Calcium Oxalate Precipitation in a Flow System: An Attempt to Simulate The Early Stages of Stone Formation in the Renal Tubules

1986 ◽  
Vol 136 (1 Part 1) ◽  
pp. 150-153 ◽  
Author(s):  
R. Azoury ◽  
J. Garside ◽  
W.G. Robertson
Keyword(s):  
Calcium Oxalate ◽  
Flow System ◽  
Stone Formation ◽  
Renal Tubules ◽  
Early Stages ◽  
Oxalate Precipitation

Nephrolithiasis

2018 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg
Keyword(s):  
Uric Acid ◽  
Calcium Oxalate ◽  
Dietary Habits ◽  
Stone Formation ◽  
Urine Volume ◽  
First Episode ◽  
Dietary Advice ◽  
Dietary Recommendations ◽  
Genetic Traits ◽  
Oxalate Precipitation

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.

Nephrolithiasis

2017 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg
Keyword(s):  
Uric Acid ◽  
Calcium Oxalate ◽  
Dietary Habits ◽  
Stone Formation ◽  
Urine Volume ◽  
First Episode ◽  
Dietary Advice ◽  
Dietary Recommendations ◽  
Genetic Traits ◽  
Oxalate Precipitation

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.

Calcium-Oxalate Precipitation in a Flow System

Urolithiasis ◽  
1989 ◽  
pp. 61-63
Author(s):  
R. Azoury ◽  
W. G. Robertson ◽  
J. Garside
Keyword(s):  
Calcium Oxalate ◽  
Flow System ◽  
Oxalate Precipitation

Nephrolithiasis

2017 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg
Keyword(s):  
Uric Acid ◽  
Calcium Oxalate ◽  
Dietary Habits ◽  
Stone Formation ◽  
Urine Volume ◽  
First Episode ◽  
Dietary Advice ◽  
Dietary Recommendations ◽  
Genetic Traits ◽  
Oxalate Precipitation

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.

Nephrolithiasis

2018 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg
Keyword(s):  
Uric Acid ◽  
Calcium Oxalate ◽  
Dietary Habits ◽  
Stone Formation ◽  
Urine Volume ◽  
First Episode ◽  
Dietary Advice ◽  
Dietary Recommendations ◽  
Genetic Traits ◽  
Oxalate Precipitation

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.

Involvement of Cellular Membranes and their Lipids in Nucleation of Stone Forming Crystals

1999 ◽  
Vol 599 ◽  
Author(s):  
S. R. Khan ◽  
J. M. Fasano ◽  
R. Backov ◽  
D. R. Talham
Keyword(s):  
Calcium Phosphate ◽  
Calcium Oxalate ◽  
Kidney Stones ◽  
Membrane Lipids ◽  
Stone Formation ◽  
Rat Kidney ◽  
Langmuir Monolayers ◽  
Membrane Vesicles ◽  
In Vivo Studies ◽  
Renal Tubules

AbstractMore than 80% of human kidney stones consist of calcium oxalate and/or calcium phosphate. Human urine is generally metastable with respect to these salts and their nucleation is heterogeneous. Based on: 1. ultrastructural and immunohistochemical studies of stones in which cellular degradation products and lipids were commonly seen in association with calcific crystals and 2. in vivo studies of nephrolithiasis in rat models where calcium oxalate (CaOx) and calcium phosphate (CaP) crystals almost always formed and seen in association with cell membranes, we proposed that membranes and their lipids are involved in crystallization of these salts. To test our hypothesis we isolated organic matrix of kidney stones, its lipid contents and membrane vesicles from epithelial cells of rat kidney and incubated them in metastable solution of CaOx. Both membrane vesicles and matrix from the stones supported crystallization of CaOx and crystals formed in association with the membranes. Lipids of the stone matrix appeared better nucleators than whole matrix. Urine spends only minutes within the kidneys thus any nucleation which can lead to stone formation has to occur rapidly. In studies described here, we demonstrate that under specific circumstances relevant to conditions in the kidney, membrane vesicle- supported CaOx crystallization can occur within seconds, demonstrating the possibility of such events happening in the kidneys. We also studied CaOx monohydrate (COM) precipitation at Langmuir monolayers of dipalmitoylphosphatidylglecerol (DPPG), dipalmitoylphosphatidylcholine (DPPC), dipalmitoylphosphatidylserine (DPPS) showed precipitation to be heterogeneous and selective with a majority of crystals orienting with the 101 face of COM facing the monolayer. Our results show that membrane lipids can initiate nucleation of calcium oxalate crystals in solutions similar to those present in the kidneys. In addition these crystals form within the time urine spends inside the renal tubules demonstrating for the first time the likelihood of occurrence of such a phenomenon in the kidneys during stone formation.

Molecular modulation of calcium oxalate crystallization

2006 ◽  
Vol 291 (6) ◽  
pp. F1123-F1132 ◽  
Author(s):  
James J. De Yoreo ◽  
S. Roger Qiu ◽  
John R. Hoyer
Keyword(s):  
Molecular Modeling ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Energy Levels ◽  
Critical Role ◽  
Specific Interactions ◽  
Crystal Surfaces ◽  
Site Specific

Calcium oxalate monohydrate (COM) is the primary constituent of the majority of renal stones. Osteopontin (OPN), an aspartic acid-rich urinary protein, and citrate, a much smaller molecule, are potent inhibitors of COM crystallization at levels present in normal urine. Current concepts of the role of site-specific interactions in crystallization derived from studies of biomineralization are reviewed to provide a context for understanding modulation of COM growth at a molecular level. Results from in situ atomic force microscopy (AFM) analyses of the effects of citrate and OPN on growth verified the critical role of site-specific interactions between these growth modulators and individual steps on COM crystal surfaces. Molecular modeling investigations of interactions of citrate with steps and faces on COM crystal surfaces provided links between the stereochemistry of interaction and the binding energy levels that underlie mechanisms of growth modification and changes in overall crystal morphology. The combination of in situ AFM and molecular modeling provides new knowledge that will aid rationale design of therapeutic agents for inhibition of stone formation.

Control of cell shape by calcium in the euglenophyceae

1981 ◽  
Vol 49 (1) ◽  
pp. 99-117 ◽  
Author(s):  
J.M. Murray
Keyword(s):  
Endoplasmic Reticulum ◽  
Atpase Activity ◽  
Calcium Oxalate ◽  
Cell Shape ◽  
Motor Units ◽  
Astasia Longa ◽  
Oxalate Precipitation ◽  
Entire Cell ◽  
The Individual ◽  
Euglenoid Movement

The euglenoid flagellates are able to change their shape rapidly in response to a variety of stimuli, or sometimes spontaneously. Two extremes of shape can be identified: the “relaxed” form is cylindrical; the contracted form is a somewhat distorted disc. These 2 forms can be interconverted by treatments that alter the Ca2+ concentration of the entire cell. The level of Ca2+ is believed to be normally controlled by a system of calcium-accumulating membranes, identified in Astasia longa by the technique of calcium oxalate precipitation. The system forms a set of parallel tubes of endoplasmic reticulum, one of which lies immediately below each of the ridges of the pellicle. The individual ridges, each with its associated reticulum, microtubules and other elements are suggested to be independent motor units. Local activation of a small number of these units by Ca2+ is made possible by the arrangement of Ca2+ -sequestering reticulum, producing the characteristic squirming euglenoid movement. Uniform activation or suppression of all units produces the 2 extremes of shape. The pellicle of A. longa with its associated microtubules has been purified and shown to contain a Ca2+ -binding site and ATPase activity.

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