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)

Uninephrectomy (uNX) usually induces compensatory hyperfunction of the remaining kidney in an attempt to preserve the homeostasis of body fluid composition. The present study used uninephrectomized Sprague-Dawley rats on a lithogenic diet (0.5% ethylene glycol, EG) to evaluate the influence on urinary stone formation and calcium oxalate crystal deposition of compensatory excretion of lithogenic substances in the remnant kidney. The results showed that there were no urinary stones or calcium oxalate crystal deposits in the intact or uNX rats fed a normal diet. In the EG feeding groups, the incidence of massive (grade 3) crystal deposits was significantly higher in the uNX rats (87.5%) than that in the intact rats (37.5%; P less than 0.05). The incidence of urinary stone formation was also higher in the uNX rats as compared to that of the intact rats, although the difference did not achieve statistical significance. The serum magnesium, phosphorus and creatinine increased significantly, whereas creatinine clearance (CCr), 24-hour urinary excretions of citrate, sodium, potassium and chloride decreased significantly in the uNX rats fed EG. These data indicate that uninephrectomy increases the vulnerability of the contralateral remnant kidney to urolithiasis and crystal deposition when the lithogenic risk factors are present. Furthermore, once the remnant kidney forms urolithiasis or massive calcium oxalate crystal deposits, the renal function is severely compromised.
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PMID:Uninephrectomy enhances urolithiasis in ethylene glycol treated rats. 140 14

Chondroitin polysulfate (CPS) have inhibitory activity on stone formation of calcium oxalate. This study compared the inhibitory effect of three CPS (CPS S-I, CPS S-II, CPS S-III) with sodium pentosan polysulfate (SPP) and chondroitin sulfate (CS). Crystal growth inhibition was measured in a seeded crystal growth system with 14C-oxalate, and CPS S-I and CPS S-II were the most active substances inhibiting crystal growth. Since CPS S-II and CPS S-III had remarkable hemorrhagic adverse effect, these two substances were excluded from the following study. The study of administration of the rest of the substances (CPS S-I, SPP, CS) to rats revealed that CPS S-I highly inhibited formation of stone in kidney. About 65 percent of CPS S-I administered subcutaneously was excreted in 24 hours urine. Therefore it may be of value to study clinical usefulness of CPS S-I for treatment of patient with urolithiasis.
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PMID:[A study of inhibitory effect of chondroitin polysulfate on stone formation of calcium oxalate]. 143 67

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

A sixty nine-year-old woman was admitted to the hospital because of further examination of hypercalcemia. On July 1990, she complained of general fatigue and loss of appetite. She was pointed out to have hypercalcemia (15.1mg/dl), urolithiasis, and renal insufficiency. CT films of the chest showed swelling of the mediastinal lymphnodes and CT of the abdomen nephrocalcinosis. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in the mediastinum. Levels of the parathyroid hormone was normal. Levels of the serum calcium (13.7mg/dl), angiotensin converting enzyme (30.4IU/L) and 1.25 (OH)2D (87PG/ml) were elevated. Giant cells were found in the biopsy specimen of the lung. A significant relationship between the serum calcium and creatinine were observed (r = 0.76, p < 0.02). Proximal fractional reabsorption of sodium showed to be suppressed (47.7%), and distal fractional reabsorption of sodium showed to be normal (88.4%). From these findings hypercalcemia and urolithiasis was suggested to result from sarcoidosis. The hypercalcemia and renal insufficiency improved with corticosteroid therapy.
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PMID:[A case of sarcoidosis with hypercalcemia, urolithiasis, nephrocalcinosis and renal insufficiency]. 148 16

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.
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PMID:Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers. 154 Oct 59

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

A total of 15 patients with unilateral nephrostomy tubes after extracorporeal shock wave lithotripsy received either 0 (placebo), 100, 500, 1,000 or 2,000 mg. ascorbic acid on days 2 and 3 postoperatively. Before and after administration, successive 6-hour urine specimens were collected from the nephrostomy tube and from the contralateral kidney directly into a preservative to stabilize ascorbic acid and oxalate. In 1 patient in each group preservative was omitted from the collection pouch. Urinary oxalate was then measured enzymatically after removal of ascorbic acid with sodium nitrite. Preservatives proved necessary for full recovery of analyte. At doses of 500 mg. or more of ascorbic acid there was a statistically significant increase in urinary oxalate equivalent to 1.2 to 1.8% of the millimoles of ascorbate administered. This represented an increase in urinary oxalate excretion of 6 to 13 mg. per day per 1,000 mg. ascorbic acid supplement. This amount would increase the risk of calcium oxalate urolithiasis.
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PMID:Ascorbic acid overdosing: a risk factor for calcium oxalate nephrolithiasis. 848 36

Increasing the concentration of urate promotes the crystallization of calcium oxalate in human urine. In this study the possibility that this effect might be attributable to the attenuation of the inhibitory activity of urinary glycosaminoglycans (GAGs) was explored. Urine sample were collected from 20 men with no history of urolithiasis and the intact GAGs removed by 10 kDa ultrafiltration. Ten of these specimens, designated type A, spontaneously precipitated calcium oxalate crystals when the median urate concentration was increased from 3.13 to 7.33 mmol/liter by the addition of a saturated solution of sodium urate. In the remaining more dilute urines, which were designated type B, spontaneous calcium oxalate crystallization did not occur when the median urate concentration was raised from 2.20 to 6.40 mmol/liter. In these samples crystallization was induced by a standard load of oxalate above the empirically determined metastable limit. Addition of urate significantly reduced the median metastable limit from the control value of 125 to 46 mumol oxalate, and the volume of calcium oxalate deposited was increased fourfold from 25,000 to 104,000 microns 3/microliters. The median size of the precipitated particles was also increased in the presence of urate from 12.06 microns to 14.3 microns; this was confirmed by scanning electron microscopy, which demonstrated that the crystals precipitated in the presence of added urate, though individually smaller, were markedly more numerous and more highly aggregated than those deposited in the control. Re-ultrafiltration of the urines to which urate had been added did not alter the urate concentration, and SEM examination of the ultrafiltration membranes did not reveal the presence of any particulate material.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium oxalate crystallization in urine: role of urate and glycosaminoglycans. 159 51

The interaction between calcium and glycosaminoglycans (GAGs) was studied using a calcium ion-selective electrode. The Ca-binding capacity of GAGs involved 16% of total calcium in the presence of chondroitin sulphate and 28% in the presence of pentosan polysulphate. The action of GAGs on the nucleation of uric acid and sodium urate was examined and inhibitory effects were observed. The action of uric acid as a heterogeneous nucleant of calcium oxalate was studied, and considerable promotion of the heterogeneous nucleation of calcium oxalate by uric acid was found, which could be inhibited by the action of GAGs. From these summarised in vitro results, we conclude that uric can constitute an important risk factor for calcium oxalate urolithiasis through heterogeneous nucleation and the GAGs can play an important role as preventive agents.
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PMID:Glycosaminoglycans, uric acid and calcium oxalate urolithiasis. 175 32

In Self-defense Force Hospitals we often treat pilots with renal stones who will be exposed to high gravity (G) load after the treatment. Because the regulation prohibits the flight of a pilot with urolithiasis, the stone must be removed completely by noninvasive procedure. Percutaneous nephrolithotomy, therefore, is one of the treatment of choice in such patients. The effect of G load on the kidney, in particular, on the renin-angiotensin-aldosterone (R-A-A) system and the safety of percutaneous nephrolithotomy in a pilot who is exposed to high G load have not been adequately investigated. In this study, I examined the effect of G load in canine kidney model. The effect of G load on R-A-A system: Twenty-two adult mongrel dogs of a mean weight of 10.9 kg. maintained on a normal Na+ intake were studied. To dogs in the sitting position, high G load was given. The exposure to G load consisted of maximum load of 8 G for 45 seconds with the onset ratio of 0.1 G/sec. for group 1, and 5 courses of maximum G load of 8 G for 10 seconds with the onset ratio of 2.5 G/sec., followed by 1.5 G for 60 seconds for group 2. Plasma renin activity was unchanged in group 1, but it increased in group 2. Plasma aldosterone increased from 68.6 +/- 17.9 to 252.0 +/- 56.4 pg/ml (p less than 0.005) in group 1. and from 191.8 +/- 40.6 to 479.2 +/- 76.0 pg/ml (p less than 0.005) in group 2 after G load. Angiotensin II decreased from 129.0 +/- 19.4 to 84.7 +/- 19.1 pg/ml (p less than 0.05) after G load in group 2. These data suggest that the increase in plasma aldosterone after G load in independent of the renin-angiotensin system. It is considered that the alteration of R-A-A system was caused by the change of blood flow distribution due to the effect of G load. The tolerance to G load on the kidney following subcutaneous nephrostomy: Unilateral subcutaneous nephrostomies were carried out under pentobarbital anesthesia in 15 adult female mongrel dogs. Each experimental dog was exposed to high G load 2 or 4 weeks after removal of the nephrostomy tube. Excretory urography, renal angiography and renal function tests were performed before and after G load. Excretory urograms demonstrated no remarkable changes at all after G load in all dogs. Renal angiograms revealed small renal infarction along the nephrostomy tract in almost all dogs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The effects of gravity load on the canine kidney]. 176 62


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