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)

From September 1986 to August 1987, heavy precipitation of amorphous calcium phosphate, that is phosphaturia, was found at our outpatient clinic in 153 postprandial urine specimens from 115 patients, in 1.5% of all the specimens examined during this period. One patient was excluded because he had both urolithiasis and urinary tract infection. The remaining 152 specimens with phosphaturia were then divided into 3 groups; Group I from patients with urolithiasis, Group II from patients with urinary tract infection and Group III from patients without either urolithiasis or urinary tract infection (Phosphaturia Group, Table 1). It is evident from this table that phosphaturia is repeated more frequently in patients with urolithiasis than in patients without urolithiasis (p less than 0.01). 200 urine specimens examined during this period were selected randomly. Three bloody or purulent specimens were excluded. The remaining 197 specimens from 189 patients were divided into 3 groups, as in the phosphaturia group (Control Group, Table 2). When the proportion of the number of specimens to the total is compared between the phosphaturia group and the control group, it is clear that phosphaturia is found more frequently in specimens from patients with urolithiasis than in specimens from patients without urolithiasis (p less than 0.01). Since phosphaturia was almost always found in the specimens with urine pH greater than or equal to 7, 486 patients, in whom the pH of the first urine specimen was equal to or above 7, were selected from among 1434 patients undergoing urinalyses during this period and divided into 3 groups as has been described above (Table 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical significance of phosphaturia]. 275 94

A total of 191 children with oxalate-phosphate urinary concrements and 28 virtually healthy ones were studied for the main parameters of acid-base blood status with the use of Astrup's microtest. Besides, the urine circadian levels of acid and ammonium were followed up too. The proportion of the main and H+-secreting insertion cells of collecting tubes were calculated in 46 operative biopsy specimens, cells studied with electron microscopy. Advanced metabolic acidosis associated with a decrease in acid and ammonium titration was diagnosed in all patients with bilateral and in 81.6 per cent with unilateral nephrolithiasis. Regardless of acid-base blood status biopsy examination revealed a decrease in the number of insertion cells in renal collecting tubes of the patients mostly pronounced in those with bilateral concrement localization. Ultrastructure of insertion cells in children with oxalate-phosphate urolithiasis featured by a sharp decrease in mitochondria number, absence of smooth-walled vesicles, frequency of myelinoid lysosomes pointed to the failed competence of these cells to efficient H+ secretion. The data obtained evidence of the relationship between the metabolic acidosis and primary disability of the children's kidney to excrete H+.
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PMID:[Acid-base balance of the blood and possible renal mechanisms of its imbalance in children with oxalate-phosphate stones of the urinary tract]. 277 79

The influence of certain dietary elements on the urolithiasis syndrome in cattle calves was elucidated. Calcium, phosphorus, and magnesium measurements were conducted on feed rations as well as on serum and urine samples collected from affected and normal calves. Analysis of the rations given to the animals showed phosphorus at higher levels than calcium, indicating mineral imbalance. Serum and urine of urolithic calves were characterised by high phosphorus, calcium, magnesium, urea, and creatinine levels. Physical examination of urine of affected animals showed a high degree of turbidity, a large amount of calcium carbonate, and triple phosphate as well as abundant amount of pus cells and red blood cells. The characteristic clinical symptoms of urine retention were observed. Moreover, some animals were found to urinate through an opening in front of the scrotal region.
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PMID:Influence of dietary mineral imbalance on the incidence of urolithiasis in Egyptian calves. 277 11

The density of calcium phosphate and the pH were determined in 15 postprandial urine specimens with heavy precipitation of amorphous calcium phosphate, that is phosphaturia, collected from 5 patients with calcium urolithiasis (stone-formers) and 3 patients with no known urological disease (controls). Phosphaturia, not related to urinary tract infection or administration of alkalinizing agents, was found repeatedly at our outpatient clinic in these patients. The correlative relationship was not confirmed between the density of calcium phosphate and the pH. The concentration of calcium and phosphorus was also determined in 10 urine specimens with phosphaturia. The concentration of phosphorus was correlated significantly with the pH (r = -0.775, p less than 0.01), although the concentration of calcium was not correlated with the pH. The pH of 11 urine specimens with phosphaturia from the controls was 7.51 +/- 0.31 (mean +/- S.D.) and the pH of 18 urine specimens with phosphaturia from the stone-formers was 6.81 +/- 0.34. The pH was significantly lower in the urine specimens from the stone-formers than in those from the controls (p less than 0.01). We have noted that the occurrence of phosphaturia depends not only on the urinary pH but on the concentration of phosphorus. It is interesting that phosphaturia often occurs in urine specimens with a pH below 7 in stone-formers.
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PMID:[The role of urine pH in the occurrence of phosphaturia]. 281 12

Using an animal model involving rats fed tetraethylorthosilicate, the minimal effective dietary concentration of ammonium chloride for reduction of silica urolithiasis was determined to be approximately 0.10 equivalents/kg diet. Ammonium sulfate appeared to be only slightly less effective. The lower incidences of urolithiasis were associated with urinary pH less than 7. A subprophylactic concentration (0.067 equivalents/kg diet) of ammonium chloride was factored with three levels of supplemental phosphorus (0, 0.15 and 0.30%) from Na2HPO4 to determine whether the antiurolithic effects of dietary phosphate and urinary-acidifying salts are synergistic. Phosphate had no effect on urinary pH. A 50% urolith incidence occurred in controls; the incidence was 25% (P = 0.08) with 0.15 and 10% (P less than 0.01) with 0.30% phosphorus. Urinary pH was 7.5 in controls compared with approximately 7.2 in rats given the subprophylactic level of ammonium chloride, but ammonium chloride alone had no effect on urolithiasis. However, complete protection from urolithiasis was provided by each of the two levels of phosphorus in combination with ammonium chloride. It is concluded that supplemental dietary phosphorus is most effective for protection against silica urolithiasis under conditions contributing toward urinary acidification due to a possible synergism between dietary phosphorus and urinary acidifying salts.
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PMID:A possible synergism of dietary phosphate and urine-acidifying salts in preventing silica urolithiasis in a rat model. 282 Dec 3

Phosphate concentration and pH were studied as factors influencing the formation of insoluble protein-polysilicic acid complexes of bovine serum albumin (BSA) or urinary proteins (nondialyzable urinary solids, NDUS) with silicic acid under conditions of constant ionic strength (IS) equivalent to 0.1724 N. In the pH range 5.5-7.0, the amount of protein-silicic acid complex measured turbidimetrically increased with decreasing pH. Only a trace of precipitate occurred with use of either of the protein sources at pH 7 or with NDUS at pH 6.5. With BSA at pH 6.5, phosphate supplying the total IS of the solution completely prevented precipitation of the complex. The phosphate effect was linear when it supplied 20-50% of the IS. In this range, there was a 12.3% reduction in the amount of precipitate for each 10% of the IS supplied by phosphate. With NDUS at pH 6.0, the phosphate effect was linear over its full range of concentrations. The phosphate effect resulted in an 8.7% reduction in the amount of precipitate for each 10% of the IS supplied by phosphate. On removal of the precipitated protein-silicic acid complex from the silicic acid solution, dissolution was facilitated by increases in phosphate concentration and pH. It is concluded that phosphate inhibition of protein-polysilicic acid complex formation may play a role in the reduction of silica urolithiasis related to increases in dietary phosphate.
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PMID:Phosphate inhibition of protein-polysilicic acid complex formation in vitro: a factor in preventing silica urolithiasis. 282 32

Experiments were designed to evaluate the effects of Gray strain infectious bronchitis virus (IBV) and high dietary calcium (Ca), alone and in combination, on renal function in pullets. Eight hundred female Single Comb White Leghorn chicks were raised on starter ration. Five hundred chicks were inoculated intravenously with Gray strain IBV at 4 wk of age; the remaining chicks were not exposed to IBV. At 6 wk of age, IBV-inoculated and uninoculated chicks were randomly divided into two diet treatment groups. Half the chicks were fed commercial grower ration (approximately 1.0% Ca, .6% available P) and half were fed commercial layer ration (approximately 3.25% Ca, .5% available P). Birds remained on their respective diets until 18 wk of age. Kidney function studies were conducted on anesthetized birds at 6 wk of age prior to initiation of the diet treatments, at 10 wk of age, and at 18 wk of age. The layer ration increased Ca excretion, decreased inorganic phosphate excretion, and decreased urine hydrogen ion concentration in 10-wk-old pullets in comparison with the grower ration. These diet effects on kidney function were attenuated when the pullets reached 18 wk of age. The layer ration also caused an 11.5% incidence of urolithiasis, and significantly increased kidney asymmetry in 18-wk-old pullets relative to the effects of the grower ration. Gray strain IBV exposure significantly increased kidney asymmetry in 18-wk-old pullets, but had no gross effect on kidney function clearly related to the etiology of urolithiasis. Gray strain IBV did not enhance the incidence of urolithiasis in any of the age groups.
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PMID:Effect of Gray strain infectious bronchitis virus and high dietary calcium on renal function of Single Comb White Leghorn pullets at 6, 10, and 18 weeks of age. 284 30

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.
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PMID:[Tubular dysfunction in renal lithiasis: cause or consequence?]. 285 24

High concentrations of phosphate, oxalate, and calcium ions in urine may cause formation of mineral deposits, i.e., urolithiasis. This is prevented in healthy individuals by substances present in trace quantities. However, there is no recognizable difference between normals and stone formers in urinary substance content. The enzymes glutamic oxaloacetic transaminase and glutamic pyruvic transaminase produce glutamic acid which retards calcium oxalate crystallization. The combined transaminase activity in 70 stone former urine samples was 12.2 +/- 4.1 IU and 31.9 +/- 10.7 IU for 47 normal controls. Incubation of stone former urine with glutamic oxaloacetic transaminase improved overall inhibitory potential, raised glutamic acid levels, and decreased aspartic acid concentrations. Correlation was established between the success of therapeutic treatment and the improvement of enzyme activity. The relative content of glutamic acid is low stone former urines and high in active inhibitory fractions of urinary materials. It is suggested that part of the mechanisms of prevention of stone formation is subjected to biological control.
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PMID:Biological control to diminish dangers of urolithiasis. 286 20

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.
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PMID:Tubulopathy in nephrolithiasis: consequence rather than cause. 287 Dec 16


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