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A J Monserrat

Publications and source records attributed to A J Monserrat.

At least 37 records · Page 2Linked to original sources

Acute renal failure induced by choline deficiency: structural-functional correlations.

The wide range of lesions obtained after feeding weanling rats with hypolipotropic diets underlies the interest of this model in the study of the pathophysiology of acute renal failure. Renal functional studies (experiment A) show that the more advanced grade of morphological alteration correlates well with a progressively more severe deterioration in renal function. In animals wtih morphological evidence of repair there was an evident rise in the urinary volume of a low osmolality and a reduction in blood urea. In experiment B, where the sequential changes in urine volume and composition were analyzed, the installation of the disease is marked by a decrease in body weight, food intake and water intake, a rise in urine Na concentration and by a fall in urine flow rate and renal capacity to excrete concentrated urine. The progressive decline in renal function observed in these animals would seem more linked to a primary tubular alteration which gradually becomes more extensive than with an initial ischemic alteration. The tubular necrosis can be interpreted as the initial lesion common to the wide morphological range observed in this model (tubular necrosis of various grades, cortical necrosis or evidence of repair).

Acute Kidney Injury↗

Effects of repeated injections of sucrose on the kidney. Histologic, cytochemical and functional studies in an animal model.

In previous experiments (Monserrat, Gotelle, and Garay, 1969) we have found that the administration to rats of a single injection of 1.12 M sucrose induces a hydropic reversible vacuolation of the proximal convoluted tubules of the kidney. Along with the vacuolation the PAS and acid phosphatase positive, as well as autofluorescent granules (lysosomes) disappear and vice versa. We now report the effects of multiple intraperitoneal injections of 1.12 M sucrose. The aim of the study was to determine whether the renal cells are able to adapt to this situation or the modifications are permanent. Wistar male rats were allotted to 4 different groups (A : experimental, B, C, and D, controls) and placed in metabolic cages. Animals from group A were injected with 3.0 ml/100 gm body weight of 1.12 M sucrose at 0, 24, 48, 72, and 96 hours after the beginning of the experiment; rats of groups B and C were injected respectively at 0 and 96 hours, and finally, rats of group D were used as normal controls. All rats were killed at 120 hours. The results showed a striking vacuolation in the proximal convoluted tubules of the rats of group C, and complete regression of vacuolar changes in those of group B. Rats of group A, although they maintained the osmotic diuresis, showed mild vacuolation with persistence of acid phosphatase and PAS positive granules, as well as autofluorescent droplets (lysosomes). We postulate that these results are indicative of adaptive changes, whose mechanisms are at present being studied.

Acid Phosphatase↗

Lysosomes in the pathogenesis of the renal necrosis of choline-deficient rats.

Previously published data from our laboratories led us to postulate that alterations in lysosomes may play a cardinal pathogenic role in the fatal renal necrosis of choline-deficient weanling rats. To explore this hypothesis further a series of five different experiments were carried out. In the first two experiments the effect of a "stabilizer" of the lysosomes, hydrocortisone, was studied; conversely, in the third and fourth experiments, the effect of a "labilizer," vitamin A, was studied. Finally, in the fifth experiment, the renal levels of a lysosomal enzyme, acid phosphatase, were evaluated biochemically. Results of the first two experiments revealed a protective effect of hydrocortisone while those of the third and fourth an aggravating effect of vitamin A. Results of the fifth experiment indicated lysosomal changes in the prenecrotic and early necrotic stages. These results along with those from our previous studies, support the concept that lysosomal alterations play an important pathogenic role in renal changes of choline-deficient weanling rats.

Acid Phosphatase↗