dogs. Coincident with a dramatic rise in renal cortical citrate concentrations, there was a significant fall in tissue glutamate in both acid-base states. This was accompanied by a significant increase in total renal ammonia production. Glutamine metabolism and ammoningenesis in alkalotic dogs receiving fluorocitrate simulated that achieved in acidotic dogs. The simultaneous administration of alpha-ketoglutarate and fluorocitrate significantly diminished the fall in tissue glutamate and the rise in ammoniagenesis induced by fluorocitrate alone. These results are compatible with the hypothesis that ammonia production from glutamine is enhanced secondary to increased glutamate deamination. We postulate that this chain of events may be the consequence of impaired alpha-ketoglutarate production from citrate.

Acidosis↗
PubMed1979

Metabolism of p-aminobenzoic acid in the perfused livers of chronically uraemic rats.

1. Chronic renal failure was induced in rats by surgical removal of thirteen-sixteenths of renal tissue. 2. The metabolism of p-amino[14C]benzoic acid was studied in the isolated perfused livers of control and chronically uraemic rats. There was a slower rate of clearance and decreased overall metabolism of the compounds in the uraemic rats. 3. Conjugation of p-amino[14C]benzoic acid with glycine and the formation of p-aminobenzoic acid glucuronide were both significantly decreased in the uraemic rats, but there was a significant increase in acetylation of both p-aminobenzoic acid and its glycine conjugate.

4-Aminobenzoic Acid↗
PubMed1979

Lymphocyte sequestration by the liver in alcoholic hepatitis.

The possibility that lymphocytes are sequestered by the liver in patients with alcoholic hepatitis was investigated. Sixteen patients who had liver biopsy specimens taken were studied as follows: The T- and B-lymphocyte populations of the peripheral blood and liver biopsy digest were quantitated. The liver biopsy specimens were studied by light and electron microscopy for lymphocyte-hepatocyte interaction. The data were analyzed by comparing the results of patients with and without the presence of Mallory bodies (MBs) in the liver. When MBs were present, the percentage of T cells was significantly increased in the liver compared with peripheral blood. By electron microscopy, two livers with MBs showed lymphocyte-hepatocyte interaction. The results support the concept that lymphocytes participate in a cell-mediated immune process when MBs are present in the liver.

Adult↗
PubMed1978

Juvenile nephronophthisis, congenital hepatic fibrosis and retinal hypoplasia in twins.

Juvenile nephronophthisis has been recognized recently as an important cause of chronic renal failure in childhood and adolescence. This report describes clinical and morphological findings in monozygotic twins in whom the triad of juvenile nephronophthisis, congenital hepatic fibrosis and retinal hypoplasia coexisted. The findings are discussed in relation to previous reports of nephronophthisis associated with either retinal abnormalities or congenital hepatic fibrosis. The occurrence of similar ocular and hepatic anomalies with the other cystic kidney diseases, polycystic disease and medullary sponge kidney disease is reviewed. A spectrum of oculo-hepato-renal syndromes is identified with many interrelated features which suggest a shared basic aetiology.

Child, Preschool↗
PubMed1977

Acid-base induced alterations in glutamine metabolism and ureogenesis in perfused muscle and liver of the rat.

The effects of altered acid-base balance on the production of urea and the metabolism of glutamine were investigated in the isolated perfused liver and hindquarter of the rat. In the isolated perfused rat liver, lowering of perfusate pH without altering bicarbonate concentration significantly reduced urea production and increased net glutamine synthesis, although the converse did not obtain. In the isolated perfused rat hindquarter when perfusate pH and bicarbonate were simultaneously reduced glutamine synthesis was significantly increased. The combined hepatic and muscle increase in glutamine synthesis accounted for 89% of the decrease in hepatic urea synthesis under these experimental conditions. These changes in nitrogen metabolism are interpreted in terms of adaptations which offset the initial alterations in hydrogen ion homeostasis.

Acid-Base Imbalance↗