Abstract
In infants and children with type 1 renal tubular acidosis (RTA) after chronic acidosis, short stature, stunting (height. < 2.5 SD from mean for age- and sex- matched normals) and nephrocalcinosis occur1–12. Nephrocalcinosis is invariable by age 4 years in children with type I RTA who are maintained on low-dose alkali therapy.(< 3 mEq/kg/d) since infancy1–6. Recently we have shown that nephrocalcinosis has not occurred over observation periods of 10–20 years in 7 children with type 1 RTA in whom sustained correction of acidosis with high dose alkali therapy (5-14 mEq/kg/d) was maintained since infancy7-9. In these children, we demonstrated that urinary excretion of citrate rose to normal values: whereas on low-dose alkali, < 3 mEq/kg/d, it remained subnormal7-9. Citrate is a chelator and complexor of urinary calcium and also, acts as an inhibitor of urinary crystal formation13,14.
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McSherry, E., Gates, J., Pialaet, M. (1981). The Incidence of Nephrocalcinosis and the Urinary Excretion of Citrate and Calcium in Patients with Non-Azotemic type 4 Renal Tubular Acidosis. In: Smith, L.H., Robertson, W.G., Finlayson, B. (eds) Urolithiasis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8977-4_120
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DOI: https://doi.org/10.1007/978-1-4684-8977-4_120
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