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Biomedical subjects

J M Castrillo

Publications and source records attributed to J M Castrillo.

At least 55 records · Page 3Linked to original sources
PubMed1984

Immunoreactive pancreatic polypeptide components in plasma from normal subjects and patients with chronic renal failure in basal and postprandial conditions.

Gel filtration of plasma from normal subjects and patients with chronic renal failure (CRF) yielded four immunoreactive human pancreatic polypeptide (IRhPP) peaks of approximately greater than 20,000, 10,000, 4200, and 2000 daltons. In normal subjects, the basal plasma distribution was 36 +/- 2%, 16 +/- 3%, 25 +/- 1% and 23 +/- 2%, respectively. In the CRF patients, the total plasma IRhPP was close to ten times higher than in the normal group. This difference was due to an increase in IRhPP10000 and IRhPP4200 plasma levels. After a standard breakfast, plasma IRhPP10000 and IRhPP4200 levels increased in the normal subjects and in the CRF patients, while the levels of the other two plasma components were not affected by the meal. In a patient with multiple endocrine adenomatosis type 1, the basal plasma levels of IRhPP10000 and IRhPP4200 were, respectively, 41 and 44 times higher than the mean value in the normal subjects; these fractions appeared to be further increased after breakfast. In trying to characterize the IRhPP10000, it was found that treatment with urea, guanadium hydrochloride, and acetic acid (pH 2.2) did not alter its molecular size, whereas limited trypsin treatment was able to destroy part of the immunoreactivity and to produce greater than 20,000-dalton and 4200-dalton immunoreactive materials. Plasma IRhPP10000 seems to be a co-secretory product of the PP cell, and the kidney plays a role in its catabolism as well as in that of the IRhPP4200 component. The IRhPP10000 component may correspond to a PP precursor.

Adult↗
PubMed1979

[Nephrocalcinosis as a clinical syndrome. Study of 77 cases (author's transl)].

Seventy-seven patients with nephrocalcinosis as revealed by X-ray studies over a 10-year period are reviewed. A programmed clinical and metabolic study was performed on each case; the author's criteria included the different pathogenic factors considered in the etiologic definition of the disease. There were 22 cases with primary hyperparathyroidism, 19 with spongy kidney, nine with tubulointerstitial nephropathy, five with hyperoxaluria, five with distal renal tubular acidosis, four with esential hypomagnesemia, and three cases of miscellaneous etiology (vitamin D intoxication, Fanconi's syndrome, Bartter's disease). Ten other cases were classified as idiopathic nephrocalcinosis since no definite cause could be found. The clinical characteristics (symptoms, associated diseases, diet and medication intake, family history) and the biochemical findings are analysed for each group. The physiopathologic mechanisms, comparisons between each etiologic group, treatment, clinical course, and prognosis are commented on. The conclusion drawn is that nephrocalcinosis is a clinical syndrome of various etiologies which in most cases arises from an underlying metabolic disease.

Acidosis, Renal Tubular↗
PubMed1977

Gout disease. Its natural history based on 1,000 observations.

Gout disease in our country as both exogenous factors (dietary habits, professions, etc.) and endogenous factors (sex, inheritance, etc.) play a polygenic role in its incidence. Those conditions resulting in hyperuricemia (diseases, drugs, etc.) facilitate the clinical manifestations. But a genetic determinant in the articular reaction in front of an accumulation of uric acid crystals or in the development of such crystallization is a fundamental factor in the manifestation of the disease. In our series we were able to confirm the high incidence of arterial hypertension, renal lithiasis and renal participation in gout. The role of lead and of certain professions in favouring the hyperuricemia is suggested. A classification of gout, from a functional point of view, must include both the clinical form and the analysis of the whole renal function, and the renal handling of uric acid. This is mandatory not only for the diagnosis and prognosis of the disease but to set the basis of its adequate management.

Calculi↗