Leading article
Molecular developments in renal tubulopathies
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Introduction |
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The renal tubule is responsible for the reabsorption of more
than 99% of the water and sodium in the glomerular ultrafiltrate. Congenital or acquired tubular dysfunction can therefore readily cause
profound electrolyte and volume disturbance. The tubule also has to
regulate acid-base balance, mineral homoeostasis, and the excretion of
organic anions and drugs. To fulfil these functions, a large number of
specialised transporters and channels are specifically localised in the
tubular cell membranes, some in the luminal border and others in the
plasma membrane border (basolateral membrane). In the past decade (and
especially in the past five years) advances in molecular genetic
research have revealed the structure, function, and effects of
mutations in these transporters, thereby greatly increasing our
understanding of the function and dysfunction of the renal tubule. Some
renal stone disorders (for example, cystinuria, Dent's disease) and rare genetic causes of hypertension (for example, Liddle's syndrome) are now
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