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PubMed1998

Amelioration of polyuria in nephrogenic diabetes insipidus due to aquaporin-2 deficiency.

OBJECTIVE: We have recently reported a large cluster of patients with nephrogenic diabetes insipidus (NDI) due to an autosomal recessive aquaporin-2 (AQP-2) early-stop codon. This paper describes the clinical manifestations and evaluation of therapeutic approaches to this new entity. PATIENTS AND DESIGN: Nine patients with an AQP-2 mutation were studied. Urine osmolality was measured in five patients before and at 3 x 30 min intervals after desmopressin given in increasing doses of 5-100 micrograms. Urinary prostaglandins PGE2 and 6-keto PGF1 alpha, were extracted from 24-h urine samples and estimated by radioimmunoassays. Eight NDI patients were given a combination of a low-sodium diet and hydrochlorothiazide. Four to 11 weeks later, ibuprofen was added, and the patients were retested within the following 4-9 weeks. RESULTS: Urine osmolality remained unchanged after supra-pharmacological doses of desmopressin, at 60-70 mOsm/kg. Urinary PGE2 in control subjects was 0.74 +/- 0.1 microgram/g creatinine (mean +/- SD) compared to 5.0 +/- 2.6 micrograms/g creatinine in AQP-2 deficient patients (P < 0.05). Urinary 6-keto PGF1 alpha, was 0.20 +/- 0.03 microgram/g creatinine in controls and 0.75 +/- 0.31 microgram/g creatinine in AQP-2 deficiency (P < 0.05). Urinary volumes decreased by a mean 31% on a low-salt diet and hydrochlorothiazide, and by a mean of 38% on the combination therapy. Plasma osmolality decreased by a mean 15 mOsm/kg on the low-salt diet and hydrochlorothiazide, and by 22 mOsm/kg on the combination therapy. Urinary osmolality increased from a mean 80 mOsm/kg to 96 mOsm/kg on the low-salt diet and hydrochlorothiazide, and to 146 mOsm/kg on the combination therapy. CONCLUSION: AQP-2 deficiency in these patients with an early-stop codon is associated with complete unresponsiveness of the collecting duct to vasopressin, implying an indispensable role for AQP-2 in vasopressin antidiuresis. Urinary PGE2 and 6-keto PGF1 alpha are elevated, the former being extremely high, apparently due to the extreme vasopressin unresponsiveness. Combination therapy with a combination of a low-salt diet, thiazide and non-steroidal anti-inflammatory drug is partially effective.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Atrial natriuretic peptide mediated polyuria: pathogenesis of polyhydramnios in the recipient twin of twin-twin transfusion syndrome.

We studied the role of atrial natriuretic peptide (ANP) in the pathophysiology of polyhydramnios in monochorionic (MC) twins with and without twin-twin transfusion syndrome (TTTS). Matched maternal, fetal blood samples and amniotic fluids (AF) were obtained in utero (n=12) and at birth (n=20) from MC twins with TTTS. Blood and amniotic fluid samples were also collected from non-TTTS MC twin pairs in utero (n=6) and at birth (n=20). In both groups cellular localization of ANP in the fetal kidney and heart was performed using anti ANP rabbit polyclonal antibody. Concentrations of ANP in pg/ml were determined by radioimmunoassay.In recipient fetuses, ANP levels were higher than the donors both in utero (P< 0.001) and at birth (P< 0.001). No such differences were found between the non-TTTS twins. In the TTTS group maternal ANP levels were lower than the non-TTTS group (P< 0.05). A linear relationship was found between fetal ANP levels and the AF volumes removed at fetal blood sampling (r(2)=0.68;P< 0.01, n=12). ANP was localized predominantly to the cytoplasm of the distal convoluted tubules of the fetal kidney and heart, and the intensity of immunostaining for ANP in kidney and heart were markedly greater in the recipient than the donor twin. No such differences were found between the twin pairs. These data suggest that polyhdramnios in the recipient twin occurs as a consequence of ANP mediated increase in fetal urine output and raises the possibility of direct fetal therapy with ANP blocking agents.

Amniotic Fluid↗