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Biomedical subjects

M García-Fuentes

Publications and source records attributed to M García-Fuentes.

6 recordsLinked to original sources
PubMed1987

Hypomagnesaemia of hereditary renal origin.

Cases of hypomagnesaemia of hereditary renal origin represent at least three different congenital disorders of tubular reabsorption of magnesium (Mg). Isolated familial hypomagnesaemia has been reported in a heterogeneous group of patients and an autosomal dominant pattern of inheritance has often been found to be present. Familial hypokalaemia-hypomagnesaemia, inherited as an autosomal recessive trait, has been reported in 17 patients and we now describe 3 additional cases. Hypomagnesaemia is accompanied by hypokalaemia, metabolic alkalosis, hypocalciuria and moderate sodium chloride wasting. Titration of renal Mg reabsorption indicates the presence of a low threshold but a normal Tm. The inherited defect is probably situated at the level of the distal convoluted tubule and mimics the therapeutic effect of thiazides. This condition is frequently confused with Bartter's syndrome. Familial hypomagnesaemia-hypercalciuria, also inherited as an autosomal recessive trait, has been reported in at least 15 patients and we now add 3 new cases. Hypomagnesaemia is always accompanied by hypercalciuria and nephrocalcinosis. Ocular abnormalities such as myopia and horizontal nystagmus are often present. Hypermagnesiuria is of a greater degree than that observed in the previous entity and reflects a low Tm of Mg reabsorption. The defect must be situated at the level of the ascending limb of the loop of Henle and affects the transport of both calcium and Mg but not of sodium and chloride. This condition has not been clearly separated from hereditary distal renal tubular acidosis in the literature.

Humans↗
PubMed1986

Immunoglobulin-producing cells in IgA nephropathy.

The number of peripheral blood mononuclear cells (PBMC) producing IgA, IgG and IgM spontaneously, after in vitro polyclonal stimulation with pokeweek mitogen (PWM) and in response to autologous mixed lymphocyte reaction (AMLR), were determined by a protein A hemolytic plaque assay in 23 patients with IgA nephropathy confirmed by renal biopsies and in 24 normal controls. The geometric mean of circulating IgA-producing cells in Berger's disease (689 +/- 1.73 cells/10(6) PBMC) was increased when compared with the normal controls (332 X divided by 1.52 cells/10(6) PBMC; p less than 0.001). To a lesser degree, there was also an increase in the number of IgG-secreting cells (98 +/- 3.97 cells/10(6) PBMC vs. 38 +/- 2.90 cells/10(6) PBMC; p less than 0.05). After PWM stimulation, although the number of IgA-producing cells was increased in patients with IgA nephropathy, no significant differences were observed between the 2 groups. In response to AMLR, the number of IgA-secreting cells was significantly higher in the cases with Berger's disease (1,979 +/- 1.76 cells/10(6) non-T cells vs. 783 +/- 1.95 cells/10(6) non-T cells; p less than 0.001). Although it did not reach statistical significance, the patient group had also an increase in the number of IgG-producing cells (884 +/- 2.64 cells/10(6) non-T cells vs. 317 +/- 5.05 cells/10(6) non-T cells). These data support the existence of some abnormalities in the mechanisms regulating the synthesis of IgA in Berger's disease which might contribute to its pathogenesis.

Adolescent↗
PubMed1981

[Poststreptococcal glomerulonephritis].

Acute poststreptococcal glomerulonephritis is one of the best defined renal diseases and it is the commonest form of acute glomerulonephritis in children. Antigen-antibody complexes formed in the circulation or "in situ" seem to play an important role in the pathogenesis and even though antiglobulins have recently been incriminated, there is still controversy over the nature of the antigen/s involved. Usually the clinical picture is very characteristic, but in those cases of atypical presentation mainly in those without urinary abnormalities, the diagnosis could be resolved by demonstration of well defined histological lesions. Although it is generally agreed upon, on the basis of clinical observations, that recovery from acute glomerulonephritis generally occurs in children, confusion still exists concerning the precise frequency with which chronicity may happen in this disease. There is no specific treatment for the immunological processes but symptomatic therapy has considerably reduced early mortality.

Antibodies, Anti-Idiotypic↗
PubMed1980

Serum levels of alpha 1-antitrypsin and Pi types in children with bronchiolitis.

Alpha 1-antitrypsin levels were determined at the beginning of the disease and after clinical recovery in a group of 51 infants with bronchiolitis, and the results were compared to those obtained in 24 normal infants and in 15 infants with viral bronchopneumonia. Distribution of Pi types in the patients with bronchiolitis was also compared to that observed in a control population of 170 blood donors of the same ethnic background. Both serum levels of alpha 1-antitrypsin and prevalence of non-M phenotypes were not statistically different from the values found in the control groups, thus not supporting the hypothesis that a deficiency of alpha 1-antitrypsin plays a role in the pathogenesis of bronchiolitis. A non explained finding was the lack of elevation of serum level of alpha 1-antitrypsin during the acute phase of the bronchiolitis process, a fact present in the group of patients with bronchopneumonia.

Bronchiolitis, Viral↗