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NITROGEN, POTASSIUM, SODIUM, AND CHLORINE METABOLISM IN RICKETS, WITH SPECIAL REFERENCE TO BILIARY FISTULA RICKETS IN PUPPIES.

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1. Rickets developed in three puppies deprived of vitamin D and sunlight since birth, in which, at the age of 6 to 7 weeks gall bladder fistula was established. The results of studies of their bones and of the calcium and phosphate metabolism have previously been published (2). Studies on the

Normal left ventricular performance in children with X-linked hypophosphatemic rickets: a Doppler echocardiography study.

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To determine if chronic hypophosphatemia causes myocardial dysfunction, we explored one model for this metabolic derangement by prospectively investigating 11 patients (aged 5-18 years) with X-linked hypophosphatemic rickets (XLH) by M-mode, two-dimensional, and Doppler echocardiography. Inorganic

A case report of nephrogenic diabetes insipidus with idiopathic Fanconi syndrome in a child who presented with vitamin D resistant rickets.

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Fanconi syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells, occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycemic glycosuria, tubular proteinuria without hematuria,

Hypophosphatemic rickets due to Dent's disease: A case report and review of literature.

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We report a case of rickets due to Dent's disease in a two-year-old boy. He was treated with sodium phosphate, calcitriol and potassium citrate supplements, following which there was a remarkable improvement in mobility, growth and bony deformities. The hypercalciuria associated with Dent's disease

EXPERIMENTAL RICKETS IN RATS : I. A DIET PRODUCING RICKETS IN WHITE RATS, AND ITS PREVENTION BY THE ADDITION OF AN INORGANIC SALT.

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1. A simple diet is presented which regularly induced rickets in young rats. 2. The substitution of 0.4 per cent secondary potassium phosphate for a small part of calcium lactate in this diet completely inhibited the development of rickets. 3. Quantitative determinations of calcium in the bodies of

Selective modulation by vitamin D of renal response to parathyroid hormone: a study in calcitriol-resistant rickets.

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Calcitriol-resistant rickets (CRR) is an autosomal recessive disease caused by mutated nonfunctioning vitamin D receptors. Because of their lack of biological activity of vitamin D, CRR patients were studied to investigate whether vitamin D modulates the effects of PTH on renal tubules. Five

Nephrogenic diabetes insipidus with idiopathic Fanconi's syndrome in a child who presented as vitamin D resistant rickets.

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Fanconi's syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycaemic glycosuria, tubular proteinuria without

[Aspects of juvenile rickets/osteopenia in black children].

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Juvenile rickets or osteopenia in rural black children is thought to be due to low calcium intake. Characteristic findings include mild calcium deficiency, normal serum phosphate levels, increased alkaline phosphatase concentrations and normal plasma vitamin D levels. The present series consisted of

Rare tubulopathy - primary hypophosphatemic rickets (case report).

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Primary hypophosphatemic rickets is a rare disorder caused by inborn defect of renal tubular reabsorbtion and usually manifested in childhood and infancy with stunted growth and deformities of lower limbs. Patient 12 years old, female, was born to healthy parents, at 41 weeks of gestation by normal

Rickets with hypophosphatemia, hypokalemia and normal anion gap metabolic acidosis: not always an easy diagnosis.

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Rickets other than those associated with advanced kidney disease, isolated distal renal tubular acidosis (dRTA) and hypophosphatasia (defective tissue non-specific alkaline phosphatase) are associated with hypophosphatemia due to abnormal proximal tubular reabsorption of phosphate. dRTA, however, at

[Effect of potassium orotate on metabolism in chickens under different provision with vitamin D3].

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Vitamin D3 induction of the vitamin-D3-dependent proteins biosynthesis and certain indexes characterizing the rachitic state in animals were studied as affected by potassium orotate. Introduction of potassium orotate to the rachitogenic diet in combination with vitamin D3 is shown to normalize the

[Effect of potassium orotate and guanine on calcium uptake in small intestine of chickens with different amounts of vitamin D3].

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Potassium orotate and guanine are established to accelerate the duodenum physiological response of chickens with experimental rachitis to administration of vitamin D3 in the in vivo experiments. They stumulate the uptake and transport of calcium, increase the content of calcium-binding protein and

Hypophosphatemic rickets: results of a long-term follow-up.

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This study reports the benefits and side effects of conventional treatment, phosphate and calcitriol supplementation in patients with heritable hypophosphatemic rickets and a long-term follow-up, median of 60.9 months. The group is composed of 17 patients (ten girls). Sixteen patients presented with

Idiopathic Fanconi's syndrome with nephrogenic diabetes insipidus in a child who presented as vitamin D resistant rickets--a case report and review of literature.

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EXPERIMENTAL RICKETS IN RATS : V. THE EFFECT OF VARYING THE ORGANIC CONSTITUENTS OF A RICKETS-PRODUCING DIET.

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1. Casein phosphorus does not completely prevent the development of rickets when substituted in Diet 84 in amount equivalent to a protective dose of basic potassium phosphate. 2. The protection given by lecithin is equivalent to its phosphorus content. 3. The protection given by yeast is at least

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