scholarly journals Evaluation of biochemical parameters in calcium oxalate renal stone formers

2013 ◽  
Vol 13 (2) ◽  
pp. 27-35
Author(s):  
Mannal Abd AL-Monim Ibrahim
Keyword(s):  
Calcium Oxalate ◽  
Biochemical Parameters ◽  
Renal Stone ◽  
Stone Formers

The Evaluation of Some Biochemical Parameters in Pyridoxine-Treated Calcium Oxalate Renal Stone Formers

1977 ◽  
Vol 32 (4) ◽  
pp. 348-352 ◽  
Author(s):  
V. Revúsová ◽  
J. Gratzlová ◽  
V. Zvara ◽  
J. Krídl ◽  
B. Suchánek ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Biochemical Parameters ◽  
Renal Stone ◽  
Stone Formers

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.

Circadian Periodicity of Urinary Inhibitor of Calcium Oxalate Crystallization in Healthy Indians and Renal Stone Formers

1993 ◽  
Vol 24 (3) ◽  
pp. 387-392 ◽  
Author(s):  
R.K. Singh ◽  
A. Bansal ◽  
S.K. Bansal ◽  
A.K. Singh ◽  
A.A. Mahdi
Keyword(s):  
Calcium Oxalate ◽  
Renal Stone ◽  
Circadian Periodicity ◽  
Calcium Oxalate Crystallization ◽  
Stone Formers

Calcium Oxalate Crystalluria and Inhibitors of Crystallisation in Recurrent Renal Stone Formers

2015 ◽  
pp. 302-306
Author(s):  
W. G. Robertson ◽  
M. Peacock ◽  
C. F. Knowles
Keyword(s):  
Calcium Oxalate ◽  
Renal Stone ◽  
Stone Formers

Inhibitory effect of bikunin on calcium oxalate crystallization in vitro and urinary bikunin decrease in renal stone formers

1999 ◽  
Vol 27 (1) ◽  
pp. 69-75 ◽  
Author(s):  
J. Médétognon-Benissan ◽  
S. Tardivel ◽  
C. Hennequin ◽  
M. Daudon ◽  
T. Drüeke ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Renal Stone ◽  
Inhibitory Effect ◽  
Calcium Oxalate Crystallization ◽  
Stone Formers

Effects of High Intake of Dietary Animal Protein on Mineral Metabolism and Urinary Supersaturation of Calcium Oxalate in Renal Stone Formers

1984 ◽  
Vol 56 (3) ◽  
pp. 263-269 ◽  
Author(s):  
B. Fellström ◽  
B. G. Danielson ◽  
Brita Karlström ◽  
H. Lithell ◽  
S. Ljunghall ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Renal Stone ◽  
Mineral Metabolism ◽  
Animal Protein ◽  
High Intake ◽  
Stone Formers ◽  
Urinary Supersaturation

Abnormal Urate Transport in Erythrocytes of Patients with Idiopathic Calcium Nephrolithiasis: A Possible Link with Hyperuricosuria

1993 ◽  
Vol 85 (1) ◽  
pp. 41-44 ◽  
Author(s):  
Giovanni Gambaro ◽  
Massimo Vincenti ◽  
Francesco Marchini ◽  
Angela D'Angelo ◽  
Bruno Baggio
Keyword(s):  
Uric Acid ◽  
Urinary Excretion ◽  
Calcium Oxalate ◽  
Metabolic Disorder ◽  
Renal Stone ◽  
Heparan Sulphate ◽  
Anion Transport ◽  
Stone Disease ◽  
Urate Transport ◽  
Stone Formers

1. The demonstration of an inheritable anomaly of erythrocyte oxalate transport in ‘primary’ calcium nephrolithiasis suggested that this disease might be a generalized metabolic disorder characterized by a defect in cellular anion transport. 2. To determine whether this anomaly is restricted to oxalate alone, we studied erythrocyte transmembrane urate self-exchange in calcium-oxalate renal stone formers in whom urinary excretion of uric acid is frequently increased. 3. Abnormal urate self-exchange was found in 30% of the patients. The urate self-exchange rate constant was correlated with 24 h urinary excretion of uric acid; the erythrocyte anomaly was also associated with the frequency of hyperuricosuria and a more intense disease activity. Transmembrane urate self-exchange was inhibited by stilbene and heparan sulphate. Morphazinamide administration did not reduce urinary urate excretion in patients with abnormal urate erythrocyte self-exchange. 4. These findings suggest that hyperuricosuria during calcium-oxalate renal stone disease might be due to a cellular defect in urate transport, and further support the hypothesis that idiopathic nephrolithiasis is a metabolic disorder characterized by a defect in cellular anion transport.

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