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Biomedical subjects

D Brancaccio

Publications and source records attributed to D Brancaccio.

At least 55 records · Page 3Linked to original sources
PubMed1986

Insulin resistance in uremia: in vitro model in the rat liver using human serum to study mechanisms.

We have previously demonstrated in a rat model of chronic uremia that the liver is resistant to insulin. To further investigate the mechanism(s) of insulin resistance in uremia, primary cultures of normal rat hepatocytes were incubated with varying dilutions (1/10 to 1/10,000) of sera from undialyzed end stage uremic and normal humans for 20 hours. We then studied insulin action, binding, and postbinding events. Dilutions of uremic sera as low as 1/1,000 rendered the hepatocytes resistant to maximal concentrations of insulin with regard to [14C]acetate incorporation into lipids. The dose response curve for insulin-stimulated [14C]aminoisobutyric acid uptake demonstrated a shift to the right in hepatocytes incubated with uremic sera when compared with those incubated with normal sera. The 125I-insulin binding sites and affinity, 125I-insulin internalization and degradation, insulin receptor structure, autophosphorylation of the insulin receptor, and its tyrosine-specific kinase activity were normal in the hepatocytes rendered resistant to insulin by uremic sera. However, these cells failed to generate the chemical mediator or second messenger of insulin action, as assessed by its ability to stimulate pyruvate dehydrogenase (PDH) in liver mitochondria from normal rats. We concluded that uremic sera renders normal rat hepatocytes resistant to insulin. Insulin resistance is a postinsulin receptor kinase defect possibly due to lack of the generation of the chemical mediator of insulin action. This in vitro cell model may be useful to further define the mechanism(s) and the serum factor(s) responsible for insulin resistance in uremia in the absence of complicating hormonal and substrate changes that occur in vivo.

Adult↗
PubMed1985

Progressive dialytic encephalopathy and the problem of aluminum neurotoxicity.

Some clinical, epidemiological, and pathological aspects of the progressive dialytic encephalopathy have been considered with the aim to clarify the nature of the disease as well as to identify factors that possibly favor the neurotoxic effect of aluminum in uremic patients. The role of the blood-brain barrier has been outlined. The concept of a delayed neurotoxicity of aluminum has been introduced to face the problem of the risk of mental deterioration and neuromyopathies in patients on oral aluminum administration. A comparison has been made with the dementias of the Alzheimer type and with amyotrophic lateral sclerosis in which aluminum is regarded as a possible etiologic factor. Finally, a proposal has been made of monitoring aluminum levels in blood serum and cerebrospinal fluid as well as the results of electrodiagnostic tests, CT scan, and language and psychometric examinations, that may help in clarifying the problem of aluminum neurotoxicity in uremic patients.

Aluminum↗
PubMed1984

Glomerular disease and pregnancy. A study of 123 pregnancies in patients with primary and secondary glomerular diseases.

The clinical course of 123 pregnancies in 86 patients with biopsy-proven glomerular diseases have been studied. In 35 women the onset of nephropathy occurred during pregnancy. No complications were observed in more than half of the pregnancies. In the others, one third of the complications were obstetrical or fetal accidents, one third were renal manifestations (hypertension or deterioration of renal function) and one third were both causes. The lowest incidence of complications was observed in patients with membranous nephropathy and the highest in membranoproliferative glomerulonephritis patients. There were 6 spontaneous late abortion, 6 stillbirths and 5 neonatal deaths. 17 deliveries were preterm and 7 fetuses were small for gestational age. Hypertension appeared in 24 pregnancies, in 13 of which it was reversible and related to superimposed preeclampsia and in 11 it persisted after delivery (5 of these 11 pregnancies were in patients with IgA nephropathy). Renal function deteriorated in 10 cases during pregnancy. The deterioration was reversible in 6 and progressive in 4 (2 of whom had membranoproliferative glomerulonephritis). It is suggested that in most patients pregnancy does not change the natural history of glomerular disease.

Diabetic Nephropathies↗
PubMed1984

Dopamine and frusemide in oliguric acute renal failure.

Into 24 oliguric patients with acute renal failure (ARF) for whom mannitol and high-dose frusemide had failed to promote a diuresis, dopamine (3 micrograms/kg/min) plus frusemide (10-15 mg/kg/h) were infused for 6-24 h. In 19 of the 24 patients this treatment produced significant increases in diuresis (from 11 +/- 7 to 85 +/- 51 ml/h; p less than 0.001) and natriuresis (from 45 +/- 13 to 88 +/- 22 mEq/1; p less than 0.001), without any significant modification of blood pressure, pulse rate or central venous pressure. 10 of the 24 patients required dialysis: 5 because therapy failed to promote diuresis and the other 5 because of their hypercatabolic state in spite of polyuria. 5 patients died of causes unrelated to ARF. Since all patients who responded were treated within 24 h after the onset of oliguria, it appears to be crucial to administer dopamine and frusemide early, before more severe anatomical and functional damage develops.

Acute Kidney Injury↗
PubMed1983

Dopamine-frusemide therapy in acute renal failure.

In 16 patients with ARF and in three with hepatorenal syndrome we infused dopamine (3 micrograms/kg/min) and frusemide (10-15 mg/kg/day) for 6-24 hours. This treatment produced in all patients a significant diuresis and natriuresis without any modification of blood pressure, pulse rate, and central venous pressure. In three patients with hepatorenal syndrome diuresis was established during dopamine and frusemide infusion, but severe oliguria again reappeared when drug infusion was stopped. This experience suggests that this therapy may avoid fluid overload and hyperkalaemia in oliguric patients reducing the need for dialysis. It is also the first successful approach in the treatment of hepatorenal syndrome although its effect is transient.

Acute Kidney Injury↗
PubMed1981

Bone changes in end-stage oxalosis.

Primary hyperoxaluria is a rare metabolic disease characterized by exaggerated production of oxalic acid. Clinically the disease is characterized by recurrent calcium nephrolithiasis, progressive renal failure, and early death in uremia. As the regular dialysis treatment may prolong survival, a new syndrome may develop. This is due to intense and continuous deposition of calcium oxalate crystals in soft and bone tissues. The radiologic aspects of oxalate deposition in four adult patients on chronic renal dialysis with histologic and clinical evidence of massive bone oxalosis are reported.

Adolescent↗
PubMed1979

Thiazide diuretics in renal hypercalciuria.

Forty-six renal hypercalciuric normocalcaemic patients were treated with hydrochlorothiazide (50mg/day) and amiloride (5 mg/day), both to reduce new stone formation and to suppress parathyroid hyperfunction. A reduction of hypercalciuria and suppression of parathyroid hyperactivity were observed in 41 patients, while in the other five patients no evidence of parathyroid suppression was found and hypercalcaemia developed. Four of five patients underwent parathyroidectomy which was followed by a normalisation of biochemical signs of hyperparathyroidism. These results suggest that the appearance of hypercalcaemia in renal hypercalciuric patients during hydrochlorothiazide/amiloride treatment may be of diagnostic value in unmasking pharmacologically non-suppressible normocalcaemic hyperparathyroidism.

Adult↗