Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Struvite nephrolithiasis is caused by infection with bacteria that possess the enzyme urease, and convert urea to ammonia that raises urine pH and crystallizes with magnesium and trivalent phosphate ion. Of the 75 of our 1431 stone patients with struvite stones 52 were women. Struvite stones occurred almost exclusively in women; a minority of women and most men had mixed stones of struvite and calcium oxalate. Increased serum creatinine levels and reduced creatinine clearance were common in patients with struvite stones, not in those with mixed stones; both were rare in calcium stone disease. Men and women with mixed struvite, calcium oxalate stones were hypercalciuric, but women with struvite stones were not. Patients with mixed stones usually had initial symptoms of stone passage, and were less likely to need surgery, including nephrectomy, or to form contralateral stones. Patients with struvite stones usually presented with infection or no symptom, not passage. We conclude that struvite stones occur in two forms. The struvite stone is a disease of women, presumably occurring de novo from infection. The mixed stones occur in both sexes, presumably from secondary infection in hypercalciuric patients who begin with calcium-oxalate stone disease.
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PMID:Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis. 343 Sep 61

Undiluted human urine and synthetic urine were inoculated with urease. No inhibitory activity against urease enzymatic activity could be detected in human urine. The urease-induced crystallization of both calcium phosphate and magnesium ammonium phosphate differed markedly, however, between the individuals studied, and it was less pronounced in human urine than in synthetic urine. This supports the observation made in experiments using diluted urine that human urine possesses an inhibitory activity against urease-induced crystallization and suggests that it has a large interindividual variation.
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PMID:The effects of urease in undiluted human urine. 373 63

Kidney stones have an overall incidence of two to three percent in western countries. In many patients, the disease process is difficult to control and recurrence rates are high: 20 to 50 percent over the subsequent ten years. The pathogenesis and standard methods of treatment for the five major types of stones (i.e., calcium oxalate, struvite, calcium phosphate, uric acid, and cystine) are reviewed. Three new drugs are reviewed in the context of their roles in the selective treatment of kidney stones. Cellulose sodium phosphate (Calcibind) is a nonabsorbable ion-exchange resin with a limited indication for the treatment of calcium stones associated with absorptive hypercalciuria Type I. Acetohydroxamic acid (Lithostat) is an urease-inhibitor that is indicated as adjunctive therapy in patients with chronic urea-splitting urinary tract infections and struvite stones. Potassium citrate (Urocit) is an investigational agent that has clinical efficacy in patients with calcium oxalate and calcium phosphate stones who are hypocitraturic. In addition, potassium citrate is an alkalinizing agent that can be used in patients with uric acid stones.
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PMID:New drug therapy for kidney stones: a review of cellulose sodium phosphate, acetohydroxamic acid, and potassium citrate. 389 14

To study whether human urine contains inhibitors against urease-induced crystallization, Jackbean urease and human urine, in amounts small enough (0.5 to 10 per cent) not to influence the ion concentration, buffering capacity or pH, were added to synthetic urine. The ammonia production and alkalinization that followed were independent of the amounts of human urine added. The addition of human urine gave a dose-related decrease in the amount of calcium phosphate and struvite precipitated on glass rods immersed in the synthetic urine, however. Addition of only 0.5 per cent human urine gave a reproducible decrease and when 10 per cent human urine was added to the synthetic urine the precipitation of calcium phosphate was reduced by 50 per cent and that of struvite by 75 per cent. The results thus indicate that human urine contains components with the ability to reduce the urease-induced crystallization.
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PMID:The inhibitory effect of human urine on urease-induced crystallization in vitro. 394 82

The urease-induced crystallization of magnesium ammonium phosphate and calcium phosphate was studied at different alkalinization degrees by incubating synthetic urine with increasing Jack Bean urease concentrations. The crystallization was studied as precipitation on glass rods immersed in synthetic urine. The calcium phosphate precipitation on the glass rods occurred when the pH reached 6.8. Magnesium ammonium phosphate precipitation occurred when the pH reached 7.0. The maximal crystallization occurred at a pH between 7.5 and 8.0; at higher pHs the precipitation was considerably lower. The possible mechanisms and clinical implications behind this narrow pH optimum for urease-induced crystallization, which also have important implications for future experimental studies, are discussed.
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PMID:Urease-induced crystallization in synthetic urine. 397 8

The fastidious growth requirements of mycoplasmas and ureaplasmas necessitated development of special growth media for them. The 1st mycoplasma was isolated from humans in 1937, and in 1954 a previously unknown mycoplasma was isolated from men with nonspecific urethritis. This organism, Ureaplasma urealyticum, is found most frequently in the genitourinary tract, followed by Mycoplasma hominus. M. fermentans and other mycoplasmas are isolated only rarely. Mycoplasmas and ureaplasmas have been implicated in pelvic inflammatory disease, puerperal infection, septic abortion, low birth weight, nongonococcal urethritis, and prostatisis, as well as spontaneous abortion and infertility, but there are no clinical symptoms pathognomonic of these infections. In spite of clinical suggestions of Mycoplasma or Ureaplasma infection, only a properly obtained specimen evaluatd with the use of selective cultures can lead to unequivocal diagnosis. The cultural characteristics and hence diagnostic procedures for Mycoplasma and Ureaplasma are quite different. Sterile calcium alginate swabs are used for obtaining urethral specimens, while sterile cotton swabs can be used for prostatic or vaginal secretions or semen. The swab should not touch antiseptic solutions, creams, or jellies, and the specimen must not dry out. Urine, if cultured, is best examined after centrifugattion at 600 g. Several different transport media are available. Optimally the specimen should be taken directly to the laboratory and subcultured on arrival. The metabolic activity of Mycoplasmas and Ureaplasmas is used in their detection. A phenol red indicator is added to the medium and the color change to or from yellow to pink indicates metabolic change. The growth medium is supplemented with glucose and phenol red for M. fermentans and arginine and phenol red for M. hominis. After color change is observed, the growth medium is subcultured on solid medium, which is obtained by adding .6-.8% Noble agar to the growth medium. Colonies develop best in an atmosphere of 95% N2 and 5% CO2 and reach approximately 200-300 mcm in diameter. They have a fried-egg appearance. Staining with Dienes stain, use of specific antisera, or incident light fluorescence microscopy are used for identification of the classic mycoplasmas. To isolate ureaplasmas, the specimen is transferred on arrival in the laboratory to urease color test broth U9C. During incubation the presence of Ureaplasma induces a rapid color change usually observable in 24-48 hours. A subculture should be done on fresh U9C broth media and on agar media once a color change is observed. Serologic tests for detection of antibodies to mycoplasmas and ureaplasmas are still in the developmental stage.
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PMID:Diagnosis of genital Mycoplasma and Ureaplasma infections. 402 Jul 82

Interexperimental variation in the incidence of tibial dyschondroplasia of chickens that occurred in studies on the effect of dietary calcium, phosphorus and cholecalciferol metabolites was apparent from previous reports from this laboratory. Since the source of commercial soybean meal used in the diets was known to change, studies were conducted to evaluate different sources of soybean meal on the incidence of tibial dyschondroplasia. A series of experiments demonstrated that the soybean meals from one source consistently produced a high incidence of tibial dyschondroplasia (34-69%); whereas soybean meals from a different source consistently produced low incidences (14-28%). This same relationship was found with soybean meals from these two plants produced a year apart. When the levels of two soybean meals that produced a high incidence of tibial dyschondroplasia were reduced in the diet from 35 to 24 12% the incidence of tibial dyschondroplasia was reduced from 60 and 69% to 25 and 20% to 15 and 10%, respectively. The most striking difference between the meals observed by chemical analysis was in the high antitrypsin and urease values of the meals that induced tibial dyschondroplasia. Chickens fed the soybean meal that reduced tibial dyschondroplasia also had reduced pancreas size in one experiment but not another. The soybean meals that induced tibial dyschondroplasia caused an increase in testes size but had no effect on liver, adrenal and thyroid size or plasma levels of calcium, phosphorus and triiodothyronine (T3). No difference in the utilization of the diets as measured by metabolizable energy values and lipid calcium, phosphorus or phytin phosphorus retention was found between the soybean meals that induced high or low incidence of tibial dyschondroplasia with chickens at 19-21 d of age.
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PMID:Effects of different soybean meals on the incidence of tibial dyschondroplasia in the chicken. 404 May 57

A retrospective study of the case records of 391 adult patients with spontaneously passed or surgically removed concrements from the upper urinary tract during the period 1982-1983 was performed. According to chemical analysis, 66% of the stones were calcium stones, 30% were infection stones, 4% were uric acid/urate stones and 1% were cystine stones. Of the infection stones 12 (10%) were staghorn calculi. The infection stones placed a greater strain on the patients than the calcium stones. Thus, infection stones were significantly more often recurrent stones and required surgery significantly more often than the calcium stones. Only 6% of the patients with infection stones had proved abnormalities predisposing to upper urinary tract infection. Urinary tract infection with a urease-producing microorganism was detected in only 52% of the patients with infection stones. As infection with a urease-producing microorganism is a prerequisite for the formation of infection stones in the urinary tract a careful microbiological investigation to find and treat the infection responsible for the stone formation is mandatory.
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PMID:The severity of infection stones compared to other stones in the upper urinary tract. 408 54

Escherichia coli with no demonstrable urease activity was inoculated into filter sterilized urine obtained from a healthy volunteer subject with no history of stone disease and then incubated at 37 degrees C. Bacteria were recovered at intervals between 1 and 10 days. Urinary pH was stable as compared to control urines and spontaneous crystal precipitation was not noted in controls. Recovered organisms were analyzed by x-ray powder diffractometry. An uncharacterized mineral phase (UMP) was first evident after 6 days. Calcium phosphate in the form of brushite and hydroxyapatite was apparent at 7 and 10 days respectively. This suggests a role for bacteria in calcium phosphate crystal formation in urine apart from urease activity and may contribute to the calcium phosphate component of urinary calculi.
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PMID:Calcium phosphate crystal formation in Escherichia coli from human urine: an in vitro study. 627 77

Crystallization of struvite and calcium phosphates was studied in vitro as encrustations on glass rods immersed in synthetic urine, to evaluate the crystallization capacity of Ureaplasma urealyticum and compare it with that of known urease and non-urease-producing bacteria. Inoculation of the synthetic urine with Ureaplasma urealyticum resulted in alkalinization of the synthetic urine and crystallization of struvite and brushite. Inoculation with Proteus mirabilis caused a faster and more pronounced alkalinization as well as crystallization of struvite and apatite. The alkalinization and crystallization caused by Ureaplasma urealyticum and Proteus mirabilis was completely prevented by acetohydroxamic acid, a potent urease inhibitor, linking the crystallization to the urease activity of the microorganisms. When the synthetic urine was inoculated with urease-negative Escherichia coli no alkalinization and no crystallization were seen.
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PMID:Ureaplasma urealyticum-induced crystallization of magnesium ammonium phosphate and calcium phosphates in synthetic urine. 638 69


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