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)

The problem of abacterial nephropathies associated with impaired calcium metabolism is discussed from the standpoint of membranous pathology. The data are presented on the similarity of the calciphylaxis pathogenesis described for the first time by H. Selye to calcium nephrolithiasis. The disease is viewed as the result of pronounced modification of the phospholipid layer of cell membranes under the influence of peroxidation, phospholipase activity and other processes induced by calcium-regulating hormones (parathyroid hormone, D3 and calcitonin). It is assumed that the clinical manifestations of renal pathology during calciphylaxis depend on the hereditary and environmental factors that determine the gravity of membranous pathology of renal cells. Recommendations as to the treatment and prevention of renal pathology during calciphylaxis based on the results of the authors' own experience are given.
 ...
PMID:[Clinical aspects of metabolic nephropathies, interstitial nephritis and urolithiasis in calciphylaxis]. 271 Jun 2

In 76 patients with active nephrolithiasis and in 28 normal subjects the influence of an Ca-load on the calcitonin and glucagon secretion and on the serum calcium, phosphate and magnesium levels was examined. In the patients with active nephrolithiasis a significant suppression of Ca-induced calcitonin secretion and absence of glucagon secretion was found. Simultaneously the patients showed a lower decrease of serum Mg and reduced increase of serum phosphate levels. The authors suggest participation of the above mentioned biochemical and endocrine abnormalities in the pathogenesis of the active nephrolithiasis.
 ...
PMID:[Calcitonin and glucagon secretion in active nephrolithiasis]. 363 Feb 89

24-h urinary cyclic adenosine 3', 5'-monophosphate/creatinine (cAMP/Cr) ratio was assessed in 10 patients with hypoparathyroidism, 6 with primary hyperparathyroidism, 7 with normocalcemic hypercalciuria and recurrent nephrolithiasis, 14 with osteomalacia, 25 with Paget's disease and 53 with symptomatic postmenopausal osteoporosis. In hypoparathyroid subjects the mean values of 24 h cAMP/Cr ratio were significantly lower than the control values, whereas in patients with parathyroid adenoma the mean values were higher and fell after parathyroid surgery. Patients with nephrolithiasis due to absorptive hypercalciuria showed low or normal cAMP/Cr ratio, whereas in those with osteomalacia and mean values of cAMP/Cr ratio were significantly higher than the control values and decreased after vitamin D treatment. The mean value of the 24 h urine cAMP/Cr ratio was normal in patients with Paget's disease or postmenopausal osteoporosis and increased significantly after long term treatment with calcitonin or diphosphonate. This increase paralleled a significant decrease of calcium plasma level. A significant improvement of fractional calcium absorption was observed in women with postmenopausal osteoporosis at the end of treatment with calcitonin or diphosphonate.
 ...
PMID:The 24-h urinary cyclic adenosine 3', 5' monophosphate/creatinine ratio: an useful approach to the diagnosis of parathyroid disorders and function. 627 46

Reduced citrate in urine and increased fasting excretion of calcium are abnormalities frequently reported in stone forming (SF) patients. Increased dietary acid (or reduced alkali) introduction or absorption may be a potential cause of both these pathological findings. To test this hypothesis, we studied 64 SF patients (32 with fasting hypercalciuria (FH) and 32 without FH (NFH)). After a basal evaluation for nephrolithiasis, while on a 500 mg calcium diet, they were evaluated for: (1) daily intestinal alkali absorption (IAA), by urinary electrolyte excretion; (2) basal concentrations of PTH, calcitonin (CT) and 1,25(OH)2-VitD; (3) oral calcium load for evaluation of changes in calcium and hydroxyproline urinary excretions; (4) intestinal calcium absorption (18 patients), with double curve analysis (stable Sr as tracer); and (5) changes in citrate excretion after an alkali load (50 mEq of a mixture of calcium gluconate, lactate and carbonate) in 10 patients. The results demonstrated: (1) FH stone formers had reduced citrate excretion and lower mean IAA levels than NFH stone formers; (2) FH stone formers also had higher bone resorption levels with lower PTH and higher CT levels; (3) IAA levels were related to both citrate excretion and bone turnover indices; and (4) the increases in citrate excretion after oral alkali load were strictly related to basal IAA values (index of alkali absorption and/or generation after oral load), demonstrating that a different absorptive capacity of alkali rather than a different dietary content may underlie these metabolic abnormalities.
 ...
PMID:Urinary citrate, bone resorption and intestinal alkali absorption in stone formers with fasting hypercalciuria. 774 55

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.
 ...
PMID:[The physicochemical and biochemical signs of nephrolithiasis]. 816 Mar 12

Idiopathic infantile hypercalcemia is recognized as a rare cause of infantile hypercalcemia. Its renal consequences include nephrocalcinosis with distal tubular dysfunction, nephrolithiasis, and finally renal failure. Herein we report the case of a two-month-old infant presenting with idiopathic infantile hypercalcemia complicated with distal renal tubular acidosis (RTA) and nephrocalcinosis. Despite correction of acidosis and dehydration, the persistant hypercalcemia could only be ameliorated with calcitonin treatment. Early diagnosis and appropriate treatment is life-saving in such cases.
 ...
PMID:Idiopathic infantile hypercalcemia and renal involvement. 1797 58

The objective of this article is to review the literature regarding the treatment of primary hyperparathyroidism (PHPT) with a focus on cinacalcet. A MEDLINE (1965-June 2009) and bibliographic search of the English-language literature was conducted using the search terms cinacalcet, calcimimetics, primary hyperparathyroidism, and treatment. All articles identified in the search were included. Parathyroidectomy is curative for patients with PHPT; however, there are few options for patients who are not surgical candidates, who refuse surgery, or those with refractory PHPT after parathyroidectomy. Possible treatment options include estrogens, raloxifene, bisphosphonates, calcitonin, and cinacalcet. Cinacalcet has been shown to decrease serum calcium and parathyroid hormone serum levels in patients with PHPT. These trials, however, have not studied the effect of cinacalcet on patient-oriented outcomes such as bone mineral density, nephrolithiasis, or other complications of PHPT. Cinacalcet may be considered to reduce serum calcium and parathyroid hormone serum levels in patients with PHPT who cannot or will not undergo surgery and those with refractory PHPT after parathyroidectomy. Because the effects of cinacalcet on bone mineral density are uncertain, more frequent monitoring of bone mineral density may be required along with a medication proven to improve bone mineral density. Future studies should evaluate the effect of cinacalcet on complications of PHPT.
 ...
PMID:Cinacalcet for the treatment of primary hyperparathyroidism. 2022 75

Calcium is essential for many metabolic process, including nerve function, muscle contraction, and blood clotting. The metabolic pathways that contribute to maintain serum calcium levels are bone remodeling processes, intestinal absorption and secretion, and renal handling, but hypercalcemia occurs when at least 2 of these 3 metabolic pathways are altered. Calcium metabolism mainly depends on the activity of parathyroid hormone (PTH). Its secretion is strictly controlled by the ionized serum calcium levels through a negative feed-back, which is achieved by the activation of calcium-sensing receptors (CaSRs) mainly expressed on the surface of the parathyroid cells. The PTH receptor in bone and kidney is now referred as PTHR1. The balance of PTH, calcitonin, and vitamin D has long been considered the main regulator of calcium metabolism, but the function of other actors, such as fibroblast growth factor-23 (FGF-23), Klotho, and TPRV5 should be considered. Primary hyperparathyroidism and malignancy are the most common causes of hypercalcemia, accounting for more than 90% of cases. Uncontrolled hypercalcemia may cause renal impairment, both temporary (alteration of renal tubular function) and progressive (relapsing nephrolithiasis), leading to a progressive loss of renal function, as well as severe bone diseases, and heart damages. Advances in the understanding of all actors of calcium homeostasis will be crucial, having several practical consequences in the treatment and prevention of hypercalcemia. This would allow to move from a support therapy, sometimes ineffective, to a specific and addressed therapy, especially in patients with chronic hypercalcemic conditions unsuitable for surgery.
 ...
PMID:Calcium metabolism & hypercalcemia in adults. 2175 30