American journal of physiology. Renal physiology
-
Am. J. Physiol. Renal Physiol. · May 2007
A new method for determining plasma water content: application in pseudohyponatremia.
Pseudohyponatremia is a clinical condition characterized by an increased fraction of protein or lipid in plasma, thereby resulting in an artificially low plasma sodium concentration ([Na(+)](p)). Since the automated method of measuring [Na(+)](p) in most laboratories involves the use of an indirect ion-selective electrode (I-ISE), this method does not correct for elevated protein or lipid concentrations. In I-ISE, the plasma sample is diluted before the actual measurement is obtained, and the [Na(+)](p) is determined based on the assumption that plasma is normally composed of 93% plasma water. ⋯ To validate this new method experimentally, we altered the PWC in vitro by dissolving varying amount of salt-free albumin in human plasma. We then measured PWC gravimetrically in each sample and compared the gravimetrically determined PWC with the ISE-determined PWC. Our findings indicate that the PWC can be accurately determined based on differences in the [Na(+)](p) as measured by I-ISE and D-ISE and that this new quantitative method can be a useful adjunct in the analysis of the dysnatremias.
-
Am. J. Physiol. Renal Physiol. · May 2007
Nephrogenic diabetes insipidus in mice caused by deleting COOH-terminal tail of aquaporin-2.
In mammals, the hormonal regulation of water homeostasis is mediated by the aquaporin-2 water channel (Aqp2) of the collecting duct (CD). Vasopressin induces redistribution of Aqp2 from intracellular vesicles to the apical membrane of CD principal cells, accompanied by increased water permeability. Mutations of AQP2 gene in humans cause both recessive and dominant nephrogenic diabetes insipidus (NDI), a disease in which the kidney is unable to concentrate urine in response to vasopressin. ⋯ By immunohistochemical and immunoblot analyses using antibody against the NH(2)-terminal region of the protein Aqp2(Delta230/Delta230) mice had a markedly reduced protein abundance. Expression of the truncated protein in MDCK cells was consistent with a small amount of functional expression but no stimulation. Thus we have generated a mouse model of NDI that may be useful in studying the physiology and potential therapy of this disease.