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Early polyuria and urinary concentrating defect in potassium deprivation
1Department of Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio 45267-0585, USA.
American Journal of Physiology. Renal Physiology
|September 21, 2000
Summary
Potassium deprivation causes nephrogenic diabetes insipidus early, preceding hypokalemia. This urinary concentrating defect is linked to reduced aquaporin-2 (AQP2) expression in rat kidneys.
Area of Science:
- Nephrology
- Molecular Biology
- Physiology
Background:
- Nephrogenic diabetes insipidus (NDI) is a condition characterized by the kidneys' inability to respond to antidiuretic hormone.
- The precise onset of NDI and its molecular underpinnings during potassium deprivation (KD) are not well understood.
Purpose of the Study:
- To investigate the time course of NDI development in rats subjected to potassium deprivation.
- To examine the relationship between KD, urinary concentrating ability, and aquaporin-2 (AQP2) expression.
Main Methods:
- Rats were placed on a potassium-free diet for varying durations (12 hours to 21 days).
- Measurements included serum potassium, urine osmolality, water intake, and urine volume.
- Aquaporin-2 (AQP2) protein and mRNA levels were assessed in renal medulla and cortex using immunoblot and Northern blot analyses.
Main Results:
- Urinary osmolality decreased significantly as early as 12 hours of KD, preceding the drop in serum potassium concentration.
- Both AQP2 mRNA and protein levels were reduced in the cortex and outer medulla within 12-24 hours of KD.
- Water intake increased and urine volume rose after 24 hours of KD, indicating impaired water reabsorption.
Conclusions:
- The urinary concentrating defect in KD is an early event that precedes hypokalemia.
- Early NDI (12-24 hours) is primarily associated with suppressed cortical AQP2 expression.
- Later NDI (after 24 hours) involves downregulation of both cortical and medullary AQP2, contributing to the persistent defect.
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