Transport of Oxalate in Intact Red-Blood Cells can Identify Potential Stone Formers

Narula, Ravinder; Sharma, Shweta; Sidhu, H.; Thind, S. K.; Nath, R.

doi:10.1007/978-1-4899-0873-5_146

Urolithiasis 1989

DOI: 10.1007/978-1-4899-0873-5_146

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Transport of Oxalate in Intact Red-Blood Cells can Identify Potential Stone Formers

Ravinder Narula

Shweta Sharma

H. Sidhu

et al.

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1998

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“…57 Ion transport is also affected by the assembly of the cytoskeleton to the membrane, which modifies sodium fluxes mediated by Na-K cotransport, 58 and intracellular proteases, which influence calcium pump function. 45 The existence of an abnormal RBC oxalate flux was confirmed by Narula et al, 61 in a group of Indian nephrolithiasic patients, Jenkins et al, 62 and Motola et al 63 in renal stone patients in the U.S., and Takahiro et al 64 in Japanese patients. Intermediate phenotypes found in erythrocytes could have a physiopathological importance, and may be clinical and epidemiological markers for subjects predisposed to kidney stones.…”

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confidence: 87%

Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

Baggio

Plebani

Gambaro

1998

Critical Reviews in Clinical Laboratory Sciences

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Idiopathic calcium nephrolithiasis (ICN) is a frequent disease in Western countries. The physicochemical theory of lithogenesis, which explains stone formation by the precipitation, growth, and crystalline aggregation of lithogenic salts in the urine, has contributed greatly to the understanding of the pathogenesis of calcium urolithiasis. However, several aspects are still unexplained; the co-existence of familial occurrence, primary tubular dysfunctions with ICN, and anomalies in the systemic handling of oxalate and calcium led to the development of a cellular hypothesis of ICN. A number of cellular defects in the handling of ions has been reported that involves both anion and cation transport. These anomalies are probably the expression of a still unknown cellular defect in idiopathic calcium stone formers. We suggested that an anomaly in the cell membrane composition might be responsible for the complex array of cell ion flux abnormalities observed in ICN. Recently, a disorder in the n-6 polyunsaturated fatty acid series has been described; it is characterized by a lower linoleic acid content and a higher arachidonic acid concentration in both plasma and erythrocyte membrane phospholipids of renal calcium stone patients. This anomaly could cause an increased activity of ion carriers; furthermore, it may lead to increased prostaglandin synthesis and to secondary phenomena at the kidney, skeletal, and intestinal level. As a consequence, critical conditions for lithogenesis in the kidney may ensue. The data suggest a common pathogenesis for hypercalciuria and hyperoxaluria. The systemic defect in the phospholipid arachidonic acid level may be both of dietary or genetic origin; experimental data suggest that the increase in delta-6 desaturase activity, the limiting enzyme in the metabolic pathway of polyunsaturated fatty acids, might be relevant to the pathogenesis of lipid abnormalities observed in nephrolithiasis and to the pathogenesis of ICN and its related problems (at the kidney, intestinal, and bone level).

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confidence: 87%

Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

Baggio

Plebani

Gambaro

1998

Critical Reviews in Clinical Laboratory Sciences

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Transport of Oxalate in Intact Red-Blood Cells can Identify Potential Stone Formers

Cited by 1 publication

References 0 publications

Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

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