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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of citrate on intestinal calcium absorption (CaA) was studied in eight healthy males. On separate occasions, either a load containing 5 mmol of calcium chloride and 21 mmol of citrate in the form of sodium potassium citrate or a citrate-free vehicle load corrected for pH and cations was ingested. CaA was measured over 3 h with a 47Ca-85Sr double tracer method. After citrate administration, 10 min fractional CaA decreased significantly from 30 to 110 min post-load, and 3 h cumulative CaA dropped to 54.6 +/- (SEM) 6.1% of the total dose as opposed to 76.3 +/- 4.5% after vehicle administration (P less than 0.002). Citrate administration raised serum and urinary citrate, but had little effect on blood acid-base status. After both loads, urinary specific activity of 47Ca significantly correlated with 3 h cumulative CaA, while citrate administration decreased urinary calcium excretion only slightly as compared with vehicle. The results suggest that, in man, higher doses of oral citrate inhibit CaA, probably by way of intraluminal complexation of calcium by citrate. The finding might help explain the fall in urinary calcium excretion observed in patients treated with alkali citrate for recurrent calcium urolithiasis.
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PMID:The influence of oral alkali citrate on intestinal calcium absorption in healthy man. 360 72

Urolithiasis (kidney stone formation) is an acquired degenerative kidney lesion affecting sexually mature and immature domestic fowl. For the present study, uroliths were collected from three commercial flocks during outbreaks of urolithiasis. Uroliths also were collected from a research flock in which urolithiasis was induced by feeding immature chickens a diet formulated to contain excess calcium (3.25% Ca) and .4% available phosphorus. All uroliths were tested by x-ray diffractometry, infrared spectrophotometry, and emission spectrography. With one exception, the stones were composed of compact masses of microcrystalline to fine pleomorphic crystals of calcium sodium urate, with random substitution of magnesium for calcium, and potassium for sodium. No initiating nidus was evident. One of four stones from one laying hen flock was positively identified as an ammonium acid (hydrogen) urate. The unique calcium-sodium-urate stone composition in all but one of the stones tested suggests that similar processes were involved in stone formation in the four different flocks.
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PMID:Characterization and composition of uroliths from domestic fowl. 373 19

Six children with idiopathic hypercalciuria and their families were examined with an oral calcium loading test. Family members were divided into two clinical categories: group 1 consisted of the six index children and their parents and siblings with urolithiasis or unexplained hematuria; group 2 comprised the remaining parents and siblings without signs or symptoms associated with hypercalciuria. The results revealed that fasting urinary excretion of calcium was similar in both groups, but group 1 displayed a greater calciuric response to an oral calcium load. Serum concentrations of calcitriol (1,25-dihydroxyvitamin D3) and calcium were higher in group 1 than in group 2, while parathyroid activity was lower in group 1 patients. Urinary excretion of sodium, phosphorus, and magnesium, urine pH, serum levels of calcifediol (25-hydroxyvitamin D3) and phosphorus, and the renal tubular threshold for phosphate were not significantly different in the two groups. These findings suggest that idiopathic hypercalciuria may arise from a disturbance in the regulation of vitamin D metabolism that mediates enhanced intestinal absorption of calcium.
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PMID:Families of children with idiopathic hypercalciuria. Evidence for the hormonal basis of familial hypercalciuria. 383 4

Patients with recurrent non-infectious calcium urolithiasis were classified metabolically (122 patients). When the magnesium excretion was measured in the metabolic subgroups, a subset of patients (21.6%) could be identified with marked hypomagnesuria as the only metabolic abnormality. A significantly reduced rate of magnesium excretion was found in these normocalciuric stone formers while assessing the overall 24-h urine magnesium excretion or the 24-h urine and fasting urine magnesium to calcium ratio. These differences were apparently not due to factors that might modify renal magnesium excretion, such as parathyroid function, hypercalcemia, hypophosphatemia, alimentary sodium load, age and sex.
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PMID:[Magnesium excretion in recurrent calcium urolithiasis]. 406 Mar 80

The urinary excretion of various substances involved in kidney stone formation was evaluated in 67 patients with hypercalciuric lithiasis (HCl), 36 lithiasis patients with normal calciuria (NCl) and 21 controls without urinary stones. All subjects were hospitalized for 3 days and given a calcium, phosphorous and sodium-controlled diet. The 24-hour urine volume was significantly larger in the HCl and NCl groups than in controls. The 24-hour Ca, Na and uric acid excretion was significantly greater in the HCl group than in the NCl and control groups. Oxalate and pyrophosphate excretion was the same in all three groups. Urinary Ca correlated with urinary creatinine in the HCl and control groups, but the slope and ordinate of the regression line were significantly higher in the former group. Similarly, urinary Na correlated with urinary creatinine in the HCl and control groups with a significantly steeper slope in the HCl group. These data are suggestive of abnormalities in the tubular reabsorption of Ca and Na in HCl patients. Finally, there was no correlation between the values obtained and the activity of the disease, as evaluated by the finding of at least 3 urinary stones or one staghorn calculus during the 5 years preceding the study. It is concluded that measurements of Ca, Na, uric acid, creatine, oxalates and phosphates during a stay in hospital provide pathophysiological information but cannot be taken as indices of urolithiasis activity.
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PMID:[Urinary excretion of lithogenic substances in hospitalized patients with calcium lithiasis. Physiopathologic meaning and prognostic value]. 622 Feb 70

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.
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PMID:Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. 624 14

The urine to blood carbon dioxide tension gradient (U-B PCO2) following alkalinization of the urine (pH = 7.8) has been widely used to assess distal tubular hydrogen secretion. The magnitude of the U-B PCO2 is influenced not only by the rate of hydrogen secretion but also by bicarbonate concentration and water abstraction. Simultaneous administration of sodium bicarbonate and dDAVP improve the reliability of the test in healthy children. Children with distal renal tubular acidosis were not able to increase urinary PCO2, while a normal increase was found in patients with proximal renal tubular acidosis and the Fanconi Syndrome. Four out of nine patients with urolithiasis failed to increase urinary PCO2 following NaHCO3 and dDAVP-administration, despite a normal ability to acidify the urine following NH4Cl administration. To assess the effect of acute alterations in urinary concentration on urinary PCO2, the test was carried out in children with central diabetes insipidus. Despite sharp increase in urinary bicarbonate concentration these patients failed to increase urinary PCO2.
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PMID:The diagnostic value of the urine to blood carbon dioxide tension gradient for the assessment of distal tubular hydrogen secretion in pediatric patients with renal tubular disorders. 640 15

The pathophysiologic consequences of renal function impairment and chronic renal failure among others result from the loss of excretory and regulatory functions of the kidneys. The role of the exchange of cellular hydrogen ions of tubular fluid in the reabsorption of bicarbonate and in the urinary excretion of titratable acid and ammonia (acid-base regulation) is outlined. The effects of decreased glomerular filtration rate on calcium and phosphorus homeostasis are discussed. De novo urolithiasis in these patients is uncommon. However, it is well recognized that they may form matrix stones with calcium oxalate inclusions. Of greater significance is the prophylaxis in those patients, in whom urolithiasis has been the cause of chronic renal failure. In these patients it is of importance to modify the drug dosage or to abandon the prophylaxis when it interferes with the metabolic changes of renal function impairment. Some agents require no modification, others minor or major modifications. Some are even contraindicated. Hazards of stone prophylaxis in chronic renal failure: Acidification - cave metabolic acidosis! Cave RTA! Antibiotic agents - special rules to prevent accumulation. Thiazides - contraindicated! Hypokalemia; hyperuricemia; cave HPT! Triamterene - contraindicated! Acetazolamide (cystinuria) - contraindicated. Spironolactone - contraindicated. Sodium-cellulose-phosphate - Hyperoxaluria, hypomagnesiuria , hyperphosphatemia, cave HPT. Orthophosphate - cave urinary infection, cave poor renal function, cave obstruction. Allopurinol - dose reduction advisable. Brenzbromaron - contraindicated.
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PMID:[Prevention of calculus recurrence in impaired kidney function]. 653 25

Renal function evaluations were conducted on pullets and laying hens during outbreaks of urolithiasis. The following parameters were measured: kidney weights; hematocrits; plasma concentrations of uric acid, calcium, inorganic phosphate, magnesium, sodium, and potassium; urine flow rates; glomerular filtration rates; renal plasma flow rates; urine pH; and relative clearances of inorganic phosphate, calcium, magnesium, sodium, potassium, and para-amino hippuric acid. The adequacy of renal portal perfusion was estimated by timed phenol red extraction. Considerable interindividual variability was noted, presumably due to differences in age and reproductive status. Intraindividual left versus right kidney comparisons also were made, since urolithiasis often is associated with macroscopic lesions of one kidney but not the other. The results indicate that even when gross lesions of only one kidney were present, specific tubular transport processes were similar in both kidneys. Urolithiasis did cause significant alterations in urine flow rates, glomerular filtration rates and renal plasma flow rates. it was concluded that the changes associated with urolithiasis reflect the expected compensatory hypertrophic responses of surviving kidney tissue to a reduction of renal mass. The physiological impact of this form of kidney damage appears to arise from reduced renal mass rather than from inappropriate renal handling of minerals or electrolytes.
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PMID:Kidney function of pullets and laying hens during outbreaks of urolithiasis. 663 78

Exposure of male weanling Fischer 344 rats to 4.0% terephthalic acid (TPA) in the diet (positive controls) for two weeks (postnatal days 28-42) resulted in a 50% incidence of bladder calculi, aciduria, elevated urinary excretion of calcium (Ca) and magnesium (Mg), and slightly elevated serum levels of Ca and Mg relative to negative controls. Possible mechanisms of TPA-induced urolithiasis were examined by daily oral administration of allopurinol, chlorothiazide, or neutral phosphates, at their recommended therapeutic doses during exposure to dietary 4.0% TPA. An additional group was fed 4.0% TPA and 4.0% sodium bicarbonate in the diet for two weeks. Chlorothiazide or dietary bicarbonate abolished TPA-induced urolithiasis, but allopurinol and neutral phosphates had no effect. Bicarbonate increased water intake above that of positive controls and ameliorated the TPA-induced aciduria. It also increased urinary Mg and TPA above positive control values. Chlorothiazide reduced urinary Ca and TPA levels below those of positive controls. Treatment with chlorothiazide, neutral phosphates or bicarbonate slightly reduced serum Ca below the levels in either positive or negative controls. Drug treatment did not alter TPA-induced elevated serum Mg levels, but bicarbonate reduced serum Mg levels to negative control values. In conclusion, TPA-induced urolithiasis in male weanling rats was abolished by therapeutic agents which reduced urinary Ca and TPA excretion (chlorothiazide), or which enhanced water intake, urinary Mg and TPA excretion, and ameliorated TPA-induced aciduria (dietary bicarbonate). These factors appear to be critical for TPA-induced urolithiasis.
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PMID:Effects of selected therapeutic agents on urolithiasis induced by terephthalic acid in the male weanling Fischer 344 rat. 666 96


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