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Biomedical subjects

A M Robson

Publications and source records attributed to A M Robson.

At least 55 records · Page 3Linked to original sources
PubMed1980

Effects of dietary intake and hemodialysis on protein turnover in uremic children.

The dynamic aspects of protein metabolism in uremic children were studied by using newly developed gas chromatography and mass spectrometry micromethods for determining nitrogen-15 enrichment in plasma lysine during a continuous i.v. infusion of 15N-lysine. Protein flux in uremic children was low and varied directly with protein and energy intake, which themselves were closely related in the diets consumed by the study subjects. Hemodialysis did not alter acutely protein flux. Protein flux in children undergoing chronic hemodialysis was still reduced below normal but was higher than that in nondialyzed uremic children at each level of protein-energy intake. The ratio of protein flux to protein intake was 0.05 +/- 0.003 g of protein x kg-1 x day-1 x kcal ingested in the nondialyzed uremic children, but it increased to a normal vaue of 0.11 +/- 0.03 g x kg-1 x day-1 x kcal in those on longterm hemodialysis. We conclude that the low protein turnover rates in our uremic population reflect the decreased protein-energy intake commonly found in such patients and that reduction of azotemia by chronic hemodialysis may improve whole body transport at a given energy intake.

Adolescent↗
PubMed1980

Inhibitory factors of lymphocyte transformation in sera from patients with minimal change nephrotic syndrome.

This study was undertaken to establish the specificity and relation to disease activity of serum inhibitors of lymphocyte function in minimal change nephrotic syndrome (MCNS). Sera from 21 children with MCNS were evaluated for their effect on blast transformation of normal human lymphocytes after stimulation with E-PHA, ConA, PWM or allogeneic cell surface antigens (mixed lymphocyte cultures;MLC). Sera from patients in relapse on no medication (n = 12), in relapse on steroids (n = 5), and in remission on steroids (n = 7) were significantly more inhibitory than sera from patients in late remission off steroids (n = 14 both in mitogen induced blast transformation and in MLC. Sera from eight children with other forms of nephrotic syndrome exhibited the same degree of inhibition of E-PHA, ConA, and PWM induced mitogenesis but significantly less inhibition of MLC when compared to 12 MCNS patients in untreated relapse. Thus serum inhibition of mitogen induced blast transformation is not specific for MCNS but occurs in other forms of nephrotic syndrome as well. Conversely, sera from MCNS patients does selectively inhibit MLC. Finally, the inhibitory activity of MCNS sera for both mitogen and cell surface antigen stimulation correlates with the course of the disease.

Adolescent↗
PubMed1979

Congenital glomerulosclerosis and nephrotic syndrome in two infants. Speculations and pathogenesis.

The incidental finding of hyalinized glomeruli in otherwise normal infant kidneys is referred to as congenital glomerulosclerosis. Two infants had extensive glomerulosclerosis manifested by nephrotic syndrome, severe oliguria, and progressive renal failure. Both patients were believed to have had intrauterine infections. These two cases have unequivocally identified congenital glomerulosclerosis as one of the causes of nephrotic syndrome in infancy. In addition, they suggest that extensive glomerulosclerosis in some cases may be a result of congenital infections.

Female↗
PubMed1979

Severe immobilization hypercalcemia, renal insufficiency, and calcification.

Severe hypercalcemia with decreased renal function, hypertension, and renal calcifications developed in a 14-year-old boy who required prolonged immobilization for multiple fractures. Parathyroid hormone was not detectable in the serum. Urinary calcium excretion was high. Initially, mobilization was impossible and the patient was treated with a high fluid intake, low calcium intake, acidification of the urine, furosemide, and a passive exercise program. Renal function improved and renal calcifications resolved but hypercalcemia did not resolve. After mobilization the serum calcium concentration became normal rapidly. This treatment regimen is suggested for use in patients with immobilization hypercalcemia when mobilization is impossible.

Accidents, Traffic↗
PubMed1978

Maturation of p-aminohippuric acid transport in the developing rabbit kidney: interrelationships of the individual components.

The excretion of both endogenous organic (aryl) acids, such as benzoic acid, and exogenous ones, such as p-aminohippuric acid (PAH), penicillin, and furosemide, is reduced in the human neonate and other immature animals. The unique developmental pattern of aryl acid transport in immature rabbit kidney cortex slices is produced by the interrelationships of PAH uptake, efflux, and amount of intracellular binding protein, all of which reach mature levels at different ages.

Aminohippuric Acids↗
PubMed1977

Severe glomerulonephritis complicated by coagulopathy: treatment with anticoaguland and immunosuppresive drugs.

Serial determinations, using plasma fibrinogen gel chromatography as well as standard methodology, demonstrated that six children with severe glomerulonephritis, characterized on renal biopsy by glomerular necrosis and crescent formation, had persistent evidence of intravascular coagulation. Based on these observations, therapy with anticoagulants and azathicoagulants and azathioprine was instituted for one year; treatment with anticoagulants was continued for a second year. Anticoagulant therapy was initiated with heparin, followed by oral anticoagulation with phenindione and dipyridamole. In contrast to our earlier experience with similar patients, each of the present patients improved. Urinalyses returned to normal and glomerular filtration rates to near normal values in all patients at the end of the treatment period and have remained so for up to 3.9 years since treatment has been completed. Post-treatment biopsies showed remarkable improvement, with virtually no glomerulosclerosis even in patients who had had a high incidence of glomerular crescents before treatment. It is suggested that the therapeutic regimen favorably influenced the natural history of disease and that plasma fibrinogen chromatographic findings may be helpful in selecting patients likely to benefit from the use of anticoagulant therapy.

Acute Disease↗
PubMed1976

Recurrent hypernatremia; a proposed mechanism in a patient with absence of thirst and abnormal excretion of water.

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

Child↗
PubMed1976

"Pulse" methylprednisolone therapy in the treatment of severe glomerulonephritis.

Eight patients with severe glomerulonephritis and an average inulin clearance of 21.7 ml/min/1.73 m2 body surface were treated with high-dosage intravenous methylprednisolone, 30 mg/kg given over a one-hour period on each of six alternate days. The mean inulin clearance rate doubled after this "pulse" therapy. In the six patients treated early in the course of their disease, GFR increased to a mean of 100.2 ml/min/1.73 m2 during the follow-up period extending for up to three years and was accompanied by clinical improvement. These observations suggest that "pulse" methylprednisolone may be beneficial in treating some patients with potentially life-threatening severe glomerulonephritis.

Adolescent↗
PubMed1976

Pathophysiological response of the blood coagulation system in acute glomerulonephritis.

A new procedure, plasma fibrinogen chromatography, has been utilized, together with other blood coagulation assays, to quantify fibrin formation in 43 children with acute poststreptococcal glomerulonephritis (AGN) from the time of hospitalization until recovery. During the prediuretic phase of AGN, significant evidence for substantial increase in fibrin formation (intravascular coagulation) included gross increase in plasma high molecular weight fibrinogen complexes (HMWFC), the development of either hypo- or hyperfibrinogenemia and gross depression of coagulation factor XIII concentration and of alpha2-macroglobulin concentration. During the diuretic phase of the disease, these abnormalities regressed and evidence of enhanced plasma fibrinolytic activity, documented by an increase in fibrinogen first derivative, was detected. Concomitantly, urinary excretion of fibrin(ogen) degradation products (FDP) underwent substantial increase. With disease recovery, which occurred in all children, urinary FDP excretion ceased and all coagulation findings normalized.

Acute Disease↗
PubMed1975

Serum immunoglobulins in the nephrotic syndrome. A possible cause of minimal-change nephrotic syndrome.

To assess immunologic factors in the pathogenesis of idiopathic minimal-change nephrotic syndrome (INS), serum immunoglobulin concentrations were measured in 37 children with this syndrome and compared with those found in 36 with nephrotic syndrome secondary to chronic glomerulonephritis (CGN). Serum IgG and IgA levels were significantly reduced in nephrotic patients with either INS or CGN, IgG averaging 18.5 and 25.9 per cent of normal (P less than 0.001) and IgA 59.8 and 44.1 per cent of normal (P less than 0.01) respectively. Values increased after treatment of INS with prednisone, but mean values remained low. Serum IgM concentrations in INS averaged more than twice normal before, during, and after successful treatment with steroids. Patients with CGN did not have equivalent elevations of serum IgM. Thus, the primary defect in INS may be immunologic and could consist of deficiency in the T-cell function that mediates conversion of IgM synthesis to IgG synthesis.

Animals↗