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)

In male patients with idiopathic recurrent calcium urolithiasis (RCU) the effects of oral potassium sodium citrate (PSC) on acid-base, citrate and mineral metabolism were investigated. There were 17 normocitraturic and 15 hypocitraturic patients. The examination time points in our clinical laboratory were prior to medication and after 3, 6 and over 12 months of medication. Urine collection periods were over 24 h, 2 h--after an overnight fast--3 h postprandially. Acceptance by the patients was poor, a large number refusing to take PSC for 12 months. Compliance of the patients continuing with the study was adequate as assessed by the urinary excretion of potassium and sodium. No unwanted side effects were observed. After 3 months of PSC medication a compensated metabolic alkalosis developed; in the urine calcium was decreased, while citrate, pH and oxalate were increased, as were hydroxyapatite supersaturation and calcium phosphate particles. After more than 12 months of PSC medication, citrate and pH tended toward the pretreatment baseline values, while hydroxyapatite supersaturation and calcium had already returned to pretreatment values. Despite ongoing PSC intake, patients with pre-existing hypocitraturia had lower urinary citrate than patients with previous normocitraturia, while the concomitant pH and hydroxyapatite supersaturation in the urine of the former remained at levels close to those of the latter. Under the influence of PSC, parathyroid gland function remained unchanged, but serum levels of bone alkaline phosphatase and osteocalcin were low, and urinary hydroxyproline was high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium sodium citrate administered as short-, medium- and long-term to male stone patients. 145 67

In idiopathic recurrent calcium urolithiasis (RCU) in men (n = 37) the metabolic effects of oral tripotassium citrate (PC) were investigated in a longitudinal field study. The patients were either normo- (n = 22) or hypocitraturic (n = 15). Laboratory examinations were performed before, and after 3, 6, and more than 12 months of medication. Acceptance of PC was poor, mainly because of the salty taste of the tablet preparation chosen, and a number of participants dropped out of the study. In the remaining participants, compliance was acceptable when evaluated on the basis of urinary potassium and undesired side effects did not occur. In the short term (up to 3 months), PC evoked compensated metabolic alkalosis (pH and citrate in urine increased; blood gases remained normal), a drop in urinary calcium, together with increasing oxaluria, hydroxyapatite supersaturation, and calcium phosphate crystalluria. In the long term (greater than 12 months) PC urinary pH and citrate "dissociated", in that pH returned to pretreatment baseline values, whereas citrate stayed at high levels. In normocitraturics but not in hypocitraturics, urinary urea and sodium increased with PC. Hypocitraturics appeared to be less sensitive to the effects of PC, as reflected by the relatively small rise in urinary pH and citrate, and they maintained higher mean levels of indicators of bone metabolism (osteocalcin, alkaline phosphatase, hydroxyproline) despite continuous administration of PC. It was concluded that although the PC tablet preparation was effective it may not be an ideal anti-stone drug treatment in the long term and that, especially in hypocitraturics, the intrinsic metabolic defect of RCU may not be sufficiently well controlled.
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PMID:Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium citrate administered over the short-, medium- and long-term medication of male stone patients. 155 90

Experiments were designed to determine if Gray strain infectious bronchitis virus (IBV) infection increases the incidence of urolithiasis type kidney damage when the urine is already high in Ca and relatively alkaline due to a high Ca-low available P diet (i.e., layer ration). In addition, experiments were conducted to determine the effects of Gray strain IBV on pullet renal function of 6 and 14-wk-old pullets at 2, 5, and 10 days postinoculation (PI). Blood gas parameters were measured to determine the mechanism by which layer ration decreases hydrogen ion concentration [( H+]). Urine flow rate, glomerular filtration rate, electrolyte excretion (Na, K, Ca, P), free water clearance, urine osmolality, urine [H+], and renal plasma flow (para-aminohippuric clearance) were measured to assess renal function. Gray strain IBV increased urine [H+] and decreased renal plasma flow in 6-wk-old pullets, and induced a diuresis in 14-wk-old pullets between 5 and 10 days PI. The layer ration increased Ca excretion and induced a metabolic alkalosis, thus decreasing urine [H+] and causing urolith formation. Feeding layer ration followed by Gray strain IBV infection had an additive effect on the incidence of urolithiasis and gross kidney damage. Gray strain IBV infection 8 wk prior to feeding layer ration did not induce urolithiasis. The results suggest that the additive effect of Gray strain IBV on the incidence of urolithiasis is probably due to tubular damage rather than direct changes in renal function parameters.
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PMID:Order of exposure to high dietary calcium and gray strain infectious bronchitis virus alters renal function and the incidence of urolithiasis. 255 68

Urinary acidification previously was shown to be an effective treatment for calcium-induced urolithiasis in domestic fowl, but diuresis caused by the acidifying agent (ammonium chloride) was an undesirable side effect. Because supplemental dietary methionine reportedly acidifies mammalian urine, an experiment was conducted to evaluate the efficacy of the free acid form of methionine hydroxy analog (MHA) as an acidifying agent for treating avian urolithiasis. From 5 to 17 wk of age, immature Single Comb White Leghorns were fed diets containing normal calcium (1%) or high calcium (3.5%). Diets were supplemented with 0, 0.3 or 0.6% MHA. Relative to birds fed the normal calcium diets, birds fed the high calcium diet without added MHA were in a state of metabolic alkalosis and excreted more alkaline urine containing high levels of calcium. Birds fed the high calcium diet without MHA also had significantly higher kidney asymmetry ratios, a higher incidence of gross kidney damage, and a higher incidence of urolith formation when compared with birds fed normal calcium diets. When compared with the high calcium diet without MHA, the high calcium diet supplemented with 0.6% MHA significantly acidified the urine without causing detectable metabolic acidosis, significantly reduced kidney asymmetry and gross kidney damage, and reduced the incidence of urolith formation without increasing water consumption or urine flow. These data demonstrate that MHA effectively prevents calcium-induced kidney damage in domestic fowl without causing undesirable side effects. MHA did increase both fractional and absolute calcium excretion during calcium loading.
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PMID:Methionine hydroxy analog (free acid) reduces avian kidney damage and urolithiasis induced by excess dietary calcium. 272 31

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 objective of the present study was to investigate the matrix protein of a rare urinary stone that contained calcium carbonate. A urinary stone was extracted from a 34-year-old male patient with metabolic alkalosis. After X-ray diffractometry and infrared analysis of the stone, proteomic analysis was carried out. The resulting mass spectra were evaluated with protein search software, and matrix proteins were identified. X-ray diffraction and infrared analysis confirmed that the stone contained calcium carbonate and calcium oxalate dihydrate. Of the identified 53 proteins, 24 have not been previously reported from calcium oxalate- or calcium phosphate-containing stones. The protease inhibitors and several proteins related to cell adhesion or the cytoskeleton were identified for the first time. We analyzed in detail a rare urinary stone composed of calcium carbonate and calcium oxalate dihydrate. Considering the formation of a calcium carbonate stone, the new identified proteins should play an important role on the urolithiasis process in alkaline condition.
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PMID:Proteomic analysis of a rare urinary stone composed of calcium carbonate and calcium oxalate dihydrate: a case report. 2411 10

The SFBC working group aimed to deal with biological tests outside the french nomenclature that may be useful in the context of urinary exploration of metabolism. This section will be divides into three parts: 1) nutritional assessment using urinary urea; 2) metabolic assessment of urolithiasis; 3) exploration of tubulopathies. National and international recommendations support the evaluation of nutritional status from urea measurements in urine and dialysate with the following indications: primary metabolic evaluation of urolithiasis patients, monitoring of protein intake in chronic renal failure stage 3 or stage 5D with residual diuresis. For the management of the urolithiasis disease, biomedical tests recommended by the national and international guidelines are the measurement of the urinary density using refractometry in the primary metabolic evaluation as well as the determination of oxalemia in the diagnosis (patients with GFR< 30 mL/min/1.73 m2) and follow-up (patients with GFR< 60 mL/min/1.73 m2) of primary hyperoxaluria. The determination of the bicarbonaturia is retained for the in depth exploration of urolithiasis and tubular acidosis. The measure of chlore in urine is used to evaluate the volume status during metabolic alkalosis and to calculate the urinary anionic gap during metabolic acidosis.
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PMID:Urinary exploration of metabolism: nutrition assessment, urolithiasis and tubulopathy. 3141 99