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

As calcium oxalate stones are the most important component in urolithiasis, an experimental model has to be designed to clarify the pathogenesis and aid in their prevention. Hyperoxaluria as well as hypercalciuria were produced in rats by administering ethylene glycol (0.5%, in drinking water administered ad libitum) and 1-alpha (OH) D3 (0.5 micrograms/rat given every other day), respectively, for three to four weeks. Neither drug alone produced stones efficiently as did the combination regimen of these two compounds. The occurrence of stones was 77.3%, and with only a moderate degree of renal functional impairment. Biochemical and histological data were obtained using this model.
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PMID:[Experimental and clinical studies on calcium urolithiasis: (I) Animal model for calcium oxalate urolithiasis using ethylene glycol and 1-alpha (OH) D3]. 403 34

Urinary stones are much more common in subjects with intestinal diseases than in the general population. The chemical composition of the stones depends on the type of intestinal disease. In diarrhoeas with loss of water and electrolytes (inflammatory colitis and, chiefly, ileostomy), the urine is acid and concentrated and the stones are composed of uric acid. Extensive lesions of the ileum or wide resections of the small bowel increase the intestinal absorption of oxalates and expose the patients to oxalate stones. Treatment, which must be preventive, is based upon a knowledge of the pathophysiology of urolithiasis.
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PMID:[Urinary lithiasis secondary to intestinal diseases]. 622 18

We report about a case with simulated recurrent urolithiasis. The patient introduced foreign bodies (gypsum) into the bladder. Often the stones had to be removed from the bladder and the right refluxing ureter. The diagnosis of the foreign bodies was made after 2 years of malingering by X-ray diffraction (analysis: gypsum = CaSO4 . 2 H2O).
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PMID:[Recurring pseudo-urolithiasis]. 634 39

A diet providing less than 20 mg of magnesium per 100 kcal that maintains urine pH near 6.0 3 to 5 hours after eating, or a diet providing this amount fo magnesium (see Table 2) with 1 gm of ammonium chloride or 1.5 gm of dl-methionine added daily, should be fed for 1 to 3 months to dissolve struvite uroliths (see Fig. 1). The low-magnesium diet should be fed indefinitely to prevent recurrence, because struvite urolithiasis and all of its effects (hematuria, pollakiuria, and/or complete to partial obstruction to urinary excretion) recurs repeatedly in cats that have previously experienced the condition if they are returned to regular cat food. In contrast, if a diet low in magnesium is fed, recurrence is uncommon. For cats that have never been affected, feeding a low-magnesium ration is unnecessary. For all cats, the following measures are recommended: encourage exercise, allow frequent urination, prevent obesity, decrease confinement, keep the litter box clean, and always have palatable water readily available.
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PMID:Treatment and prevention of feline struvite urolithiasis. 637 67

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

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

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.
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PMID:Effects of magnesium deficiency on intratubular calcium oxalate formation and crystalluria in hyperoxaluric rats. 706 46

High concentration of iron (greater than or equal to 1.5 mg/l) and high total hardness of household water (greater than or equal to 7.0 dH0) in residence community were associated with low hospital admission rate for urolithiasis in a population of about 1.2 million during one year. The incidence of ureteral and renal stone did not vary according to natural fluoride content of drinking water, but it was lower in a city with fluoridated water than in a reference city.
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PMID:Incidence of urolithiasis and composition of household water in southern Finland. 720 23

The results of the second year of the project confirmed most of the major findings from the initial year. Feeding cornsilage, particularly as the major roughage in the first month after arrival was associated with excess mortality. Mixing of cattle from different sources and vaccinating against respiratory disease appeared to be the most important additional factors that increased mortality rates. Delaying vaccination at least two days postarrival may have prevented the negative effects of vaccination but only in calves fed cornsilage. Morbidity rates were highly variable among farms but were positively correlated with mortality rates and treatment costs. The occurrence of infectious thromboembolic meningoencephalitis appeared to share some of the same risk factors as mortality; whereas, urolithiasis did not. Water deprivation may be a risk factor in the occurrence of urolithiasis. Fibrinous pneumonia was again the most frequent cause of death. Relative to year one, infectious thromboembolic meningoencephalitis increased in frequency and only one death was attributed to bovine virus diarrhea.
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PMID:Factors associated with morbidity and mortality in feedlot calves: the Bruce County beef project, year two. 726 Jul 27


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