scholarly journals Hippuric Acid as a Significant Regulator of Supersaturation in Calcium Oxalate Lithiasis: The Physiological Evidence

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Stoyanka S. Atanassova ◽  
Ivan S. Gutzow
Keyword(s):  
Calcium Oxalate ◽  
Human Urine ◽  
Hippuric Acid ◽  
Clinical Laboratory ◽  
Stone Formation ◽  
Control Group ◽  
Stone Formers ◽  
Artificial Urine ◽  
Kinetics Of

At present, the clinical significance of existing physicochemical and biological evidence and especially the results we have obtained from our previousin vitroexperiments have been analyzed, and we have come to the conclusion that hippuric acid (C6H5CONHCH2COOH) is a very active solvent of Calcium Oxalate (CaOX) in physiological solutions. Two types of experiments have been discussed: clinical laboratory analysis on the urine excretion of hippuric acid (HA) in patients with CaOX lithiasis and detailed measurements of the kinetics of the dissolution of CaOX calculi in artificial urine, containing various concentrations of HA. It turns out that the most probable value of the HA concentration in the control group is approximately ten times higher than the corresponding value in the group of the stone-formers. Ourin vitroanalytical measurements demonstrate even a possibility to dissolve CaOX stones in human urine, in which increased concentration of HA have been established. A conclusion can be that drowning out HA is a significant regulator of CaOX supersaturation and thus a regulation of CaOX stone formation in human urine. Discussions have arisen to use increased concentration of HA in urine both as a solubilizator of CaOX stones in the urinary tract and on the purpose of a prolonged metaphylactic treatment.

scholarly journals In Vivo Entombment of Bacteria and Fungi during Calcium Oxalate, Brushite and Struvite Urolithiasis

Kidney360 ◽  
2020 ◽  
pp. 10.34067/KID.0006942020
Author(s):  
Jessica J. Saw ◽  
Mayandi Sivaguru ◽  
Elena M. Wilson ◽  
Yiran Dong ◽  
Robert A. Sanford ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Human Kidney ◽  
Rrna Gene ◽  
Bacterial Cells ◽  
Stone Formers ◽  
Bacteria And Fungi ◽  
Struvite Stones

Background: Human kidney stones form via repeated events of mineral precipitation, partial dissolution and reprecipitation, which are directly analogous to similar processes in other natural and man-made environments where resident microbiomes strongly influence biomineralization. High-resolution microscopy and high-fidelity metagenomic (microscopy-to-omics) analyses, applicable to all forms of biomineralization, have been applied to assemble definitive evidence of in vivo microbiome entombment during urolithiasis. Methods: Stone fragments were collected from a randomly chosen cohort of 20 patients using standard percutaneous nephrolithotomy (PCNL). Fourier transform infrared (FTIR) spectroscopy indicated that 18 of these patients were calcium oxalate (CaOx) stone formers, while one patient each formed brushite and struvite stones. This apportionment is consistent with global stone mineralogy distributions. Stone fragments from 7 of these 20 patients (5 CaOx, 1 brushite and 1 struvite) were thin sectioned and analyzed using brightfield (BF), polarization (POL), confocal, superresolution autofluorescence (SRAF) and Raman techniques. DNA from remaining fragments, grouped according to each of the 20 patients, were analyzed with amplicon sequencing of 16S rRNA gene sequences (V1-V3, V3-V5) and internal transcribed spacer (ITS1, ITS2) regions. Results: Bulk entombed DNA was sequenced from stone fragments in 11 of the 18 CaOx patients, as well as the brushite and struvite patients. These analyses confirmed the presence of an entombed low-diversity community of bacteria and fungi, including Actinobacteria, Bacteroidetes, Firmicutes, Proteobacteria, and Aspergillus niger. Bacterial cells ~1  µm in diameter were also optically observed to be entombed and well-preserved in amorphous hydroxyapatite spherules and fans of needle-like crystals of brushite and struvite. Conclusions: These results indicate a microbiome is entombed during in vivo CaOx stone formation. Similar processes are implied for brushite and struvite stones. This evidence lays the groundwork for future in vitro and in vivo experimentation to determine how the microbiome may actively and/or passively influence kidney stone biomineralization.

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.

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.

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.

scholarly journals Escherichia coli Aggravates Calcium Oxalate Stone Formation via PPK1/Flagellin-Mediated Renal Oxidative Injury and Inflammation

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Lingyue An ◽  
Weizhou Wu ◽  
Shujue Li ◽  
Yongchang Lai ◽  
Dong Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Bacterial Species ◽  
Oxidative Injury ◽  
Wild Type ◽  
E Coli ◽  
Crystal Aggregation ◽  
Stone Formers

Escherichia coli (E. coli) is closely associated with the formation of kidney stones. However, the role of E. coli in CaOx stone formation is not well understood. We explored whether E. coli facilitate CaOx stone formation and its mechanism. Stone and urine cultures were reviewed from kidney stone formers. The ability of calcium oxalate monohydrate (COM) aggregation was detected to evaluate the influence of uropathogenic E. coli, then gel electrophoresis and nanoLC-MS/MS to detect the crystal-adhered protein. Flagellin (Flic) and polyphosphate kinase 1 (PPK1) were screened out following detection of their role on crystal aggregation, oxidative injury, and inflammation of HK-2 cell in vitro. By transurethral injection of wild-type, Ppk1 mutant and Flic mutant strains of E. coli and intraperitoneally injected with glyoxylate in C57BL/6J female mice to establish an animal model. We found that E. coli was the most common bacterial species in patients with CaOx stone. It could enhance CaOx crystal aggregation both in vitro and in vivo. Flagellin was identified as the key molecules regulated by PPK1, and both of them could facilitate the crystal aggregation and mediated HK-2 cell oxidative injury and activated the inflammation-related NF-κB/P38 signaling pathway. Wild-type strain of E. coli injection significantly increased CaOx deposition and enhanced oxidative injury and inflammation-related protein expression, and this effect could be reversed by Ppk1 or Flic mutation. In conclusion, E. coli promotes CaOx stone formation via enhancing oxidative injury and inflammation regulated by the PPK1/flagellin, which activated NF-κB/P38 pathways, providing new potential drug targets for the renal CaOx calculus precaution and treatment.

Abnormal Erythrocyte and Renal Frusemide-Sensitive Sodium Transport in Idiopathic Calcium Nephrolithiasis

1994 ◽  
Vol 86 (3) ◽  
pp. 239-243 ◽  
Author(s):  
Bruno Baggio ◽  
Giovanni Gambaro ◽  
Francesco Marchini ◽  
Massimo Vincenti ◽  
Giulio Ceolotto ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Renal Stone ◽  
Stone Formation ◽  
Fractional Excretion ◽  
Cation Transport ◽  
Anion Transport ◽  
Kinetic Properties ◽  
Distal Nephron ◽  
Stone Formers ◽  
Na Efflux

1. Anomalous transmembrane anion transport has been observed in erythrocytes of patients with idiopathic calcium nephrolithiasis. 2. To verify whether cation transport is also abnormal, we investigated the frusemide-sensitive Na+ efflux from Na+-loaded erythrocytes and the natriuretic response to acute intravenous frusemide administration in calcium oxalate renal stone formers. 3. Frusemide administration induced a statistically significant smaller increase in the fractional excretion of Na+ in patients than in control subjects. Abnormal kinetic properties of erythrocyte Na+-K+-2Cl− co-transport were observed in approximately 60% of stone formers. The Km for Na+ of Na+-K+-2Cl− co-transport correlated with urinary Ca2+ excretion. 4. The abnormal kinetic properties of Na+-K+-2Cl− co-transport may be relevant for stone formation, hampering renal Ca2+ reabsorption in the distal nephron and determining critical physicochemical conditions for calcium/oxalate crystallization.

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