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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of parathyroidectomy on the crystallization of calcium salts in urine was examined in seven stone-forming patients with primary hyperparathyroidism. After parathyroidectomy, urinary calcium decreased significantly from 205 +/- 30 to 67 +/- 11 mg per day (P less than 0.01); there were no significant changes in urinary phosphorus, oxalate, magnesium, sodium, potassium, uric acid, pH, or total volume. The urinary activity product ratio (state of saturation) of brushite (CaHPO4.2H2O) and calcium oxalate decreased significantly from 1.34 +/- 0.14 to 0.75 +/- 0.18 and from 3.20 +/- 0.56 to 1.53 +/- 0.21 respectively (P less than 0.05), owing principally to the decline in urinary calcium. Moreover, the urinary formation product ratio of calcium oxalate, which reflects the minimum supersaturation required for spontaneous nucleation, increased significantly after parathyroidectomy, from 7.19 +/- 1.19 to 12.99 +/- 1.69 (P less than 0.001). The results indicate that parathyroidectomy restores the normal urinary environment with respect to saturation and inhibitor and/or promoter activity.
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PMID:Effect of parathyroidectomy on crystallization of calcium salts in urine of patients with primary hyperparathyroidism. 46 14

An increase in the average calcium oxalate content and decrease in average calcium phosphate content of stones received for analysis has been noted in a 9-year study. These changes appear to be due to a progressive increase in the number of patients with noninfected upper urinary tract stone and to the gradual elimination of phosphatic stones as a result of improved diagnosis and treatment. Some of the conditions associated with calcium phosphate stones are examined, particularly primary hyperparathyroidism, renal tubular acidosis, and medullary sponge kidney. These results further emphasize the importance of calcium oxalate in idiopathic stone disease and the need for a fuller understanding of the factors influencing calcium oxalate crystallization.
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PMID:Changes in the composition of urinary tract stones. 118 36

The physicochemical factors involved in the formation of calcium-containing renal stones have been elucidated previously and some of the techniques for their quantitation are currently available. Accordingly, urinary activity product ratio (state of saturation), formation product ratio (limit of metastability), and crystal growth of brushite and calcium oxalate in 24-hr urine samples were compared between a control group without stones and stone-forming groups composed of patients with absorptive hypercalciuria, normocalciuric nephrolithiasis, and primary hyperparathyroidism. The activity product ratios of brushite and calcium oxalate were significantly elevated in stone-forming groups, largely because of the high renal excretion of calcium. The formation product ratios were reduced in most stone-forming groups, and the crystal growth was increased in the group with primary hyperparathyroidism. Thus, the physicochemical environment of urine in stone-forming groups was favorable to the nucleation of the nidi of brushite and calcium oxalate; in primary hyperparathyroidism, it may be conducive to the subsequent growth of nidi as well.
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PMID:Nucleation and growth of brushite and calcium oxalate in urine of stone-formers. 127 73

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95

In normal individuals, 1,25-dihydroxyvitamin D (1,25-D) levels regulate calcium (Ca) absorption according to Ca intake; its synthesis is stimulated by low Ca intake, probably via increased parathyroid hormone (PTH) secretion, to increase Ca absorption, and suppressed during high intake to reduce Ca absorption. The body also adapts Ca absorption in response to renal Ca excretion, and phosphate absorption in response to phosphate intake. These adaptations may fail or be impaired in certain diseases. In disorders of overadaptation, the intestinal tract absorbs excessive amounts of Ca due to overproduction of 1,25-D, as in absorptive hypercalciuria, sarcoidosis, primary hyperparathyroidism, and tumoral calcinosis. Intestinal hyperabsorption and hypercalciuria may occur on both low- and high-Ca diets. Primary hyperparathyroidism and hypoparathyroidism are bihormonal, related to over- and underproduction, respectively, of both 1,25-D and PTH. Underadaptation disorders are typically related to low 1,25-D synthesis or resistance to this metabolite; examples include postmenopausal osteoporosis, chronic renal failure, and osteomalacia. Many of these adaptational disorders can be relieved or improved by manipulating Ca, phosphate, sodium, or protein intake or by administering exogenous 1,25-D. Overabsorption of Ca and other substances, such as oxalate, may be responsible for Ca nephrolithiasis. Hypocitraturia (which may be a complication of certain diseases or the result of unbalanced diet or excessive exercise), diets high in readily metabolizable sugars and purine-rich proteins (meat, poultry, and fish), and low fluid intake can all contribute to stone formation. Various regimens may reduce the risk of Ca nephrolithiasis.
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PMID:Calcium metabolism. 268 27

The initial part of this presentation deals with the sensitivity of tests commonly used in the diagnosis of primary hyperparathyroidism. Total serum calcium levels often are normal in patients with small parathyroid adenomas but levels of serum ultrafilterable and/or ionized calcium usually are elevated in these patients. The recent introduction of improved radioimmunoassays for measurement of circulating parathyroid hormone has led to greatly improved sensitivity of this test for the diagnosis of primary hyperparathyroidism. However, measurement of total urinary cyclic adenosine monophosphate, even when expressed as a function of glomerular filtration rate, is an extremely insensitive test in patients who have parathyroid adenomas weighing less than 1 gm. Consequently, this test no longer is used for diagnostic purposes in our laboratory. Data relating to the prevalence and causes of hyperoxaluria in patients with idiopathic calcium oxalate stones also are presented. Hyperoxaluria (more than 450 mumol. per 24 hours) was found in 21 of 99 consecutive untreated male patients. Approximately a third of the patients with high normal or increased urinary oxalate excretion also have increased urinary glycolate excretion, which is indicative of increased endogenous oxalate production. This metabolic abnormality was unresponsive to pyridoxine administration but preliminary findings suggest that it may be corrected by restricting dietary protein.
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PMID:Clinical and laboratory approaches for evaluation of nephrolithiasis. 291 16

Urine from patients with calculi produced by primary hyperparathyroidism was examined to determine its promotive effect on calcium oxalate crystal aggregation. The study was carried out in an in vitro whole urine system and the particle size distribution assay was done by Coulter Counter, Model TAII. Of urine samples from 19 hyperparathyroid patients, 15 showed obvious promotion of calcium oxalate crystal aggregation. It is not known what kind of substances in such urine led to this phenomenon and whether these unknown factors act by actually promoting crystal aggregation or by blocking substances of inhibitors.
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PMID:Promotive effect of urine from patients with primary hyperparathyroidism on calcium oxalate crystal aggregation in an in vitro whole urine system. 319 46

Primary hyperparathyroidism resulted in calcium urolith formation and calcium nephropathy in 2 dogs. Uroliths composed of calcium phosphate were surgically removed from the bladder of one dog 3 months after surgical removal of a parathyroid adenoma. Five years later, hypercalcemia and urolithiasis had not recurred. In a second dog, calcium oxalate renal and bladder uroliths remained unchanged in size at 11 months after removal of a parathyroid adenoma. The possibility of primary hyperparathyroidism should be considered in any dog with calcium urolithiasis.
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PMID:Calcium urolithiasis in two dogs with parathyroid adenomas. 369 84

Three cases of mild metabolic hyperoxaluria (with glycollaturia) are described. They showed different types of response to pyridoxine. One responded to low dose, one responded at first to low dose but became resistant, and the third showed temporary response to high dose. One case also had primary hyperparathyroidism and one had medullary sponge kidneys and hypercalciuria. It is important to measure urinary oxalate (and glycollate) in all cases of calcium oxalate urolithiasis.
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PMID:Mild metabolic hyperoxaluria and its response to pyridoxine. 381 Oct 39

We measured the rate of oxalate flux across the red-cell membrane in the steady state in 114 patients with a history of calcium oxalate kidney stones and in 25 controls. Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria. Oxalate exchange was significantly higher in the 98 patients with idiopathic stone formation than in the controls (-1.10 +/- 0.95 [SD] X 10(-2) min-1 vs. -0.31 +/- 0.12 X 10(-2); P less than 0.001); it was above the upper limits of normal in 78 of these patients. All 8 patients with hyperparathyroidism and the patient with primary hyperoxaluria had values in the normal range; 2 of the patients with renal or urinary tract malformation had values at the upper normal limit. A study of five families indicated that the abnormality is an autosomal monogenic dominant trait with complete penetrance and variable expressivity. Oxalate-tolerance tests were carried out in five pairs of brothers. One brother in each pair had the abnormality in oxalate flux, and had a significantly higher percentage of oxalate excretion at two hours after oxalate loading (18.09 +/- 3.07 [SD] vs. 10.37 +/- 3.08 percent; t = 3.97; P less than 0.005) and four hours (14.87 +/- 2.91 vs. 9.89 +/- 2.93 percent; t = 2.70; P less than 0.05). Treatment with oral hydrochlorothiazide (50 mg per day) or amiloride (5 mg per day) or both restored normal or nearly normal red-cell oxalate exchange in all of 33 patients who initially had increased rates. We conclude that an inherited cellular defect in oxalate transport may be a factor in "primary" calcium oxalate stone formation and that this defect may be corrected with diuretics.
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PMID:An inheritable anomaly of red-cell oxalate transport in "primary" calcium nephrolithiasis correctable with diuretics. 394 45


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