Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.5 (urease)
7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many hypotheses have been proposed for renal stone formation. It has been argued that with infection-induced renal stones the hydrolysis of urea by bacterial urease increases urinary pH, with consequent stone formation. Unfortunately, this theory is not applicable to the micro-organisms that do not produce urease (e.g. Escherichia coli). It has been recently reported that E. coli reduces the urinary urokinase activity of male rats, but does not influence the urinary sialidase activity. This study has now been expanded to the urease-producing bacteria Proteus mirabilis, Staphylococcus aureus, S. epidermidis, Pseudomonas aeruginosa and Micrococcus luteus. Subcutaneous injections with these bacteria were found to significantly (P < 0.003) reduce the UK activity of extrarenally obstructed kidneys. The urease-producing mammalian skin bacterium, M. luteus, was, however, the exception (P = 0.1079). In contrast to S. epidermidis, P. aeruginosa and M. luteus (P < 0.0213), P. mirabilis and S. aureus had no effect on renal sialidase activity (P < 0.4047). These results may explain why Proteus species are predominant in infection-induced renal stones. According to the urokinase-sialidase hypothesis, a decrease in urinary urokinase activity should increase the uromucoid levels, whilst no effect on the urinary sialidase activity should favour conversion of urinary uromucoid to mineralizable matrix. These conditions may lead to renal stone formation. An increase in urinary pH resulting from urease-producing micro-organisms will increase salt precipitation on the uromucoid. It is thus concluded that urease-producing bacteria may play a double role in renal stone formation.
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PMID:In vivo effects of urease-producing bacteria involved with the pathogenesis of infection-induced urolithiasis on renal urokinase and sialidase activity. 883 91

Renal tubular acidosis (type I) is characterized by alterations that lead to disturbed acidification in the tubule. As a result of these alterations, the excretion of uromucoid (formed in the distal tubule), citrate and glycosaminoglycan (GAG) is considerably reduced. There have been numerous investigations on changes in urine pH, citrate and calcium, but few, if any studies on the excretion of uromucoid and GAG. Apart from calcium, phosphate, pH and urease, the present study investigated the excretion of uromucoid, citrate and GAG in a collective of 41 stone patients with renal tubular acidosis (type I). We found that uromucoid excretion was reduced on 90.5%, GAG in 72.2% and citrate in 96% of cases. The reduction of uromucoid excretion in particular is characteristic of RTA I, and it has the function of a marker.
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PMID:[The significance of citrate, uromucoid and GAG for diagnosis of renal tubular acidosis in patients with urinary calculi]. 884 53