Biopathological Crystallization: A General View About the Mechanism of Renal Stone Formation

Grases, F.; Costa-Bauzà, Antònia; García-Ferragut, L.

doi:10.1016/s0022-5347(01)62025-1

Cited by 3 publications

(4 citation statements)

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“…Urine, because of its unique combination of anions and cations and small and macromolecular organic components, is capable of holding ions in solution at levels above saturation conditions in a pure aqueous environment. However, the crystal nucleation process can be influenced by the urine chemistry in the presence of particles of organic matter and cellular debris [33]. These organic molecules serve as the nidus for nucleation.…”

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Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Selvam

2002

Urological Research

185

105

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Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.

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mentioning

confidence: 99%

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Selvam

2002

Urological Research

185

105

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“…La historia de expectoración con arenilla en la infancia y expulsión objetivada de cálculos durante meses en ausencia de una calcificación intratorácica es excepcionalmente infrecuente, pero podría explicarse por un mecanismo de formación de cálculos similar a la producción de urolitos o sialolitos 19,20 , que tienen una estructura similar a la de los broncolitos de nuestro paciente. La producción de cálculos en los líquidos orgánicos se debe a las características fisicoquímicas de éstos.…”

Section: Discussionunclassified

“…La sangre y los líquidos intersticiales están sobresaturados de fosfatos cálcicos (hidroxiapatita). En el caso de la hidroxiapatita, los detritus celulares y otros restos orgáni-cos (como los residuos de bacterias) pueden actuar como nucleantes heterógenos muy efectivos 19,20 . Los escasos estudios previos sobre la composición de los broncolitos se limitaban a identificar la presencia de calcio y fósforo.…”

Section: Discussionunclassified

“…Así, la composición y microestructura de los broncolitos encontrados en este caso son totalmente análogas a las de los cálculos renales de hidroxiapatita de origen no infeccioso y a las de los sialolitos. Por este motivo, sus mecanismos de formación han de ser muy parecidos, e implican factores relativos al déficit de inhibidores de la cristalización, presencia de materia orgánica y estasis líquida 19,20 . La formación de arenilla en el árbol bronquial precisa, pues, el déficit de inhibidores, la presencia de líquido intraluminal durante tiempo prolongado (por exceso de filtración o defecto de reabsorción) y presencia de abundante materia orgánica (en este caso, mucoproteínas).…”

Section: Discussionunclassified

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