[PDF][PDF] X-linked hypercalciuric nephrolithiasis: clinical syndromes and chloride channel mutations
SJ Scheinman - Kidney international, 1998 - core.ac.uk
SJ Scheinman
Kidney international, 1998•core.ac.ukThe original report of this family included several patients with moderate renal insufficiency
in whom calcium excretion was normal [1], but with further study of a larger number of
patients it became clear that hypercalciuria was present in all affected individuals if studied
at a time when renal function was still preserved [2]. The most consistent urinary abnormality
of all, however, was excessive excretion of low-molecular-weight (LMW) proteins, in both
affected males and carrier females. Moderate
in whom calcium excretion was normal [1], but with further study of a larger number of
patients it became clear that hypercalciuria was present in all affected individuals if studied
at a time when renal function was still preserved [2]. The most consistent urinary abnormality
of all, however, was excessive excretion of low-molecular-weight (LMW) proteins, in both
affected males and carrier females. Moderate
The original report of this family included several patients with moderate renal insufficiency in whom calcium excretion was normal [1], but with further study of a larger number of patients it became clear that hypercalciuria was present in all affected individuals if studied at a time when renal function was still preserved [2]. The most consistent urinary abnormality of all, however, was excessive excretion of low-molecular-weight (LMW) proteins, in both affected males and carrier females. Moderate
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