Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-seven male patients with idiopathic calcium urolithiasis and 17 normal male subjects were studied to evaluate the mechanism of idiopathic hypercalciuria with an oral calcium tolerance test, which has been useful in differentiating hypercalciuria. The changes in parathyroid function, such as parathormone and urinary cyclic AMP, and calcium after calcium load differed between absorptive hypercalciuria and renal hypercalciuria. We have confirmed that the change in serum calcitonin after calcium load was also different in these two hypercalciurias. The increase in serum calcium was sufficient to reduce parathyroid function but serum calcitonin was unchanged after calcium load in the control group, in patients with normocalciuria, and those with renal hypercalciuria. Although serum and urinary calcium were more elevated in absorptive hypercalciuria than in the other three groups, parathyroid function was not significantly reduced after loading in absorptive hypercalciuria. In this group only, the serum calcitonin was significantly elevated after calcium load. It is reasonable to suggest that, in this group, because parathyroid function is usually suppressed by intestinal hyperabsorption of calcium, parathyroid function may not be further suppressed by even calcium load. Possibly the significant stimulation of calcitonin may compensate for the lack of suppression of parathyroid function and maintain normal serum calcium levels in absorptive hypercalciuria. These results suggest that the change in serum calcitonin is also useful to differentiate abnormalities of calcium metabolism in patients with hypercalciuria.
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PMID:Oral calcium tolerance test and serum calcitonin in calcium stone formers. 630 68

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

Previous work in younger males with recurrent idiopathic calcium urolithiasis (RCU) demonstrated inappropriately high postprandial phosphaturia, hyperinsulinemia and insulin resistance, but normal glycemia. To investigate further whether these abnormalities occur also in RCU patients with a mean age corresponding to the life period with peak formation of calcium-containing stones, two trials were carried out in 155 males of comparable age and body mass index. All participants underwent a standardized laboratory examination, including collection of urine and blood before and following a test meal rich in carbohydrate and calcium but low in phosphorus. In trial 1, comprising control subjects (n = 12, mean age 42 years) and RCU patients (n = 24, mean age 41 years), phosphate (Pi) excretion and fractional Pi excretion in postprandial urine of controls did not change compared with the values in fasting urine, but were significantly increased in RCU, despite the fact that there was almost equal suppression of serum parathyroid hormone (PTH) and increase in serum calcitonin. Postprandially, RCU patients were hyperinsulinemic but still normoglycemic versus controls. In trial 2, carried out in unclassified (in terms of calciuria) RCU patients (n = 119, mean age 40 years) only, the post-load Pi-uria was similar in magnitude to Pi-uria of RCU patients in trial 1; increased postprandial Pi-uria was a phenomenon also of normocalciuria but was slightly more pronounced in hypercalciuria, while changes in calcium phosphate (brushite) and calcium oxalate supersaturation of urine were unrelated to calciuria. In RCU patients, but not controls, there was a tendency toward higher urinary glucose in post-load as compared with fasting urine. When urinary Pi and fractional Pi excretion in trial 2 were considered as dependent variables in multivariate regression analysis, they appeared unrelated to age, but positively associated with postprandial glycemia as the best predictor, followed by insulinemia, insulin resistance, to a lesser degree fasting serum PTH and the metabolic activity of stone disease, negatively associated with blood total lipids and very low density lipoprotein (VLDL) cholesterol. It was concluded that RCU males (1) show low Pi-uria during fasting but impaired renal Pi conservation in response to a mixed meal, a situation carrying the risk of Pi deficiency over the long term; (2) represent a population developing hyperPi-uria despite suppressed PTH; (3) exhibit insulin resistance but are still able to maintain normoglycemia at the expense of hyperinsulinemia. It is suggested that calcium-containing renal stones are related to impaired Pi and glucose translocation across cell membranes, and that the role of lipids in this setting deserves further investigation.
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PMID:Urinary phosphate excretion in the pathophysiology of idiopathic recurrent calcium urolithiasis: hormonal interactions and lipid metabolism. 944 52

Calcium, in the form of regular food supplementation, can improve bone metabolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these two aspects, ten healthy volunteers were given a conventional test meal (breakfast; calcium content 28 mg) with or without two dosages of calcium (as calcium-sodium citrate, CSC 1, 680 mg; CSC 2 1,360 mg), taken after an overnight 12 h fast. To study the latter aspect, patients with idiopathic recurrent calcium urolithiasis (ICU) received a balanced test meal of fixed composition, containing 1,000 mg calcium either as CSC (Meal + CSC3; n = 6) or as calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate absorption; in serum, CSC increased calcitonin and suppressed parathyroid hormone, but left unchanged the markers of bone turnover, serum osteocalcin and bone alkaline phosphatase. In urine, CSC decreased bone resorption markers (collagen crosslinks) and phosphaturia increased citrate, created signs of metabolic alkalosis, and inhibited several parameters of CaOx crystallization. In ICU, the CSC3 load failed to promote the crystallization of CaOx and calcium phosphate. It was concluded that CSC supplementation of a meal: (1) is well tolerated by healthy subjects and ICU patients, renders calcium highly available to bone, and prevents post-prandial oxaluria from rising; and, (2) is followed by the inhibition of crystallization of renal stone forming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis of renal stones would appear justified.
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PMID:Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans--preliminary results in patients with idiopathic calcium urolithiasis. 1042 48

The analgesic effects of high-energy extracorporeal shock wave therapy (ESWT) were discovered by chance during its application for urolithiasis and for bone pseudarthrosis. Despite the extensive use of ESWT, the mechanisms of its antinociceptive effects are still unclear. A gate control mechanism and other antinociceptive mechanisms have been postulated. The aim of this study was to investigate the possible influence of low-energy ESWT on the expression of the transmitters substance P (SP) and calcitonin gene-related peptide (CGRP) in the lumbar spinal cord of the rat. Immunohistochemical analysis of the expression of the neuropeptides CGRP and SP was performed in rats treated either once with 1000 impulses or three times with 1000 impulses, with two different energy flux densities being used (0.043 and 0.11 mJ/mm2). The animals were killed either 4 or 72 h after the ESWT. No regulatory effect of ESWT on the expression of SP or CGRP in the dorsal horns was found. Because the application of ESWT showed no significant changes in the sensory system, it is unlikely that the application of ESWT triggers the endogenous pain control system of the rat through hyperstimulation analgesia. Furthermore, these results show that low-energy ESWT had no side effects on the rat spinal cord.
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PMID:No influence of low-energy extracorporeal shock wave therapy (ESWT) on spinal nociceptive systems. 1181 40

Idiopathic hypercalciuria (IH) is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density (BMD), as described previously in pediatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs (gut, bone and kidney), which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins (i.e., fibroblast growth-factor-23). Usually, a primary defect in one organ induces compensatory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary to a primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular transport of this ion in intestines, kidneys and bones. Reduced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking at the end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.
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PMID:Bone disease in pediatric idiopathic hypercalciuria. 2417 42