Glycosaminoglycan Content, Oxalate Self-Exchange and Protein Phosphorylation in Erythrocytes of Patients with ‘Idiopathic’ Calcium Oxalate Nephrolithiasis

1990 ◽  
Vol 79 (2) ◽  
pp. 113-116 ◽  
Author(s):  
Bruno Baggio ◽  
Giovanni Marzaro ◽  
Giovanni Gambaro ◽  
Francesco Marchini ◽  
Hibbard E. Williams ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Calcium Oxalate ◽  
Protein Phosphorylation ◽  
Erythrocyte Membrane ◽  
Heparan Sulphate ◽  
Flux Rate ◽  
Control Subjects ◽  
Stone Formers ◽  
Membrane Phosphorylation

1. This study was performed to test the hypothesis that glycosaminoglycans may play an important role in the observed abnormalities in oxalate flux seen in patients with calcium oxalate nephrolithiasis. 2. Oxalate flux rate, erythrocyte membrane glycosaminoglycan content, membrane protein phosphorylation and effect of heparan sulphate on erythrocyte oxalate flux in vitro were studied in control subjects and patients with calcium oxalate nephrolithiasis. 3. In comparison with control subjects, renal stone-formers showed a significantly higher oxalate self-exchange, a lower erythrocyte membrane glycosaminoglycan content and a higher membrane phosphorylation rate. In stone-formers, erythrocyte glycosaminoglycan content correlated inversely with both oxalate flux rate and protein phosphorylation. In vitro, heparan sulphate promoted a significant fall in the rate of oxalate self-exchange. 4. These findings support the hypothesis that a lower erythrocyte membrane content of glycosaminoglycans enhances membrane protein phosphorylation, leading to an increased rate of transmembrane oxalate flux.

Separate Effects of Urinary Chondroitin Sulphate and Heparan Sulphate on the Crystallization of Urinary Calcium Oxalate: Differences between Stone Formers and Normal Control Subjects

1993 ◽  
Vol 85 (1) ◽  
pp. 33-39 ◽  
Author(s):  
D. K. Y. Shum ◽  
M. D. I. Gohel
Keyword(s):  
Calcium Oxalate ◽  
Normal Control ◽  
Uronic Acid ◽  
Chondroitin Sulphate ◽  
Cetylpyridinium Chloride ◽  
Heparan Sulphate ◽  
Urinary Calcium ◽  
Crystal Nucleation ◽  
Control Subjects ◽  
Stone Formers

1. Urinary glycosaminoglycans were recovered from the papain digest of polyanions precipitated sequentially by cetylpyridinium chloride and sodium acetate-saturated ethanol. Those from the early morning urine of 48 stone formers and 43 normal control subjects measured 11 and 16 μg of uronic acid/ml of urine, respectively. 2. Preparative agarose gel electrophoresis of the recovered glycosaminoglycans in barium acetate buffer (pH 5.8) yielded fractions containing purely chondroitin sulphate, co-polymeric chondroitin/dermatan sulphates and heparan sulphate. Identification was based on the susceptibility of the fractions to chondroitinase or nitrous acid treatment. Similar compositions of glycosaminoglycan classes were observed in samples from stone formers and normal control subjects. 3. The fractionated glycosaminoglycans were dissolved in urine ultrafiltrate to assay for nucleation-promoting and growth-inhibiting activities towards crystallization of urinary calcium oxalate. When compared at the same uronic acid concentration, both the urinary chondroitin sulphate isomers and heparan sulphates of stone formers demonstrated the capacity to enhance crystal nucleation from calcium oxalate endogenous in urine ultrafiltrates, whereas only urinary heparan sulphates of normal control subjects demonstrated this capacity. 4. Tissue-derived reference chondroitin sulphate, dermatan sulphate and heparin, when similarly tested, showed negligible crystal nucleation-promoting activity. The tissue-derived heparan sulphate was similar to the urinary heparan sulphates in showing marked crystal nucleation-promoting activity. 5. Crystal-growth inhibitory activity was evident in all urinary glycosaminoglycan fractions studied. In particular, urinary heparan sulphate of normal control subjects showed higher activity than that of stone formers or the chondroitin sulphate isomers of both stone formers and normal control subjects (P <0.005).

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.

scholarly journals Evidence for in vitro and in vivo expression of the conserved VAR3 (type 3) plasmodium falciparum erythrocyte membrane protein 1

2012 ◽  
Vol 11 (1) ◽  
Author(s):  
Christian W Wang ◽  
Thomas Lavstsen ◽  
Dominique C Bengtsson ◽  
Pamela A Magistrado ◽  
Sanne S Berger ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Membrane Protein ◽  
Erythrocyte Membrane ◽  
Erythrocyte Membrane Protein ◽  
In Vivo Expression ◽  
Type 3 ◽  
Falciparum Erythrocyte Membrane Protein

scholarly journals Pyridoxine Decreases Oxidative Stress on Human Erythrocyte Membrane Protein in vitro

2019 ◽  
Vol 13 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Margarita Velásquez ◽  
Darío Méndez ◽  
Carlos Moneriz
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Protein ◽  
Oxidative Damage ◽  
Erythrocyte Membrane ◽  
Cumene Hydroperoxide ◽  
Protein Carbonylation ◽  
Human Erythrocytes ◽  
Red Cell Membrane

Background: Pyridoxine has reduction and prevention against the levels of reactive oxygen species in in vitro studies. However, the biochemical mechanism that explains this behavior has not yet been fully clarified. Objective: To evaluate the effect of pyridoxine against oxidative damage on the membrane of human erythrocytes. Methods: Cumene hydroperoxide was used to induce oxidative stress in protein and lipid. Human erythrocytes were incubated with pyridoxine and cumene hydroperoxide, either alone or together for 8 h. Oxidative damage was determined by measuring lipid peroxidation and membrane protein carbonylation. Results: The results indicate that the malondialdehyde concentration decreased with increasing concentration of pyridoxine. The membrane protein content also decreased with increasing concentration of vitamin B6, which was confirmed by the decreased signal intensity in the western blot when compared to control without pyridoxine. Results demonstrate that pyridoxine can significantly decrease lipid peroxidation and protein carbonylation in red cell membrane exposed to high concentrations of oxidant agent. Conclusion: Pyridoxine showed a protective effect against the oxidative stress in human erythrocytes in vitro, inhibiting the carbonylation and the oxidative damage of erythrocyte membrane proteins. To date, such an effect has not yet been reported in terms of protein oxidation.

Somatostatin and analogs inhibit endogenous synaptic plasma membrane protein phosphorylation in vitro

1983 ◽  
Vol 88 (2-3) ◽  
pp. 185-193 ◽  
Author(s):  
Linda A. Dokas ◽  
Henk Zwiers ◽  
David H. Coy ◽  
Willem Hendrik Gispen
Keyword(s):  
Plasma Membrane ◽  
Membrane Protein ◽  
Protein Phosphorylation ◽  
Synaptic Plasma Membrane ◽  
Plasma Membrane Protein

Inhibition of calcium oxalate monohydrate crystal aggregation by urine proteins

1989 ◽  
Vol 257 (1) ◽  
pp. F99-F106 ◽  
Author(s):  
B. Hess ◽  
Y. Nakagawa ◽  
F. L. Coe
Keyword(s):  
Crystal Growth ◽  
Calcium Oxalate ◽  
Renal Stones ◽  
Calcium Oxalate Monohydrate ◽  
Assay Method ◽  
Crystal Aggregation ◽  
Stone Formers ◽  
Aggregation Inhibitors ◽  
Normal Urine

Normal urine inhibits both the growth and the aggregation of calcium oxalate monohydrate (COM) crystals but the molecules that inhibit aggregation are not well defined. We have developed a spectrophotometric assay method to measure the aggregation of COM crystals in vitro under conditions that avoid simultaneous crystal growth. At pH 7.2 and 90 mM NaCl, Tamm-Horsfall glycoprotein (THP) and nephrocalcin (NC), a major urinary inhibitor of COM crystal growth, inhibit COM crystal aggregation at concentrations as low as 2 X 10(-9) and 1 X 10(-8) M, respectively. When increasing NaCl to 270 mM or lowering pH to 5.7, inhibition by both glycoproteins, but more markedly by THP, is decreased. Urinary NC from calcium oxalate renal stone formers (SF NC) and NC isolated from calcium oxalate renal stones (stone NC) both inhibit COM crystal aggregation 10-fold less than NC from normal urine. Citrate is ineffective even at millimolar concentrations. Thus THP and NC are two major inhibitors of COM crystal aggregation in normal urine; SF NC and stone NC are defective aggregation inhibitors.

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