Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In an analysis, by both crystallographic and microbiological methods, of 50 urinary calculi recently removed by surgical operation, 33 proved to be of metabolic origin (mostly calcium oxalate and some uric acid or urate) and 17 of 'infective' origin (struvite, apatite or a mixture of the two). Metabolic stones were usually bacteriologically sterile or contained only small numbers (less than 10(3)/g of stone) of bacteria which did not produce urease, while infective stones always contained urease-producing organisms, usually Proteus mirabilis, in large numbers (greater than 10(5)/g). The combined approach of stone analysis by crystallography and microbiological culture yields more information than conventional techniques on which to base the treatment of urinary calculi and the prevention of their recurrence.
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PMID:Bacteriological and crystallographical analysis of urinary calculi: aid to patient management. 673 6

A series of 99 consecutively operated patients presenting staghorn stones has been reviewed to ascertain the factors implicated in recurrent calculogenesis. 71.7% of the calculi were infection stones; 50.7% harbored Proteus species bacteria and 33.8% Escherichia coli. Struvite stones were found in 57.6% followed at long distance (18.2%) by carbonate apatite, calcium oxalate (11.1%) and mixed (9.1%) stones. Postoperative assessment revealed 17% residual stones, which enhanced infection in 46.7% of these cases and regrew to form a new dendritic stone in 33.3%; 80% of these repeat stones were struvite. 31.5% of the patients initially freed of their calculi by the operation, had true recurrences, and 56.5% of them had resistant urinary infection, caused by Proteus or E. coli (50%-50%). Progressive growth of the recurrent lithiasis occurred in 61.5% of the infected cases, while 87.5% of the recurrences occurring in patients with sterile urine remained stabilized. In the group of nonrecurring lithiasis (56.8%) only 16% had urinary infection. These results confirm the preponderant role played by infection in the pathogenesis of staghorn "malignant' lithiasis and move the authors to make a plea in favor of postoperative integrated therapy, including the use of long-term antibacterial agents and urease inhibitors.
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PMID:The problem of recurrences and infection after surgical removal of staghorn calculi. 703 22

The analysed material includes 100 children with urolithiasis treated in the Pediatric Clinic of the National Research Institute of Mother and Child in Warsaw between 1976 and 1978. Patients' age was from 3 months to 18 years. The analysed group included 51 boys and 49 girls. Urinary tract infection was found in 54 cases, i.e. 57,4% of the analysed material. The most common bacterial strains were those producing urease. They were detected in 48 children i.e. 88,9% of cases with urinary tract infection. Mostly these were bacteria of Proteus group--sporadically Pseudomonas aeruginosa and Staphylococcus albus. In the analysed patients urinary tract obstruction was observed in 36 children, i.e. 36% of cases. In 77% of the analysed material, localization of concrements was in upper urinary tract in 19% in the ureters and in 4% in the lover urinary tract. While in adult patients the most common compound of urinary stones was calcium oxalate, in children the most common stone compounds were phosphates (found in 38 cases i.e. 58,4% of the analysed material). The second frequent compound was oxalate found in 20 cases (30,7%). Less frequent compounds were uric acid and cystine. Performed study allowed to establish the cause of urolithiasis in 93 out of 100 examined children. Metabolic reasons of urolithiasis were found in 26 cases, i.e. 26% of the analysed material. They were as follows: idiopathic hypercalciuria--12 cases, uric acid urolithiasis--8 cases, primary hyperoxaluria--3 cases, cystinuria--2 cases, and incomplete acidosis of distal renal tubuli--1 case. Urolithiasis of probably metabolic origin was detected in 13 children (13%). Other reasons of urolithiasis in children were: infection (31%), idiopathic urolithiasis (17%) and others (6%). In 7 cases the reason of urolithiasis was not established.
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PMID:[Metabolic etiology of urinary calculi in children]. 717 91

We investigated the effects of weak to moderate urease hydrolysis by optional urease-positive microorganisms in an artificial urine model enriched with calcium phosphate and calcium oxalate in respect of calcium stone formation. The incubation experiments were performed using a discontinuously running fermenter device to simulate the urinary system. The kinetics of cell division rates, pH and ammonium ion production were measured and correlated to crystallite appearance in the incubation medium. Qualitative analyses of the sediments revealed apatite. Investigations using light microscopy and scanning electron microscopy (SEM) confirmed the matrix effect of bacterial glycoproteins. It was shown that initiation of calcium oxalate stone formation is in all probability equally determined by matrix effects and by heteronuclear crystallization if the urinary tract is infected by optional urease-positive bacteria. When urinary inorganic phosphate is present, calcium phosphate nidi are always initially formed, and may subsequently be coated by calcium oxalate.
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PMID:Potential contribution of optional urease-positive bacteria to idiopathic urinary calcium stone formation. II. Microlith formation kinetics in a fermenter model of the urinary tract infected by optional urease-positive microorganisms. 874 Sep 75

Although calcium oxalate stones are the most common type of calculi found in the United States, struvite or infection stones are quite common and generally pose a difficult treatment dilemma. The presence of urinary infection with a urease-producing organism is necessary for these stones to form. Proteus species account for the majority of infections that cause struvite stones in all age ranges. However, other organisms also produce urease and may be detected in conjunction with struvite calculi. Factors that may predispose one to urinary tract infections increase the likelihood of struvite stone formation. Several options are available for the treatment of existing struvite calculi. Smaller stones may be treated with primary shock-wave lithotripsy, whereas larger stones are more appropriately managed with percutaneous or combination procedures. Medical therapy to prevent recurrent stone formation is also an essential part of the treatment of these patients, as the risk of stone recurrence is extremely high. Antibiotic therapy and urease inhibitors perhaps offer the best form of preventative treatment available today.
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PMID:Struvite calculi. 889 Mar 98

The aetiology of calcium oxalate stones, which are commonly believed to be sterile, has not yet been fully elucidated. Recent bacteriological studies and investigations using the scanning electron microscope have also shown microorganisms to be present in this type of stone. These microorganisms were assumed not to be able to split urea. To list the most common urease-negative bacteria established in the human urinary system, we isolated apparently urease-negative microorganisms from a consecutive series of 58 urinary stone-forming patients by using standard selecting agars. Pure strains were incubated in an inductive medium lacking all sources of nitrogen except urea. Induction of urease activity was monitored by a test based on the reaction of phenol/hypochlorite with ammonium ions. This test revealed whether the urease negativity of a strain indicated by the selective agar was optional or absolute. All strains we investigated by this method and which were classified by standard methods as urease-negative we found produced urease activity which was clearly measurable, though it was often comparatively small. In the light of these results, the matrix theory of calcium oxalate stone development will need some modifications.
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PMID:Potential contribution of optional urease-positive bacteria to idiopathic urinary calcium stone formation. I. Expression of urease activity in bacteria from the urinary tract that are commonly classified as urease-negative. 896 42

While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
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PMID:[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]. 1264 87

The relationship between urinary infections and stone formation has been recognized since antiquity and it has been over a century since bacterial degradation of urea was postulated to cause struvite stones. Specific therapy for urease-producing bacteria, such as urease-inhibitors and antibiotics, has allowed for treatment for this subset of urinary stones. Future directions for research include development of novel urease-inhibitors and chemicals to enhance the protective glycosaminoglycan layer. An improved understanding of the pathogenesis of calcium-based stones has led to the discovery of potential roles for nanobacteria and Oxalobacter formingenes. Methods of altering intestinal regulation of oxalate by reintroduction of lactic acid bacteria may significantly impact the treatment of calcium oxalate stones. The use of catheters, both urethral and ureteral, is common in the urinary tract and is associated with significant morbidity, primarily from associated infections. Catheters to prevent bacterial colonization and formation of biofilms have been created using various coatings, including ciprofloxacin, hydrogel, and silver. Use of these types of catheters may minimize infections and encrustation inherent with their placement in the urinary tract.
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PMID:Infections and urinary stone disease. 1267 63

Microorganisms may have a role in the pathogenesis and prevention of kidney stones. The subjects of this review include nanobacteria, Oxalobacter formigenes, and lactic acid bacteria. Not reviewed here is the well-described role of infections of the urinary tract with Proteus species and other urease-producing organisms associated with struvite stone formation. Nanobacteria have been proposed to be very small (0.08-0.5 nm), ubiquitous organisms that could play a role in stone formation. The theory is that nanobacteria can nucleate carbonate apatite on their surfaces and thereby provide the nidus for stone formation. However, their existence remains uncertain and many investigators are openly skeptical. Recent investigations suggest that they are artifacts, and not actually living organisms, but their proponents continue to study them. O. formigenes is an obligate anaerobe which may be important in the prevention of stone formation. Its sole substrate for generation of ATP is oxalate. It may thereby metabolize its human host's dietary oxalate and diminish intestinal absorption and subsequent urinary excretion of oxalate. There is evidence that the organism's absence, perhaps sometimes due to courses of antibiotics, may be a cause of hyperoxaluria and stone formation. In early investigations, patients not colonized with the organism can be recolonized. Urinary oxalate can be diminished by accompanying an oxalate-containing meal with the organism. One study demonstrated that a preparation of lactic acid bacteria successfully reduced urinary oxalate excretion in 6 patients with calcium oxalate stones and hyperoxaluria. The mechanism of this effect is uncertain since these bacteria lacked the gene possessed by O. formigenes which codes for that organism's oxalate uptake mechanism. The author is currently completing a small randomized controlled clinical trial with this preparation in calcium stone-forming patients with idiopathic hyperoxaluria.
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PMID:Microorganisms and calcium oxalate stone disease. 1549 15

About 5% of American women and 12% of men will develop a kidney stone at some time in their life, and prevalence has been rising in both sexes. Approximately 80% of stones are composed of calcium oxalate (CaOx) and calcium phosphate (CaP); 10% of struvite (magnesium ammonium phosphate produced during infection with bacteria that possess the enzyme urease), 9% of uric acid (UA); and the remaining 1% are composed of cystine or ammonium acid urate or are diagnosed as drug-related stones. Stones ultimately arise because of an unwanted phase change of these substances from liquid to solid state. Here we focus on the mechanisms of pathogenesis involved in CaOx, CaP, UA, and cystine stone formation, including recent developments in our understanding of related changes in human kidney tissue and of underlying genetic causes, in addition to current therapeutics.
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PMID:Kidney stone disease. 1620 Jan 92


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