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Biomedical subjects

E Junco

Publications and source records attributed to E Junco.

At least 19 recordsLinked to original sources
PubMed1993

Effect of zinc treatment on serum thyroid hormones in uremic patients under peritoneal dialysis.

In order to evaluate the effect of zinc (Zn) deficiency on thyroid abnormalities in chronic renal failure, a Zn supplement (100 mg/day, p.o.) was given for four weeks to eight uremic patients under peritoneal dialysis. Zn supplementation increased plasma levels of TSH (5.8 +/- 0.7 to 7.4 +/- 0.7 mU/l, p < 0.02), T4 (61.6 +/- 3.9 to 93.9 +/- 6.2 nmol/l, p < 0.01), T3 (1.31 +/- 0.14 to 1.70 +/- 0.18 nmol/l, p < 0.01) and Zn (7.23 +/- 0.45 to 12.27 +/- 0.76 mumol/l, p < 0.01). A close correlation was found between changes in plasma levels of Zn and changes in TSH (r = 0.82), T4 (r = 0.55) and T3 (r = 0.64), suggesting that Zn deficiency may play a role in the biosynthesis or release of hormones of the hypothalamic-pituitary-thyroid axis in chronic renal failure.

Adult↗
PubMed1991

[Membranous nephritis after renal transplantation].

8 cases of membranous glomerulonephritis (MG) after renal transplants (RT) are presented; one being a recurrence of the original disease and the other 7 due to a different cause of renal insufficiency. The total incidence of MG after transplantation was 1.63%; 1.39% being the incidence of MG of new cases. Only 1 patient showed decrease of renal function and in this case the MG was accompanied by chronic rejection lesions. There was no sign of neoplasias nor drugs producing MG. As far as chronic infections are concerned, only one patient showed B antigen and it was not observed during the immunofluorescent test in the biopsy. 6 patients had urological complications after the renal transplant (3 cases of urinary fistula; 2 cases of obstructive uropathy; 1 case of short ureter). 2 patients experienced the start of hemodialysis due to focal and segmentary glomerulosclerosis. The beginning of proteinuria commences between 2 and 23 months after the RT (median 13,0 +/- 7,5 moths); with a range of between 2.0 and 12.0 gr/day (median: 6.8 +/- 3,2 Z gr/day), this being nephrotic in 4 cases. Proteinuria improved 1 case, and persisted in the other patients at the same level registered previous to the diagnosis. MG is a non-frequent complication or RT and is usually benign. Patients with post-transplant urologic complications could be considered to have a higher risk of developing a MG "de novo".

Adolescent↗
PubMed1986

Renal metabolism during four types of lactic acidosis in the dog including anoxia.

The present study was undertaken to evaluate the metabolic response of the kidney to lactic acidosis. Four types of lactic acidosis were induced in the dog: infusion of lactic acid, infusion of lactic acid with phenformin, administration of phenformin alone, and hypoxia by breathing 95% nitrogen. In all groups of animals, the same degree of acidosis was observed with plasma bicarbonate ranging from 12.8 to 14.9 mM. Plasma lactate concentration ranged from 3.0 to 8.1 mumol/mL. Renal ammoniagenesis failed to be influenced by lactic acidosis. As a matter of fact, it fell during anoxia. The extraction of glutamine by the kidney rose except during anoxia where it fell. The renal production of alanine rose during the infusion of lactic acid with and without phenformin. This coincided with the extraction of glutamine. The renal extraction of lactate rose in all forms of acidosis as well as the production of pyruvate. In the renal cortical tissue, the concentration of malate, pyruvate, and lactate rose. Alanine also rose except during anoxia. An important fall in cytosolic redox potential (NAD+/NADH lactate dehydrogenase) was observed, as well as a fall in mitochondrial redox (NAD+/NADH beta-hydroxybutyrate dehydrogenase). Lactate also accumulated in the liver and in the muscle. We propose that the kidney is unable to respond to lactic acidosis in terms of ammonia production and that this phenomenon is explained by transamination of pyruvate and glutamate into alanine and also by the observed fall in cytosolic redox potential. It is likely that renal gluconeogenesis is also inhibited and this is reflected by the rise in the concentration of malate in the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1985

The metabolic response of the kidney to acute sodium lactate alkalosis.

In vivo studies were performed in the dog to verify if sodium lactate had an important effect on the metabolism of glutamine by the kidney. The animals were infused with 0.6 M sodium lactate to induce acute metabolic alkalosis with plasma bicarbonate of 29.7 mM. During these experiments, it was demonstrated that the renal uptake of glutamine increased by 46%, while the renal production of ammonia was unchanged. The renal production of alanine rose from 6.0 to 16.8 mumol/min. Plasma concentration of lactate increased from 1.3 to 19.2 mM, while that of pyruvate increased from 0.075 to 0.454 mM. In the renal tissue, alpha-ketoglutarate, malate, oxaloacetate, lactate, pyruvate, citrate, and alanine increased significantly. Similar changes were found in the liver and skeletal muscle. The observed changes are best described by transamination of pyruvate and glutamate under the influence of alanine aminotransferase (GPT). It can be calculated that this reaction was responsible for 76% of the production of ammonia from glutamine, the latter being necessary to provide glutamate for the synthesis of alanine. Dogs infused with 0.3 M sodium bicarbonate instead of sodium lactate with the same degree of acute metabolic alkalosis, showed a depression of 40% in the renal uptake of glutamine with a 38% decrease in renal ammoniagenesis and a 20% fall in the production of alanine. The present studies demonstrate that the production of ammonia from glutamine is not necessarily related to changes in acid-base balance, but may be associated with biochemical alterations related to the synthesis of alanine by the kidney.

Alanine↗
PubMed1983

Leucopenia, hypoxia and complement activation in haemodialysis. Three unrelated phenomena.

Acute, transient leucopenia occurs in uraemic patients during the first minutes of haemodialysis, haemofiltration and ultrafiltration, and this leucopenia depends on the membrane used: maximal with cuprophan, less marked using cellulose acetate in haemofiltration and minimal with polyacrylonitrile. Complement activation was noted in all dialysis procedures except ultrafiltration. However, no correlation was found between the intensity of the complement activation and the degree of leucopenia. Significant hypoxia only appeared in haemodialysis using an acetate bath even with the polyacrylonitrile membrane. Sequential ultrafiltration-dialysis studies clearly demonstrate that leucopenia and hypoxia are unrelated effects of haemodialysis. Leucopenia depends on the membrane used and hypoxia may be related to the use of an acetate dialysate. In addition, the presence of dialysis fluid was necessary for membrane-induced complement activation suggesting an important influence of the dialysate on membrane biocompatibility.

Acetates↗
PubMed1979

[Therapeutic guides in hypertonic dehydration (author's transl)].

Physiopathology of hypertonic dehydration is revised. The bases of treatment are discussed; they are based on: 1. Basal requirements of fluids. 2. Slow correction of deficit. 3. Replacement of maintaining losses. Total fluids support will carry to rehydration in 2 or 3 days. In the most severe cases peritoneal dialysis is associated. The indications, technique and realization of peritoneal dialysis during hypertonic dehydration are discussed.

Dehydration↗
PubMed1979

[Treatment and evolution of shock and acidosis in hypertonic dehydration (author's transl)].

Authors analyse treatment and clinical and analytical evolution of 80 patients with hypertonic dehydration, depending on shock and acidosis. Several considerations concerning treatment and its' influence on evolution of different patients, emphasizing both therapeutic methods: with or without use of peritoneal dialysis, according to the values of initial natraemia, are made.

Acidosis↗
PubMed1979

[Metabolic evolution of hypertonic dehydration treated with fluidotherapy: revision of 40 infants (author's transl)].

Authors study the metabolic evolution of osmolarity, natraemia, chloremia, kaliemia and uremia of 40 infants with hypertonic dehydration. They divide the serie into two groups in accordance with initial value of natraemia: more or less than 170 mEq./l. The slow average decreases by hour of osmolarity, natraemia and chloremia were evaluated, and that justifies good evolution of hypertonic dehydration and minimal neurological repercussion found. Renal function in this metabolic condition is discussed. The usefulness of the fluidotherapic technique employed is demonstrated.

Chlorides↗
PubMed1979

[Metabolic evolution of hypertonic dehydration with combined treatment of fluidotherapy and peritoneal dialysis: revision of 22 infants (author's transl)].

Metabolic evolution of osmolarity, natraemia, chloremia, kaliemia and uremia of 22 infants with severe hypertonic dehydration, treated with fluidotherapy and peritoneal dialysis, is revised. Peritoneal dialysis was prepared in accordance with a special method for this metabolic condition. The serie was divided into two groups, according to initial value of natraemia: more or less than 170 mEq./l. Average decreases per hour of osmolarity, natraemia and chloremia were evaluated, as well as the influence of peritoneal dialysis on body fluids composition. Indication of peritoneal dialysis specially prepared for severe cases is discussed.

Chlorides↗