Analysis of HK-2 cells exposed to oxalate and calcium oxalate crystals: proteomic insights into the molecular mechanisms of renal injury and stone formation

2009 ◽  
Vol 38 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Shushang Chen ◽  
Xiaofeng Gao ◽  
Yinghao Sun ◽  
Chuanliang Xu ◽  
Linhui Wang ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Renal Injury ◽  
Molecular Mechanisms ◽  
Stone Formation ◽  
Calcium Oxalate Crystals ◽  
Oxalate Crystals

The Effect of Ethane-1-Hydroxy-1,1-Diphosphonate (EHDP) on Calcium Oxalate Crystalluria in Recurrent Renal Stone-Formers

1974 ◽  
Vol 47 (1) ◽  
pp. 13-22 ◽  
Author(s):  
W. G. Robertson ◽  
M. Peacock ◽  
R. W. Marshall ◽  
F. Knowles
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Basal Diet ◽  
Sodium Oxalate ◽  
Calcium Oxalate Crystals ◽  
Calcium Oxalate Dihydrate ◽  
Calcium Oxalate Stone ◽  
Oxalate Crystals ◽  
Stone Formers

1. The volume, size and type of calcium oxalate crystals excreted in the urine of a group of patients with recurrent ‘idiopathic’ stones were studied on a controlled basal diet, after an oral supplement of sodium oxalate and after oral administration of ethane-1-hydroxy-1,1-diphosphonate (EHDP) for 4 weeks. 2. Before administration of EHDP the stone-formers passed the large crystals and aggregates of calcium oxalate dihydrate characteristic of recurrent calcium oxalate stone-formers. For the same level of urine saturation and crystalluria EHDP caused a significant reduction in the proportion of large crystals and aggregates excreted. Studies by light-microscopy confirmed that EHDP caused a striking change in the size and habit of calcium oxalate crystals in some but not all of the urine samples examined. 3. The decrease in average crystal size during the administration of EHDP was attributed to the observed increase in the ability of urine to inhibit the growth and aggregation of calcium oxalate crystals as measured by a growth system in vitro. 4. The possible use of EHDP as a therapeutic agent in the treatment of calcium oxalate stone-formation is discussed.

856 Calcium oxalate crystals could be englobed by macrophages during kidney stone formation in vitro and in vivo models

2012 ◽  
Vol 11 (1) ◽  
pp. e856-e856a
Author(s):  
A. Okada ◽  
K. Taguchi ◽  
Y. Hirose ◽  
K. Niimi ◽  
Y. Fujii ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Kidney Stone ◽  
Stone Formation ◽  
Calcium Oxalate Crystals ◽  
In Vivo Models ◽  
Oxalate Crystals ◽  
Kidney Stone Formation

scholarly journals Nucleation of calcium oxalate crystals by albumin: Involvement in the prevention of stone formation

1999 ◽  
Vol 55 (5) ◽  
pp. 1776-1786 ◽  
Author(s):  
Claire Cerini ◽  
Sophie Geider ◽  
Bertrand Dussol ◽  
Carole Hennequin ◽  
Michel Daudon ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Calcium Oxalate Crystals ◽  
Oxalate Crystals

Calcium Oxalate Crystalluria and Inhibitors of Crystallization in Recurrent Renal Stone-Formers

1972 ◽  
Vol 43 (4) ◽  
pp. 499-506 ◽  
Author(s):  
W. G. Robertson ◽  
M. Peacock
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Sodium Oxalate ◽  
Calcium Oxalate Crystals ◽  
Oxalate Crystals ◽  
Stone Formers ◽  
Large Particles ◽  
Recurrent Stone ◽  
Recurrent Stone Formers

1. The particle size distributions of calcium oxalate crystals were measured at 37°C in fresh urine from recurrent, idiopathic stone-formers and their controls under the same conditions of dietary and fluid intake. The crystals excreted by the controls were small and belonged to a unimodal distribution, whereas those excreted by the stone-formers belonged to a distribution which contained a second peak of much larger particles. The proportion of large crystals in the urines of the stone-formers was significantly higher than in the urines of the controls. 2. The difference in the proportion of large particles passed by the two groups was accentuated by adding a small quantity of sodium oxalate to their diets. Whereas the controls continued to excrete only small crystals of calcium oxalate, the stone-formers passed most of their crystals as large particles. 3. Further investigations showed that the urines of the controls contained a potent inhibitor of the growth and aggregation of calcium oxalate crystals in vitro and that the inhibitor was deficient in the urines of the recurrent stone-formers. 4. It is suggested that the inhibitor in normal urine may allow calcium oxalate to be passed harmlessly in the form of small particles, whereas the lower inhibitory activity in the urines of the recurrent stone-formers is insufficient to prevent the growth of the primary crystals into the large aggregates seen in these urines. By blocking the formation of abnormally large crystals and aggregates the inhibitor may therefore play an important role in preventing crystalluria leading to stone formation.

scholarly journals In Vitro Cell Culture Models of Hyperoxaluric States: Calcium Oxalate and Renal Epithelial Cell Interactions

Crystals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 735
Author(s):  
Ana Petrović ◽  
Tomislav Kizivat ◽  
Ines Bilić Ćurčić ◽  
Robert Smolić ◽  
Martina Smolić
Keyword(s):  
Epithelial Cell ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
In Vitro Models ◽  
High Recurrence Rate ◽  
Published Data ◽  
Calcium Oxalate Crystals ◽  
Renal Epithelial Cell ◽  
Oxalate Crystals

Urolithiasis is a multifactorial disease with a high incidence and high recurrence rate, characterized by formation of solid deposits in the urinary tract. The most common type of these stones are calcium oxalate stones. Calcium oxalate crystals can, in hyperoxaluric states, interact with renal epithelial cells, causing injury to the renal epithelia. Pathogenesis of urolithiasis is widely investigated, but underlying mechanisms are still not completely clarified. In vitro models offer insight into molecular processes which lead to renal stone formation and are significant for evaluation of prophylactic and therapeutic management of patients with urolithiasis. In this review, we summarize recently published data from in vitro studies investigating interactions of calcium oxalate crystals with renal epithelial cell lines, anti-urolithiatic mechanisms, and the results from studies exploring possible therapeutic and prophylactic options for calcium oxalate urolithiasis in cell cultures.

scholarly journals SUN-016 REGULATION OF IL-1β BY HDAC6 AND PKR IN CALCIUM OXALATE CRYSTALS INDUCED ACUTE RENAL INJURY

2020 ◽  
Vol 5 (3) ◽  
pp. S211
Author(s):  
K. SEDMAKI ◽  
K. Karnam ◽  
P. Sharma ◽  
B. Ghosh ◽  
O. Kulkarni
Keyword(s):  
Calcium Oxalate ◽  
Renal Injury ◽  
Acute Renal Injury ◽  
Calcium Oxalate Crystals ◽  
Oxalate Crystals

The Urinary F1 Activation Peptide of Human Prothrombin is a Potent Inhibitor of Calcium Oxalate Crystallization in Undiluted Human Urine in Vitro

1995 ◽  
Vol 89 (5) ◽  
pp. 533-541 ◽  
Author(s):  
Rosemary L. Ryall ◽  
Phulwinder K. Grover ◽  
Alan M. F. Stapleton ◽  
Dianne K. Barrell ◽  
Yulu Tang ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Human Urine ◽  
Stone Formation ◽  
Calcium Oxalate Crystals ◽  
Particle Volume ◽  
Calcium Oxalate Crystallization ◽  
Oxalate Crystals ◽  
Activation Peptide ◽  
Dose Dependent Decrease

1. The urinary F1 activation peptide of prothrombin is the predominant protein incorporated into calcium oxalate crystals precipitated from human urine. The aim of this study was to examine the effect of pure urinary prothrombin F1 on calcium oxalate crystallization in human urine. 2. Urinary prothrombin F1 was purified from demineralized calcium oxalate crystals precipitated from human urine, and its effects on calcium oxalate crystallization induced by addition of an oxalate load were tested in undiluted, ultrafiltered urine from healthy men, at final concentrations of 0 to 10 mg/l. 3. Urinary prothrombin F1 did not affect the amount of oxalate required to induce crystallization, but the volume of material deposited increased in proportion to increasing concentrations of urinary prothrombin F1. However, the mean particle size decreased in reverse order: this was confirmed by scanning electron microscopy, which showed it to be the result of a reduction in crystal aggregation rather than in the size of individual crystals. Analysis of 14C-oxalate data revealed a dose-dependent decrease in calcium oxalate deposition with an increase in urinary prothrombin F1 concentration, indicating that the increase in particle volume recorded by the Coulter Counter resulted from inclusion of urinary prothrombin F1 into the crystalline architecture, rather than increased deposition of calcium oxalate. 4. It was concluded that urinary prothrombin F1 may be an important macromolecular determinant of stone formation.

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