NDT Advance Access originally published online on April 9, 2008
Nephrology Dialysis Transplantation 2008 23(7):2399-2401; doi:10.1093/ndt/gfn124
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Lack of elevation of urinary albumin excretion among patients with chronic syndromes of inappropriate antidiuresis
General Internal Medicine Department, Erasme University Hospital, Brussels, Belgium
Correspondence and offprint requests to: Frédéric Vandergheynst, General Internal Medicine Department, Erasme University Hospital, Brussels, Belgium. Tel: +32-2-555-38-06; Fax: +32-2-555-32-11; E-mail: fvdgheyn{at}ulb.ac.be
| Abstract |
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Background. A recent study has revealed that acute and chronic administration of the vasopressin V2 receptor (V2R) agonist dDAVP induced a marked increase of urinary albumin excretion (UAE) in healthy rats and humans (Bardoux P et al. Nephrol Dial Transplant 2003; 18: 497–506). The occurrence of an elevation of UAE among patients with chronic syndromes of inappropriate antidiuresis has not been reported.
Methods. We looked for the elevation of UAE in 24-h urine samples of the following patients: nine chronic SIADH patients, two patients with acute post-operative SIADH, three patients of the same family with nephrogenic syndrome of inappropriate antidiuresis (NSAID) and two patients with hyponatraemia due to surdosage of dDAVP in the setting of central diabetes insipidus.
Results. There was no elevation of UAE in our patients (whether they presented with hyponatraemia or not), apart from a patient treated with supra-physiological doses of dDAVP. When she received 80 µg/day of dDAVP, her UAE was 42 mg/day. In this patient, UAE returned to the normal range (21 mg/day) when doses of dDAVP were tapered (20 µg/day).
Conclusion. The present study shows that chronic V2R stimulation generally does not result in a rise in UAE. The discrepancy between our results and those of the above-mentioned study could be explained by a dose-dependent effect of V2R stimulation on UAE.
Keywords: antidiuresis; AVP; microalbuminuria; nephrogenic syndrome of inappropriate antidiuresis; SIADH
Received for publication: 8. 8.07
Accepted in revised form: 13. 2.08