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

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
 ...
PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

Twenty-one unselected patients with recurrent nephrolithiasis and normocalcemic hypercalciuria with or without hypophosphatemia and 18 normal subjects were studied with an oral calcium tolerance test and for 3- to 5-day periods while consuming a low normal (400 mg) and high-normal (1000 mg) calcium intake. The oral calcium tolerance test consisted of the measurement of the calcemic, calciuric, and parathyroid (assessed by determinations of serum immunoreactive parathyroid hormone and nephrogenous cAMP) responses to acute 1000- or 350-mg doses of calcium. Nineteen patients displayed normal results for basal serum calcium, parathyroid function, and fasting calcium excretion, and striking calcemic (mean increase in serum calcium, 0.9 vs. 0.2 mg/dl in the normal subjects) and calciuric (mean increase in urinary calcium, 0.33 vs. 0.15 mg calcium/100 ml GF in the normal subjects) responses to the 1000-mg calcium tolerance test, associated with a mean 54% suppression in nephrogenous cAMP. These patients were operationally defined as having "absorptive" hypercalciuria. The variable occurrence of hypophosphatemia in this group suggested that the pathogenesis of "absorptive" hypercalciuria may be complex and/or multifactorial. There were strong positive correlations between the calciuric response to the calcium tolerance test and fractional isotopic calcium absorption (r = 0.75, P less than 0.00), the calcemic responses to the test (r = 0.71, P less than 0.001) and the calciuric responses noted on the 1000- vs. the 400-mg daily calcium intake (r = 0.78, P less than 0.001). Two patients displayed low or low normal basal serum calcium, increased parathyroid function, increased fasting calcium excretion, and a striking calciuric but minimal calcemic response to the 1000-mg calcium tolerance test, associated with a moderate suppression in nephrogenous cAMP. These patients were operationally defined as having "renal" hypercalciuria. Several lines of evidence indicated that the hyperparathyroidism in these patients was physiological or secondary, including the near normalization of parathyroid function on the daily 1000-mg calcium intake. A steep slope of calcium excretion on calcium intake (due to increased calcium absorption) was noted in all hypercalciuric patients and accounted for the significantly improved diagnostic accuracy of screening patients for hypercalciuria on the high-normal calcium intake. The simple measurement of total cAMP excretion (nanomoles per 100 ml GF) and urinary calcium on the 1000-mg daily calcium intake seemed to provide reliable separation of patients with "renal" from those with "absorptive" hypercalciuria. A physiological (350 mg) dose of oral calcium produced a 30% suppression of nephrogenous cAMP in normal subjects; this suggests that dietary calcium exerts an important control of parathyroid function under physiological circumstances.
 ...
PMID:Pathophysiological studies in idiopathic hypercalciuria: use of an oral calcium tolerance test to characterize distinctive hypercalciuric subgroups. 23 82

The morphologic changes in trabecular bone were studied in 60 patients with surgically proven hyperparathyroidism and in 69 patients with nephrolithiasis. The hyperparathyroid bone lesions showed substantial variation in their extent. Four, typical stages were defined. The structure of trabecular bone remained intact in most cases. Bone turnover is significantly higher in the patients with primary hyperparathyroidism. Fifty percent of all patients with nephrolithiasis had bone changes similar to those found in the surgically proven hyperparathyroidism group. In 50% of so-called asymptomatic cases of hyperparathyroidism, the iliac crest biopsy is a useful supplement to clinical and hormonal data in deciding whether to operate on the parathyroid glands. In about 45% of cases, however, no definite diagnoses is possible. The determination of serum parathyroid hormone in primary hyperparathyroidism has a greater importance for diagnostic purposes than morphologic investigation of the bone biopsy.
 ...
PMID:Histomorphometric analysis of bone changes in surgically proven primary hyperparathyroidism and nephrolithiasis--the importance of bone biopsy in diagnosis. 55 4

Serum PRL, parathyroid hormone (PTH), and plasma 1,25-dihydroxyvitamin D [1,25(OH)2D]concentrations were measured in 6 women and 2 men with hyperprolactinemia, 6 normal men and 7 normal women, 4 men and 4 women with primary hyperparathyroidism, and 16 men and 4 women with Ca nephrolithiasis. Plasma 1,25(OH)2D and serum parathyroid hormone (PTH) concentrations were normal in the women and men with hyperprolactinemia. In patients with primary hyperparathyroidism and elevated serum PTH, plasma 1,25(OH)2D concentrations were elevated but serum PRL levels were normal. Likewise, serum PRL levels were normal in patients with Ca nephrolithiasis who had significantly elevated plasma, 1,25(OH)2D concentrations and normal serum PTH concentrations. Thus, hyperprolactinemia due to pituitary adenoma or idiopathic hypersecretion is not accompanied but elevated plasma concentrations of 1,25(OH)2D.
 ...
PMID:The interrelationships among prolactin, 1,25-dihydroxyvitamin D, and parathyroid hormone in humans. 57 83

The relatives of 25 index patients with primary parathyroid hyperplasia were tested for hypercalcemia. At least 13 of these patients had one or more first degree relatives with hypercalcemia. Two familial syndromes each with autosomal dominant transmission were recognized. Two index patients were part of large kindreds categorized as having familial hypocalciuric hypercalcemia (FHH). Manifestations of multiple endocrine neoplasia type I were present in the kindreds of at least four other index patients (FMEN I). In seven other kindreds there were too few affected members to allow definitive classification. Differences between manifestations of FHH and FMEN I were described. Among offspring of affected persons in kindreds with FHH, as distinct from FMEN I, the prevalence of hypercalcemia approached the theoretic maximum of 50 per cent during the first two decades. In FHH, nephrolithiasis and peptic disease were unusual; moderate hypercalcemia occurred without hypercalciuria; and subtotal parathyroidectomy did not abolish hypercalcemia. Concentrations of peptide hormones other than parathyroid hormone (PTH) were normal in those with FHH; in FMEN I high concentrations of glucagon in plasma were found in five of six patients tested, and high concentrations of gastrin were found in three of 12 patients. Hypergastrinemia generally accompanied obvious peptic disease. Distinction of the two conditions is important since patients with FHH may not benefit from subtotal parathyroidectomy, but they generally have a better clinical prognosis than do patients with FMEN I.
 ...
PMID:Family studies in patients with primary parathyroid hyperplasia. 87 Nov 27

The familial occurrence of primary hyperparathyroidism in which the proband is a 55-year-old man is reported. His 58-year-old sister and 40-year-old brother had undergone partial parathyroidectomy, and histological examination revealed hyperplasia in both cases. Their father and a daughter of the proband had a history of nephrolithiasis. The three siblings showed high levels of plasma parathyroid hormone (even the two postoperative cases). All of them had a history of nephrolithiasis and peptic ulcers. In the proband, image studies did not reveal any abnormality in the neck region. At present, the three cases do not exhibit any abnormalities in the pancreas or the pituitary by imaging studies and endocrine tests.
 ...
PMID:Familial primary hyperparathyroidism: study of the pedigree in three generations. 135 12

Chronic metabolic acidosis results in metabolic bone disease, calcium nephrolithiasis, and growth retardation. The pathogenesis of each of these sequelae is poorly understood in humans. We therefore investigated the effects of chronic extrarenal metabolic acidosis on the regulation of 1,25-(OH)2D, parathyroid hormone, calcium, and phosphate metabolism in normal humans. Chronic extrarenal metabolic acidosis was induced by administering two different doses of NH4Cl [2.1 (low dose) and 4.2 (high dose) mmol/kg body wt per d, respectively] to four male volunteers each during metabolic balance conditions. Plasma [HCO3-] decreased by 4.5 +/- 0.4 mmol/liter in the low dose and by 9.1 +/- 0.3 mmol/liter (P < 0.001) in the high dose group. Metabolic acidosis induced renal hypophosphatemia, which strongly correlated with the severity of acidosis (Plasma [PO4] on plasma [HCO3-]; r = 0.721, P < 0.001). Both metabolic clearance and production rates of 1,25-(OH)2D increased in both groups. In the high dose group, the percentage increase in production rate was much greater than the percentage increase in metabolic clearance rate, resulting in a significantly increased serum 1,25-(OH)2D concentration. A strong inverse correlation was observed for serum 1,25-(OH)2D concentration on both plasma [PO4] (r = -0.711, P < 0.001) and plasma [HCO3-] (r = -0.725, P < 0.001). Plasma ionized calcium concentration did not change in either group whereas intact serum parathyroid hormone concentration decreased significantly in the high dose group. In conclusion, metabolic acidosis results in graded increases in serum 1,25-(OH)2D concentration by stimulating its production rate in humans. The increased production rate is explained by acidosis-induced hypophosphatemia/cellular phosphate depletion resulting at least in part from decreased renal tubular phosphate reabsorption. The decreased serum intact parathyroid hormone levels in more severe acidosis may be the consequence of hypophosphatemia and/or increased serum 1,25-(OH)2D concentrations.
 ...
PMID:Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia. 146 97

Data are presented on 97 patients with primary hyperparathyroidism who constitute a representative cohort of the disease seen today. The average calcium (11.1 +/- 0.1 mg/dl; normal 8.7-10.7), phosphorus (2.8 +/- 0.1 mg/dl; normal 2.5-4.5), and parathyroid hormone level by immunoradiometric assay (119 +/- 7 pg/ml; normal 10-65) are typical of the modern presentation of primary hyperparathyroidism. Most patients were asymptomatic in that there was evidence for nephrolithiasis in only 18% and for radiologically evident bone disease in only 1% of patients. Nevertheless, when patients were evaluated with bone densitometry and with histomorphometric analysis of the bone biopsy specimen, evidence for the hyperparathyroid process could be shown in the majority of patients. Selective reduction of cortical bone and preservation of cancellous bone were apparent. Among patients with nephrolithiasis, no particular feature distinguished them from patients without nephrolithiasis. All biochemical data were similar between both stone and non-stone formers. The selective reduction in cortical bone was seen to the same extent among those with stones as among those without stones. The average 1,25-dihydroxyvitamin D level was not increased among those with stones. When the population was divided into groups with elevated or normal 1,25-dihydroxyvitamin D levels, the incidence of nephrolithiasis was unchanged. The results indicate that bone involvement can be demonstrated among most patients with asymptomatic primary hyperparathyroidism and that no pathophysiologic mechanisms are yet apparent to account for nephrolithiasis in primary hyperparathyroidism.
 ...
PMID:Characterization and evaluation of asymptomatic primary hyperparathyroidism. 166 60

Primary hyperparathyroidism (PHPT) is characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia. PTH acts by binding to cell surface receptors coupled to G proteins. Cyclic AMP is the classic second messenger of PTH action, but substantial evidence indicates that PTH also acts to stimulate formation of the dual second messengers, inositol trisphosphate and diacylglycerol, thereby mobilizing intracellular calcium. The physiologic actions of PTH include (1) an increase in extracellular fluid ionized calcium through direct actions on kidney and bone, the classic target organs for PTH, and (2) a decrease in extracellular fluid phosphate primarily through renal action. The pathophysiologic effects of PTH arise from (1) direct actions of PTH on bone and kidney, and possibly on nonclassic target organs, and (2) indirect effects of altered mineral homeostasis. PTH hypersecretion in PHPT can lead to bony demineralization, nephrolithiasis, and hypercalcemic crisis. PHPT may also be associated with mental disturbances, neuromuscular disease, hypertension, and glucose intolerance.
 ...
PMID:Pathophysiology of primary hyperparathyroidism. 176 67

Calcium metabolism and its response to citrate were examined in 51 patients with glaucoma receiving carbonic anhydrase inhibitors (acetazolamide or methazolamide). Metabolic acidosis, hypocitraturia and increased incidence of nephrolithiasis were induced by both drugs. However, the acidosis was milder with methazolamide administration. Normocalciuria was observed in 29 patients and was shown to be a result of low filtered calcium. Renal hypercalciuria in 16 patients was associated with elevated parathyroid hormone but nephrogenic cyclic adenosine monophosphate remained within normal limits. Citrate in the form of potassium citrate (4.3 mmol.) and sodium citrate (4.0 mmol.) did not correct the metabolic acidosis or hypocitraturia but consistently decreased fasting and 24-hour urinary calcium excretion in patients with renal hypercalciuria. This event did not occur in patients with normocalciuria or absorptive hypercalciuria. These results suggest that a small amount of citrate could reverse renal hypercalciuria without correcting the metabolic acidosis.
 ...
PMID:Calcium metabolism in acidotic patients induced by carbonic anhydrase inhibitors: responses to citrate. 201 6


1 2 3 4 5 6 7 8 9 10 Next >>