Abstract
Renal calcium stone formation is often associated with hypercalciuria, but the mechanisms underlying the latter are not fully understood. Also, there is disagreement among investigators as to whether hypercalciuria originates from hyperabsorption of dietary calcium in the intestinal tract (so-called absorptive hypercalciuria; A-HC), losses of calcium at some site of the distal tubule or collecting ducts of kidney (so-called renal hypercalciuria R-HC), or represents a combination of the two (1). Based on classification of patients with idiopathic recurrent calcium urolithiasis (RCU) according to the two possible extreme sites of origin of hypercalciuria (A-HC; R-HC), much research work has been carried out in order to elucidate their functional abnormalities in gut and kidney (2).
Supported by Deutsche Forschungsgemeinschaft, Bonn; FRG
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© 1988 Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt
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Schwille, P.O., Rümenapf, G., Schreiber, B. (1988). Urinary sodium in renal calcium lithiasis — an approach to its relationship with urinary calcium, and the possible role of atrial natriuretic peptide (h-ANP). In: Gasser, G., Vahlensieck, W. (eds) Pathogenese und Klinik der Harnsteine XIII. Fortschritte der Urologie und Nephrologie, vol 26. Steinkopff. https://doi.org/10.1007/978-3-642-72416-9_36
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DOI: https://doi.org/10.1007/978-3-642-72416-9_36
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