Nephrocalcinosis may be defined as a generalized increase in the calcium content of the kidneys. This renal calcification may occur at a molecular, microscopic or macroscopic level leading to progressive amounts of renal damage. The major causes include those associated with an increase in urinary levels of calcium, oxalate and phosphate. Under these conditions, urine concentration and supersaturation leads to calcium crystal precipitation, which may be an intratubular event or initiate within the renal interstitium. The focus of discussion concerning renal calcification is often limited to factors that lead to renal stones (calculi and nephrolithiasis); however, nephrocalcinosis is a more sinister event, and often implies a serious metabolic defect. This review will discuss the hypotheses concerning initiating lesions of nephrocalcinosis using available laboratory and clinical studies and will examine whether new understanding of the molecular basis of tubulopathies, that lead to nephrocalcinosis, has given further insights.
Review Article| June 01 2004
Nephrocalcinosis: molecular insights into calcium precipitation within the kidney
John A. SAYER;
*School of Cell and Molecular Biosciences, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, U.K.
†School of Clinical Medical Sciences, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, U.K.
Correspondence: Dr John A. Sayer, School of Cell and Molecular Biosciences, Medical School, University of Newcastle Upon Tyne, Newcastle Upon Tyne NE2 4HH, U.K. (e-mail firstname.lastname@example.org).
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John A. SAYER, Georgina CARR, Nicholas L. SIMMONS; Nephrocalcinosis: molecular insights into calcium precipitation within the kidney. Clin Sci (Lond) 1 June 2004; 106 (6): 549–561. doi: https://doi.org/10.1042/CS20040048
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