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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the thyroparathyroidectomized (TPTX) rat, fasting increased urinary phosphorus excretion by decreasing the tubular reabsorption of P1 (TRP) and resulted in hypophosphatemia. The administration of either sucrose or NaHCO3 prevented the metabolic acidosis associated with fasting and decreased the phosphaturia, indicating that the phosphaturia in fasting is in part due to metabolic acidosis. In rats on partial reduction of P1 intake selectively, the phosphaturic response to parathyroid hormone (PTH) was completely suppressed. On the other hand, the fasting rat partially retained the phosphaturic response to PTH, although dietary P1 intake was totally absent. These findings suggest that the renal P1 wasting in fasting may take place by dual mechanisms: a) the PTH-independent decrease in TRP, and b) an inability to totally suppress the response to PTH. Cyclic AMP generation in response to PTH, determined both in vivo and in vitro, was not measurably altered in fasting. However, the phosphaturic response to cyclic AMP was decreased in fasting, suggesting that the mechanism of partial resistance to PTH is probably not at but after cyclic AMP generation.
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PMID:Effect of fasting on tubular phosphorus reabsorption. 22 13

Enzootic calcinosis in Corriedale sheep was characterized by degeneration and mineralization of elastic connective tissue of aorta, arteries, lung, and kidney and by ulceration of cartilage of joints of limbs. Results of serum chemical analysis revealed low Ca X P value and significantly low, but inconsistent magnesium concentration and normal inorganic phosphorus content. The Ca:P ratio in bone was low in affected sheep. Clinicopathologically, calcinosis of sheep at Mattewara, India, appeared to be similar to the disease described as Enteque seco in South America, Naalehu disease in Hawaii, Manchester wasting disease in Jamaica, and calcinosis in central Europe, Israel, and South Africa. The disease might be due to complex mineral imbalance, although the possibility of a plant poisoning has not been ruled out.
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PMID:Enzootic calcinosis in sheep: clinical signs and pathology. 127 39

A 40-year-old female suffering from recurrent migrainous strokes is reported. She did not show any muscle weakness or wasting. Ragged red and cytochrome c oxidase negative fibers were present in the muscle biopsy. Muscle mitochondrial DNA analysis showed a 5 kb deletion, without a point mutation at nucleotide pair 3243 in the mitochondrial tRNALeu(UUR) gene. Phosphorus nuclear magnetic resonance spectroscopy of brain and gastrocnemius muscle showed a defective energy metabolism in both organs. An increased inorganic phosphate to phosphocreatine ratio due to a decreased phosphocreatine content was found in the occipital lobes, while an abnormal work-energy cost transfer function and a low rate of phosphocreatine post-exercise recovery were found in the muscle.
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PMID:Muscle mitochondrial DNA deletion and 31P-NMR spectroscopy alterations in a migraine patient. 165 40

Magnesium, the second most abundant intracellular cation, is essential for life. The consequences of deficiency are severest in the smallest and youngest members of each species and may include sudden unexpected death. Magnesium deficiency, usually diagnosed by hypomagnesemia, may be congenital, as in premature infants, infants of magnesium-deficient mothers and infants with intrauterine growth retardation. It may be acquired or caused by low magnesium intake, the use of magnesium-wasting drugs, illness provoking gastrointestinal or renal losses of the mineral, or high metabolic demands imposed by catch-up growth or postsurgical healing. Finally, the deficiency may be conditioned, caused by excessive dietary calcium, phosphorus or protein in relation to dietary magnesium, especially during a period of rapid growth or tissue repair. Magnesium therapy is safe when a low dosage is given with monitoring of plasma or serum magnesium levels, with occasional checking of calcium and potassium levels. A parenteral dose of 0.1 ml/kg/day of 50% magnesium sulfate USP (approx. 0.2 mmol/kg/day or 0.4 mEq/kg/day) may be given for 5 dose days. An oral dose of 1.0 ml of 10% magnesium chloride solution providing 0.5 mmol/kg/day magnesium or 1.0 ml/kg/day of 10% magnesium chloride USP (0.5 mmol/kg/day) or magnesium magonate (Magonate) 1.0 ml/kg/day (0.45 mmol/kg/day) may be given for extended periods; higher doses may be required for malabsorption syndromes. Hypermagnesemia, which usually results from magnesium overdosage or inadequate renal function, is a potential threat to neonates born to magnesium-treated eclamptic mothers. Most show marked improvement after 36 h of conservative management that includes calcium salts and intravenous infusions of glucose and saline, but obtunded neonates may require dialysis.
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PMID:Magnesium in perinatal care and infant health. 184 56

Animals with renal failure have a number of fairly predictable metabolic abnormalities. They are commonly presented to the veterinarian in a state of negative water balance, although prior fluid therapy in an oliguric patient may result in overhydration. Animals with oliguric ARF have sodium retention; those with polyuric ARF have increased urinary sodium loss. Chronic renal failure does not necessarily affect the ability of the renal tubule to conserve or excrete sodium, although the response to changes in sodium load is much slower than in the normal animal. Potassium retention occurs in oliguric ARF and potassium wasting in polyuric ARF; potassium balance is approximately normal in animals with CRF. Both ARF and CRF cause metabolic acidosis, although the acid-base status in a given animal will be affected by respiratory compensation, as well as other problems such as vomiting. Calcium levels are usually normal to slightly decreased in renal failure, whereas phosphorus levels are generally increased. The basic principles of fluid therapy should be used when constructing a plan for such therapy in an animal with renal failure. Intravenous administration of fluids is almost always necessary. The choice of the type of fluid, solutes, and electrolytes to be administered is based on the predicted abnormalities associated with renal failure as well as the laboratory abnormalities in the animal. Careful monitoring of the patient and periodic assessment of various laboratory parameters are necessary in order to make appropriate adjustments in fluid therapy.
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PMID:Fluid therapy for acute and chronic renal failure. 264 69

The concentrations of calcium and phosphorus and the activity of alkaline phosphatase in serum were evaluated in 42 very-low-birth-weight (VLBW) and 83 low-birth-weight (LBW) infants on the 7th, 21st, and 42nd day of life. 9 VLBW and 16 LBW infants were randomized for measurement of the renal excretion of calcium and phosphorus on the 3rd, 5th, 7th, 21st, and 42nd day of life during human milk feeding and 14 VLBW-infants fed human milk supplemented with 1 mmol NaH2PO4 per 100 ml. All serum parameters were found to be normal. Supplementation of human milk with NaH2PO4 leads to a tendency of higher concentrations of phosphorus than found in VLBW-infants exclusively fed with native human milk, but all differences between the two groups were not significant. VLBW-infants appeared more than LBW-infants to be conserving phosphorus and wasting calcium during human milk feeding. Supplementation of human milk with NaH2PO4 results in higher phosphorus lower calcium excretion in urine of VLBW-infants, but they do not reach the values of LBW-infants. Because the activity of alkaline phosphatase was not different between the feeding groups and in all cases within the normal range a delayed bone mineralisation cannot be assumed in the infants studied. Thus, the phosphorus deficiency which is shown by the renal excretion of calcium and phosphorus in the VLBW-infants can be considered to be latent. In the light of our data the concentration of phosphorus in human milk seems to be too low and the calcium/phosphorus ratio too high for the optimal mineral metabolism in VLBW-infants. The supplementation used improves the situation, but the phosphorus intake seems still too low. Further investigations are needed to detect the optimal phosphorus intake for these infants. The calcium/phosphorus ratio in the urine is a good marker to estimate a latent phosphorus deficiency in VLBW-infants.
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PMID:Calcium and phosphorus homeostasis in very-low-birth-weight infants appropriate for gestational age fed human milk. 324 Mar 2

Familial glucocorticoid deficiency is a rare multisystem disorder characterized by glucocorticoid deficiency with normal mineralocorticoid activity, achalasia of the cardia, and alacrima. Familial hypophosphatemic rickets is characterized by selective renal phosphate wasting with subsequent hypophosphatemia and an inappropriately low 1,25-dihydroxyvitamin D concentration for the degree of hypophosphatemia. A 6-year-old girl with both disorders is described. A biochemical relationship between familial glucocorticoid deficiency and familial hypophosphatemic rickets could not be defined; the influence of cortisol on her serum calcium level, phosphorus level, and rickets, as well as the natural history of these two entities, is described.
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PMID:Familial glucocorticoid deficiency in a girl with familial hypophosphatemic rickets. 339 83

We report changes in renal function and growth rate in children with reduced renal function who were kept on a low normal phosphorus formula until 18 months of age. The relationship between serum creatinine values and derived creatinine clearance and residual renal function is reviewed regarding the risk of progressive loss of function. Expressing growth as growth velocity standard deviation scores over 6-month intervals gave a more accurate description of growth performance than did change in height standard deviation scores. A relationship between residual clearance and growth velocity was inferred. However, the growth of children with a less severe reduction in function was affected intermittently by intercurrent infections and inadequately treated acidosis and salt wasting. Children with a more severe reduction in function, despite maintenance on the low-phosphorus formula, had elevated serum parathormone levels. We conclude that following growth (as serial growth velocity standard deviation scores) in relation to other variables gives more insight into factors affecting growth in these children; the level of residual function affects growth potential but other complicating factors also have an effect.
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PMID:Growth rate in infants with impaired renal function. 341 9

A patient with a mesenchymal tumor and hypophosphatemic osteomalacia was studied before and after tumor excision. Initial laboratory values included normal serum calcium, decreased serum phosphorus and tubular reabsorption of phosphate, undetectable 1,25-dihydroxyvitamin D, and normal parathyroid hormone. Histomorphometry of a bone biopsy specimen showed evidence of increased osteoclastic bone resorption. By 16 hours after tumor removal, 1,25-dihydroxyvitamin D level had normalized, but serum phosphorus level was unchanged; at 28 hours, both serum phosphorus value and tubular reabsorption of phosphate were within normal limits. It is concluded that tumor removal is associated with rapid correction both of 1,25-dihydroxyvitamin D production and of renal phosphate wasting. Increased bone resorption suggests the production of an osteoclast activator by the tumor and may explain the typically normal serum calcium value in this disorder.
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PMID:Tumor-induced osteomalacia. Kinetics of calcium, phosphorus, and vitamin D metabolism and characteristics of bone histomorphometry. 381 26

During initial trials of 5-azacytidine in adults with advanced acute leukemia, we unexpectedly observed acid-base, fluid, and electrolyte abnormalities that contributed directly to the deaths of two early patients. To evaluate this toxicity further, we studied 22 patients who received a total of 33 courses of combination chemotherapy that included 5-azacytidine. During 29 courses (88%) of treatment, polyuria, glucosuria, and/or transient changes in the serum concentrations of bicarbonate or phosphorus were detected. Spontaneous polyuria with demonstrable salt wasting and orthostatic hypotension occurred during seven courses (21%) of treatment. Inappropriate glucosuria was observed in nine courses (27%). In 24 courses (73%) the serum bicarbonate fell below the normal range. The urine became alkaline during 12 of these instances; the anion gap was not increased during the acidosis. Hypophosphatemia with serum phosphorus concentrations as low as 0.3 mg/dl occurred in 21 of 32 evaluable courses (66%). In the three patients studied the tubular reabsorption of phosphorus was 10%-18%. The renal abnormalities that were observed suggest both proximal and distal tubular damage from 5-azacytidine. Patients receiving 5-azacytidine should be monitored closely for manifestations of renal toxicity.
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PMID:5-Azacytidine and renal tubular dysfunction. 616 Aug 87


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