Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium influences mineral metabolism in hard and soft tissues indirectly through hormonal and other modulating factors, and by direct effects on the processes of bone formation and resorption and of crystallization (mineralization). Its causative and therapeutic relationships to calcium urolithiasis (CaUr) are controversial despite an association between low urinary Mg and CaUr. Recent studies have also found a tendency to low serum and/or lymphocyte Mg levels in CaUr. Despite earlier studies demonstrating an inhibitory effect of Mg supplementation on experimental CaUr in animals and in spontaneous CaUr in humans, at least two properly controlled clinical trials of Mg supplementation have failed to demonstrate a beneficial effect on CaUr frequency. With regard to the skeleton, experimental studies have shown that Mg depletion causes a decrease in both osteoblast and osteoclast activity with the development of a form of 'aplastic bone disease'. At the same time, bone salt crystallization is enhanced by Mg deficiency. Conversely, Mg excess impairs mineralization with the development of an osteomalacia-like picture, and may also stimulate bone resorption independently of parathyroid hormone. Whether or not Mg depletion may be a causal factor in human osteoporosis is also controversial, and there are conflicting reports as to the Mg content of osteoporotic bone. Small decreases in serum and/or erythrocyte Mg in osteoporotic patients have been reported, and one author has noted improved bone mineral density with a multinutrient supplement rich in Mg. The extant data are sparse and indicate a clear need for more rigorous study.
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PMID:Relation of magnesium to osteoporosis and calcium urolithiasis. 184 60

Renal tubular acidosis represents a heterogenous group of disorders with various etiologies and mechanisms. The physiopathologic basis of each type of renal tubular acidosis is reviewed, focusing on the laboratory investigations necessary to define the nature of the hyperchloremic renal tubular acidosis. Clinically, the four types of renal tubular acidosis can be associated with complications such as osteomalacia, urolithiasis and failure to thrive. Very often, the chronic administration of alkali results in normal growth and development, and greatly reduces the risk of stone formation or nephrocalcinosis.
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PMID:[Renal tubular acidosis in children]. 839 83

Poor calcification of the teeth and the bones of the skull predisposes pet rabbits to dental disease. This study is a preliminary investigation into the dietary habits of pet rabbits. Owners were questioned about the feeding preferences of their pets. Manufacturers of rabbit foods were asked about the calcium, phosphorus and vitamin D content of their foods and how they had decided upon the formulation of their rations. Samples of rabbit food were analysed for calcium and phosphorus. Rabbits were found to be selective feeders. Rabbit food from pet shops consists of a mixed ration, of which the most commonly rejected ingredients were pellets and whole grain. The food manufacturers reported that calcium, phosphorus and vitamin D supplements are incorporated into the pellets. Food analyses demonstrated that rejection of the pellets and whole grain from the food can reduce a rabbit's calcium intake to below the minimum dietary requirement. The rabbit's unusual calcium metabolism is discussed. Calcium deficiency may cause osteomalacia but dietary excess may cause urolithiasis. Vitamin D deficiency may also exacerbate calcium deficiency. Recommendations are made for preventing calcium deficiency and dental disease in rabbits.
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PMID:Calcium deficiency, diet and dental disease in pet rabbits. 912 6