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Renal stones formation

The presence of Ca in kidney stones and the abnormally high Ca levels in idiopathic (absorptive) hypercalciuric individuals that are inherently more prone to kidney stones, initially led to the belief that dietary Ca may be a cause of renal stone formation (Coe et al., 1992). Recent evidence suggests that, as a therapeutic approach to reducing the risk for kidney stones, Ca-restricted diets may pose a greater risk to normocalciuric individuals prone to kidney stone formation such an approach may increase urinary oxalate and the likelihood of recurrent stones, as well as promote bone loss (Borghi et ah, 2002 Coe et al., 1997 Curhan et ah, 1997). The amoimt of oxalate excreted in urine has been foimd to be positively associated with Ca oxalate supersaturation and stone formation (Holmes et ah, 2001). While free oxalic acid is readily absorbed from the gut lumen (Morozumi et ah, 2006), an increased dietary Ca to oxalate... [Pg.306]

Phosphaturia and hypercalciuria occur during the bicarbonaturic response to inhibitors of carbonic anhydrase. Renal excretion of solubilizing factors (eg, citrate) may also decline with chronic use. Calcium salts are relatively insoluble at alkaline pH, which means that the potential for renal stone formation from these salts is enhanced. [Pg.329]

Adverse effects Metabolic acidosis (mild), potassium depletion, renal stone formation, drowsiness, and paresthesia may occur. [Pg.238]

A number of reports have suggested that high intakes of vitamin C are associated with increased excretion of oxalate however, much of the oxalate may be the result of nonenzymic formation from ascorbate under alkaline conditions, occurring either in the bladder or after collection, and thus not a risk factor for renal stone formation (Chalmers et al., 1986). Gerster (1997) suggested that people who are recurrent oxalate stone formers should, as a matter of pmdence, restrict their intake of vitamin C to 100 mg per day, but noted that the risk of stone formation in the population at large is inversely related to vitamin C intake. [Pg.381]

The incidence of urolithiasis with indinavir has been estimated at 9% (19) but, according to some, may be as high as 20%. Indinavir calculi are often radiolucent and may be missed on CT scan rather than by using a contrast medium (which is itself not without risk) (20,21). It may therefore be that in some cases in which other renal complications with indinavir have been described there was in fact undetected renal stone formation. Any patient taking indinavir who develops renal cohc should be suspected of having renal stones (22). [Pg.1736]

Analysis of small renal and biliary stones has shown that sulindac or its metabolite was present in the material (SEDA-15,99), and the labehng of suhndac was revised in 1989 to warn physicians of this phenomenon. However, despite the presence of suhndac or its metabolites in some renal stones, patients taking long-term sulindac are not at risk of an increased incidence of renal stone formation compared with those taking other NSAIDs (38). [Pg.3244]

Ito S, Hasegawa H, Nozawa S, Murasawa A, Nakano M, Arakawa M. Sulindac usage may not be associated with an increased incidence of renal stone formation in patients with rheumatoid arthritis. J Rheumatol 1999 9 119-21. [Pg.3245]

White DJ, Nancollas GH. Triamterene and renal stone formation. J Urol 1982 127(3) 593-7. [Pg.3485]

Viscosity of THP solutions increases markedly when the sodium chloride concentration is > 60 mM. Increasing the concentration of calcium and/.or a reduction in pH also increase viscosity and may account for the involvement of THP in the pathogenesis of cast nephropathy and tubulointerstitial nephritis. THP appears to have an inhibitory effect on urinary crystal arrgegation [154] and may play a role in preventing renal stone formation [155]. In some humans with calcium oxalate nephrolithiasis, a molecular abnormality of THP has been detected [156]. Other studies showed decreased urinary levels of THP in patients with nephrolithiasis [157, 158]. A relative deficiency in THP has been associated with impaired inhibition of crystal adhesion to renal epithelial cells instone formers [159]. [Pg.107]

Diuretics have been shown to have variable effects in relationship to urinary calcium excretion and supersaturation, most notably including loop diuretic induced hypercalciuria and attenuation of urinary calcium excretion by thiazide diuretics. The factors contributing to nephrotoxicity are most commonly associated with multiple factors that favor calcium salt or uric acid deposition at the tubulo-interstitial level. Management of renal stone formation and nephrocalcinosis therefore presents a unique clinical challenge, balancing factors that increase risk for abnormal calcium salt deposition or crystallization, and factors that reduce this risk. [Pg.499]

YasuiT, Sato M, Fujita K,Tozawa K, Nomura S, Kohri K. Effects of citrate on renal stone formation and osteopontin expression in a rat urolithiasis model. Urol Res 2001 29 50-6. [Pg.755]

Dental calculi, bones, renal calculi Bones, teeth, renal stone formation Renal stones, dental calculi Pseudogout (crystals in knee joints)... [Pg.24]

Renal stone formation, possibly also accompanied by intratubular precipitation of crystalline material, has been arare complication of drug therapy. Until the AIDS era, triamterene had been the drug most frequently associated with renal stone formation, with an incidence approximating 1 in 1500 users of triamterene-hydrochlorothiazide. However, it has been unclear whether triamterene or its metabolites actually initiated stone formation, or are passively absorbed onto the organic matrix of pre-existing calculi. Sulfadiazine is a poorly soluble sulfonamide that has caused symptomatic acetylsul-fadiazine crystalluria with stone formation and flank or back pain, hematuria, or renal insufficiency in up to 29% of patients treated with the drug. A high urine volume and urinary aUcalinization to... [Pg.882]

The occurrence of renal stone formation might well date back to early man. The oldest urolith ever recovered, from an Egyptian grave, has been estimated as 6000 years old. Although stone formation seems to have been common during medieval times, surgical treatment, performed by the stone cutters, was difficult if not deadly. Bladder stone formation, as opposed to upper urinary tract stone formation, appears to have been the dominant form of disease during ancient times the last century has seen a shift in dominance. [Pg.263]


See other pages where Renal stones formation is mentioned: [Pg.113]    [Pg.132]    [Pg.443]    [Pg.444]    [Pg.151]    [Pg.263]   
See also in sourсe #XX -- [ Pg.263 , Pg.270 ]




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