Role of diet in the management of vasopressin-responsive and -resistant diabetes insipidus

Blalock, Teresa L.; Gerron, Glynda G.; Quiter, Elaine; Rudman, D

doi:10.1093/ajcn/30.7.1070

Cited by 14 publications

(16 citation statements)

References 11 publications

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“…Li-containing food was offered continuously to both groups throughout the study period. Considering the role of sodium depletion in the antidiuretic effect of thiazides in NDI (14,15), no salt was added to the drinking fluid. Serum samples were collected at the time each rat was killed for determination of the serum Li concentration by a colorimetric method (VITROS 250 Chemistry System; Shanghai Golden-Grand Medical Instruments Co., Ltd., Shanghai, China) (16).…”

Section: Animals and Experimental Protocolsmentioning

confidence: 99%

Antidiuretic Effect of Hydrochlorothiazide in Lithium-Induced Nephrogenic Diabetes Insipidus Is Associated with Upregulation of Aquaporin-2, Na-Cl Co-transporter, and Epithelial Sodium Channel

Kim

Lee²,

Oh³

et al. 2004

Journal of the American Society of Nephrology

133

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Abstract. Thiazides have been used in patients with nephrogenic diabetes insipidus (NDI) to decrease urine volume, but the mechanism by which it produces the paradoxic antidiuretic effect remains unclear. Previous studies have reported that downregulation of aquaporin-2 (AQP2) is important for the development of lithium-induced (Li-induced) polyuria and that hydrochlorothiazide (HCTZ) increases renal papillary osmolality and Na ϩ concentration in Brattleboro rats. For elucidating the molecular basis of the antidiuretic action of HCTZ in diabetes insipidus, whether administration of HCTZ may affect the expression of AQP2 and major renal Na ϩ transporters in Li-induced NDI rats was investigated, using semiquantitative immunoblotting and immunohistochemistry. After feeding male Sprague-Dawley rats Li chloride-containing rat diet for 4 wk, HCTZ or vehicle was infused subcutaneously via osmotic minipump. Urine output was significantly decreased by HCTZ treatment, whereas it was not changed in vehicle-treated rats. Urine osmolality was also higher in HCTZ-treated rats than in vehicle-treated rats. Semiquantitative immunoblotting using whole-kidney homogenates revealed that HCTZ treatment caused a significant partial recovery in AQP2 abundance from Li-induced downregulation. AQP2 immunohistochemistry showed compatible findings with the immunoblot results in both cortex and medulla. The abundances of thiazide-sensitive NaCl co-transporter and ␣-epithelial sodium channel were increased by HCTZ treatment. Notably, HCTZ treatment induced a shift in molecular weight of ␥-epithelial sodium channel from 85 to 70 kD, consistent with previously demonstrated aldosterone stimulation. The upregulation of AQP2 and distal renal Na ϩ transporters in response to HCTZ treatment may account for the antidiuretic action of HCTZ in NDI.In nephrogenic diabetes insipidus (NDI), the kidney is unable to concentrate urine despite normal or elevated concentrations of the antidiuretic hormone arginine vasopressin. The acquired form of NDI is much more common than the congenital form, which has mutations either in the vasopressin V 2 receptor gene or in the aquaporin-2 (AQP2) gene (1). Lithium (Li) treatment (2), hypokalemia (3), and ureteral obstruction (4) are three common causes of acquired NDI, and all have been associated with downregulation of AQP2 (2-4).One of the recommended regimens for the treatment of NDI is low-sodium diet coupled with thiazides, although amiloride is preferably used to mitigate Li-induced polyuria in humans because of its blunting the inhibitory effect of Li on water transport in the collecting duct (5). Thiazide diuretics paradoxically decrease urine volume and increase urine osmolality presumably by producing a mild sodium depletion (6). The widely accepted hypothesis suggests that thiazide-induced sodium depletion causes a reduction in distal delivery associated with enhanced fractional water reabsorption in the collecting duct (6,7). However, the mechanism by which thiazide diuretics produce their paradoxic antidi...

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Section: Animals and Experimental Protocolsmentioning

confidence: 99%

Antidiuretic Effect of Hydrochlorothiazide in Lithium-Induced Nephrogenic Diabetes Insipidus Is Associated with Upregulation of Aquaporin-2, Na-Cl Co-transporter, and Epithelial Sodium Channel

Kim

Lee²,

Oh³

et al. 2004

Journal of the American Society of Nephrology

133

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“…Three possible mechanisms of NaCl transport in distal segments have been considered: 1) Na ϩ -Cl Ϫ cotransport, 2) Na ϩ -K ϩ -2Cl Ϫ cotransport, and 3) Na ϩ -H ϩ and Cl Ϫ /HCO 3 Ϫ parallel antiport. At present, it is generally believed that the major site of action of thiazides is located in the distal convoluted tubule, as demonstrated in in vivo micropuncture and microperfusion studies (5)(6)(7).…”

mentioning

confidence: 99%

Thiazide induces water absorption in the inner medullary collecting duct of normal and Brattleboro rats

Cesar

Magaldi

1999

American Journal of Physiology-Renal Physiology

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The reduction of urinary volume after the use of thiazide in the treatment of diabetes insipidus (DI) is known as the "paradoxical effect." Since enhanced proximal solute and water reabsorption only partially account for the reduction in urinary volume, an additional diuretic effect on nephron terminal segments was postulated. Thus the aim of our work was to investigate the effect of hydrochlorothiazide (HCTZ) on water transport in the inner medullary collecting duct (IMCD) of normal and Brattleboro rats. Osmotic water permeability (P(f)) and diffusional water permeability (P(dw)) were studied at 37 degrees C and pH 7.4 by the in vitro microperfusion technique. In the absence of antidiuretic hormone (ADH), HCTZ (10(-6) M) added to the perfused fluid enhanced P(f) from 6.36 +/- 0. 56 to 19.08 +/- 1.70 micro(m)/s (P < 0.01) and P(dw) from 38.01 +/- 4.52 to 52.26 +/- 4.38 x10(-5) cm/s (P < 0.01) in normal rats and also stimulated P(f) in Brattleboro rats from 3.53 +/- 1.41 to 11.16 +/- 1.13 micro(m)/s (P < 0.01). Prostaglandin E(2) (PGE(2)) (10(-5) M) added to the bath fluid inhibited HCTZ-stimulated P(f) (in micro(m)/s) as follows: control, 16.93 +/- 2.64; HCTZ, 29.65 +/- 5.67; HCTZ+PGE(2), 10.46 +/- 1.84 (P < 0.01); recovery, 16.77 +/- 4.07. These data indicate that thiazides enhance water absorption in IMCD from normal rats (in the absence of ADH) and from Brattleboro rats and that the HCTZ-stimulated P(f) was partially blocked by PGE(2). Thus we may conclude that the effect of thiazide in the treatment of DI occurs not only in the Na(+)-Cl(-) cotransport in the distal tubule but also in the IMCD.

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“…In our patient 1, continuous nasogastric water feeding had a sufficient effect. A reduction in salt in the diet ( Na : 1 mEq/kg/day) has also been advocated to reduce serum sodium ( Blalock et al 1977;Words 1985). The low-solute diet with restricted protein and salt intake is justified even though growth is restricted.…”

Section: Discussionmentioning

confidence: 99%

A family case of nephrogenic diabetes insipidus.

Okayasu¹,

Shigihara²,

Kobayashi³

et al. 1990

Tohoku J. Exp. Med.

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Role of diet in the management of vasopressin-responsive and -resistant diabetes insipidus

Cited by 14 publications

References 11 publications

Antidiuretic Effect of Hydrochlorothiazide in Lithium-Induced Nephrogenic Diabetes Insipidus Is Associated with Upregulation of Aquaporin-2, Na-Cl Co-transporter, and Epithelial Sodium Channel

Antidiuretic Effect of Hydrochlorothiazide in Lithium-Induced Nephrogenic Diabetes Insipidus Is Associated with Upregulation of Aquaporin-2, Na-Cl Co-transporter, and Epithelial Sodium Channel

Thiazide induces water absorption in the inner medullary collecting duct of normal and Brattleboro rats

A family case of nephrogenic diabetes insipidus.

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