Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392525 (nephrolithiasis)
 2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred fourteen nondialyzed azotemic adult patients (creatinine connentration 1.2 to 17.6 mg/dl), 78 stable renal transplant recipients (creatinine less than 1.9 mg/dl), 50 patients with idiopathic nephrolithiasis, 36 patients with surgically proven primary hyperparathyroidism, and 62 normal volunteers were studied with simultaneous serum ionized calcium, total calcium, parathyroid hormone (PTH), phosphorus, and creatinine measurements. Ionized calcium could not be reliably predicted from total calcium. Although in all patient groups values for serum ionized calcium correlated significantly with those for total calcium, the scatter around the regression line was such that a direct interpretation was not precise. With respect to reference values, significant differnces were found between ionized and total calcium in 26% of all studied patients. When compared with total serum calcium, ionized calcium appeared to be a more sensitive index of calcium metabolism. All correlations with ionized calcium had a higher r value compared with those with total serum calcium. Two findings were particularly rewarding. In patients with chronic renal failure, serum PTH showed a negative correlation with serum ionized calcium, indicating that the latter may have been largely responsible for the secondary increase in PTH; in patients after a successful transplant, serum PTH showed a positive correlation with serum ionized calcium, indicating that in the presence of normal kidney function the previously hypertrophied parathyroid glands may be largely responsible for the daily study of a large number of specimens, determinations of serum ionized calcium should be encouraged in all patients suspected of having abnormalities of renal calcium metabolism.
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PMID:Comparative studies of total and ionized serum calcium values in normal subjects and patients with renal disorders. 699 43

The metabolic picture of 32 patients with surgically proven primary hyperparathyroidism presenting with renal stones was compared with that of 37 patients without stones. Between stone-forming and nonstone-forming groups, there was no significant difference in serum 1,25-dihydroxyvitamin D [6.82 +/- 2.62 vs. 6.22 +/- 2.33 ng/dl (mean +/- SD); P greater than 0.05], fractional (intestinal) calcium absorption (0.726 +/- 0.141 vs. 0.690 +/- 0.120), urinary calcium (299 +/- 139 vs. 284 +/- 144 mg/day), serum calcium, phosphorus, and parathyroid hormone, or bone density. Similarly, no differences were found between 29 patients presenting with stones alone and 9 presenting with bone disease alone with respect to the above measures. Moreover, urinary environment was typically supersaturated with respect to stone-forming salts regardless of the presence of stones. The results indicate that there is no unique pathophysiological background for the nephrolithiasis of primary hyperparathyroidism.
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PMID:A lack of unique pathophysiologic background for nephrolithiasis of primary hyperparathyroidism. 726 39

We report on a 33-year-old man with hypercalcemia and recurrent nephrolithiasis, who underwent the first neck exploration for primary hyperparathyroidism on September 27, 1973. No tumor was found and bilateral upper normal parathyroid glands were removed. However, hypercalcemia persisted postoperatively. Selective venous sampling for radioimmunoassay of parathyroid hormone 5 years later revealed a sharp unilateral gradient in the right vertebral vein. On November 2, 1978 the second neck exploration was performed and a right lower parathyroid adenoma was removed from the right lateral wall of the esophagus. Postoperatively, the serum calcium level decreased to 8.8 to 9.3 mg./dl. and convalescence was uneventful. In this case the pathway of parathyroid venous effluent might have been changed by the previous neck exploration and probably drained anomalously through the vertrbral vein. Selective venous sampling for radioimmunoassay of parathyroid hormone should include samplings from the vertebral veins as well as the thyroid veins, especially in cases with 1 or more previous neck explorations.
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PMID:Parathyroid adenoma found by vertebral vein sampling. 738 16

The effects of total sunlight deprivation on urinary risk factors for nephrolithiasis and vitamin D metabolism were studied in 20 healthy male subjects. Blood and 24-h urine samples were collected before submarine deployment and 68 days later while still at sea. No subject received sunlight exposure during the test interval. Significant decreases in daily urinary excretion of calcium, uric acid, sodium, sulfate, and phosphorus were found. The relative supersaturation ratio of monosodium urate also fell. There was no change in urinary citrate or urine volume. Mean serum levels of 25-hydroxyvitamin D [25(OH)D] declined from 31 to 19 pg/ml (P < 0.0001), parathyroid hormone increased from 22 to 30 pg/ml (P < 0.0001), and osteocalcin (GLA) increased from 2.7 to 3.3 ng/ml (P = 0.005). Mean serum levels of 1,25 dihydroxy-vitamin D were unchanged. Four subjects had 25(OH)D levels below 10 ng/ml by the end of the submarine patrol. These findings suggest that exposure to the submarine environment produces physiologic changes that decrease the risk for renal stone formation. The data are consistent with the role of vitamin D metabolism in sunlight deprivation and demonstrate that compensatory mechanisms are well established within 68 days.
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PMID:Effects of the submarine environment on renal-stone risk factors and vitamin D metabolism. 763 76

Urolithiasis diagnosis by uroliths presence reflects insufficient knowledge of the disease pathogenesis. 42 patients with oxalocalcium nephrolithiasis and 20 healthy patients were examined for differences in the urine and plasma composition. The authors studied factors involved in regulation of mineral metabolism and urinary elimination of crystal-forming substances. The patients with urinary stones compared to the control are characterized by low total crystal-inhibiting activity, hyperosmia, hypodipsia, decreased surface free energy, high quantities of ionized calcium, low ionized magnesium in the urine, oligo- and uricosuria. Shifts in hormonal regulation in nephrolithiasis result from slight elevation of urinary cyclic adenosine monophosphate, a relative rise in the levels of aldosterone and parathyroid hormone, low blood calcitonin, all the changes being statistically significant.
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PMID:[The physicochemical and biochemical signs of nephrolithiasis]. 816 Mar 12

We report herein the unusual case of a 55-year-old man with multiple endocrine neoplasia type 1 presenting as hyperparathyroidism, hyperpituitarism, insulinoma, and gastrinoma with postbulbar duodenal ulcers. The patient was referred to our hospital for further investigations of nephrolithiasis, acromegaly, and hematemesis. Laboratory studies showed high serum levels of calcium, parathyroid hormone, growth hormone, insulin, gastrin, and prolactin. Computed tomography of the cranial cavity demonstrated an enlargement of the serra turcica and swelling of two parathyroid glands in the neck. Computed tomography and angiography of the abdomen also showed a mass in the head of the pancreas. Endoscopy demonstrated reflux esophagitis, erosive gastritis, and multiple postbulbar duodenal ulcers. We diagnosed this patient as having multiple endocrine neoplasia type 1, with concomitant lesions of the pituitary gland, parathyroid glands, and islet cells of the pancreas. Following excision of the two enlarged parathyroid glands, his serum calcium and parathyroid hormone levels fell to within the normal range. Thereafter, a total gastrectomy was performed to alleviate the frequent bleeding from the upper gastrointestinal tract. However, resection of the pancreatic mass could not be performed owing to severe inflammation around the duodenum, probably induced by the postbulbar duodenal ulcers.
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PMID:Multiple endocrine neoplasia type 1 presenting as insulinoma, gastrinoma, and postbulbar duodenal ulcers: report of a case. 855 8

1. To assess whether the mineral content of drinking water influences both risk of stone formation and bone metabolism in idiopathic calcium nephrolithiasis, 21 patients were switched from their usual home diets to a 10 mmol calcium, low-oxalate, protein-controlled diet, supplemented with 21 of three different types of mineral water. Drinking water added 1, 6 and 20 mmol of calcium and 0.5, 10 and 50 mmol of bicarbonate respectively to the controlled diet. 2. The three controlled study periods lasted 1 month each and were separated by a 20 day washout interval. Blood and urine chemistries, including intact parathyroid hormone, calcitriol and two markers of bone resorption, were performed at the end of each study period. The stone-forming risk was assessed by calculating urine saturation with calcium oxalate (beta CaOx), calcium phosphate (beta bsh) and uric acid (beta UA). 3. The addition of any mineral water produced the expected increase in urine output and was associated with similar decreases in beta CaOx and beta UA, whereas beta bsh varied marginally. These equal decreases in beta CaOx, however, resulted from peculiar changes in calcium, oxalate and citrate excretion during each study period. The increase in overall calcium intake due to different drinking water induced modest increases in calcium excretion, whereas oxalate excretion tended to decrease. The changes in oxalate excretion during any one study period compared with another were significantly related to those in calcium intake. Citrate excretion was significantly higher with the high-calcium, alkaline water. 4. Parathyroid hormone, calcitriol and markers of bone resorption increased when patients were changed from the high-calcium, alkaline to the low-calcium drinking water. 5. We suggest that overall calcium intake may be tailored by supplying calcium in drinking water. Adverse effects on bone turnover with low-calcium diets can be prevented by giving high-calcium, alkaline drinking water, and the stone-forming risk can be decreased as effectively as with low-calcium drinking water.
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PMID:Effects of mineral composition of drinking water on risk for stone formation and bone metabolism in idiopathic calcium nephrolithiasis. 886 14

We have used published rat micropuncture data to construct a matrix of ion concentrations along the rat nephron. With an iterative computer model of known ion interactions, we calculated relative supersaturation ratios in all nephron segments. The collecting ducts and urine showed expected supersaturation with stone-forming salts. Fluid in the thin segment of the loop of Henle may be supersaturated with calcium carbonate and calcium phosphate under certain conditions. Because calculations cannot predict the actual course of crystallization, we made solutions to mimic, in vitro, presumed conditions in the loop of Henle. The solid phases that formed were analyzed by X-ray powder diffraction, electron microprobe, and infrared spectroscopy. All samples were identified as poorly crystallized or immature apatite. The descending limb of Henle's loop creates a unique condition as it extracts water but not sodium, bicarbonate, calcium, or phosphate, giving a calcium concentration at the bend of 3 mM, pH 7.4, and a phosphate concentration that varies from 0.8 to 48 mM, depending on parathyroid hormone and dietary phosphate. We conclude that conditions in the thin segment potentially could create a solid calcium phosphate phase, which may initiate nucleation of calcium oxalate salts in the collecting ducts, potentiating nephrolithiasis and nephrocalcinosis.
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PMID:Evidence of calcium phosphate supersaturation in the loop of Henle. 896 38

Most cases of primary hyperparathyroidism are due to either a parathyroid adenoma or to parathyroid hyperplasia. Parathyroid carcinoma is a very rare cause of hyperparathyroidism. Although the diagnosis of parathyroid carcinoma is usually established based on pathological criteria of vascular and capsular invasion, some clinical and biochemical features differentiate it from benign forms of hyperparathyroidism. We report the case of a middle-aged woman with a long standing history of nephrolithiasis, who presented with a palpable neck mass, weight loss, severe hypercalcemia and hypophosphatemia, as well as very high serum levels of intact parathyroid hormone. Surgical neck exploration revealed a large tumor that invaded trachea, esophagus, reccurrent laryngeal nerve, right apical pleura and right carotid artery. Pathological examination confirmed the invasive nature of the tumor. Along with the case report, we review the literature and discuss the diagnostic and therapeutic options of this rare condition.
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PMID:Primary hyperparathyroidism due to parathyroid carcinoma. 920 27

In recurrent calcium stone formers interfering factors or changes in receptor sensitivity may alter the interrelationships among calcium-regulating hormones, and hormonal behavior often does not fit with the theoretical assumptions. The vitamin D system appears to have the most important metabolic and clinical effects. Abnormal up-regulation of the synthesis of calcitriol and the consequent parathyroid hormone (PTH) suppression can induce hypercalciuria. Consequently, the hypocalciuric effect of thiazide would be caused by an enhanced response to PTH and by a reduction in 1,25(OH)2-vit D. A negative role of vitamin D on the skeleton has been observed in the presence of a negative calcium balance. Moreover, vitamin D also plays a role in urine oxalate excretion. PTH seems not to be directly stimulated in hypercalciuria and recurrent calcium nephrolithiasis, and patients with hyperparathyroidism and recurrent calcium nephrolithiasis show a similar degree of bone demineralization, irrespective of the presence of absence of the so-called 'primary hyperparathyroidism.' Calcitonin plays a contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to be strictly related to dietary calcium intake. A higher sensitivity of thyroid C cells, particularly in absorptive hypercalciuric patients, could be related to the pathogenesis of hypercalciuria and contribute to its persistence.
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PMID:Calciotropic hormones and nephrolithiasis. 938 31


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