Effects of myxedema on the renal diluting and concentrating mechanism

Discala, Vincent A.; Kinney, Michael J.

doi:10.1016/0002-9343(71)90221-x

Cited by 93 publications

(51 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Western blot analyses revealed decreased renal protein abundance of transporters, including Na-K-2Cl, Na-K-ATPase, and NHE3, in HT rats as compared with CTL and HTϩT rats. Protein abundance of renal AQP1 and urea transporters UTA 1 and UTA 2 did not differ significantly among study groups. There was however a significant decrease in protein abundance of AQP2, AQP3, and AQP4 in HT rats as compared with CTL and HTϩT rats.…”

mentioning

confidence: 76%

“…Advanced hypothyroidism to the clinical stage of myxedema is associated with hyponatremia involving both the nonosmotic release of AVP and diminished GFR (1,(13)(14)(15). These events, which impair urinary dilution in advanced hypothyroidism, override the defect in urinary concentrating capacity, which also has been observed with hypothyroidism (1,2).…”

Section: Discussionmentioning

confidence: 99%

“…SDS-PAGE was performed on 8% acrylamide gels for Na-K-2Cl, Na-K-ATPase, and NHE3, on 10% acrylamide gels for UTA 1 and UTA 2 , and on 12% acrylamide gels for AQP. After transfer by electroelution to polyvinylidene difluoride membranes (Millipore, Bedford, MA), blots were blocked overnight with 5% nonfat dry milk in phosphate-buffered saline [PBS(Ϫ)] and then probed with the respective antibodies for 24 h at 4°C.…”

Section: Western Blot Analysesmentioning

confidence: 99%

“…The ability to conserve water during periods of fluid deprivation is an important function of the kidney. Hypothyroidism has been associated with an impaired urinary concentrating capacity (1,2). However, the mechanisms of this defect at the cellular and molecular level have not been defined.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Urinary Concentrating Defect in Hypothyroid Rats

Cadnapaphornchai¹,

Kim²,

Gurevich³

et al. 2003

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. Hypothyroidism is associated with impaired urinary concentrating ability in humans and animals. The purpose of this study was to examine protein expression of renal sodium chloride and urea transporters and aquaporins in hypothyroid rats (HT) with diminished urinary concentration as compared with euthyroid controls (CTL) and hypothyroid rats replaced with L-thyroxine (HTϩT). Hypothyroidism was induced by aminotriazole administration. Body weight, water intake, urine output, solute and urea excretion, serum and urine osmolality, serum creatinine, 24-h creatinine clearance, and fractional excretion of sodium were comparable among the three groups. However, with 36 h of water deprivation, HT rats demonstrated significantly greater urine flow rates and decreased urine and medullary osmolality as compared with CTL and HTϩT rats at comparable plasma vasopressin concentrations. Western blot analyses revealed decreased renal protein abundance of transporters, including Na-K-2Cl, Na-K-ATPase, and NHE3, in HT rats as compared with CTL and HTϩT rats. Protein abundance of renal AQP1 and urea transporters UTA 1 and UTA 2 did not differ significantly among study groups. There was however a significant decrease in protein abundance of AQP2, AQP3, and AQP4 in HT rats as compared with CTL and HTϩT rats. These findings demonstrate a decrease in the medullary osmotic gradient secondary to impaired countercurrent multiplication and downregulation of aquaporins 2, 3, and 4 as contributors to the urinary concentrating defect in the hypothyroid rat.Hypothyroidism is a very common clinical disorder that is associated with abnormalities in many organs, including the kidney. The ability to conserve water during periods of fluid deprivation is an important function of the kidney. Hypothyroidism has been associated with an impaired urinary concentrating capacity (1,2). However, the mechanisms of this defect at the cellular and molecular level have not been defined.In the present study, the effect of hypothyroidism in rats on the pivotal components of the urinary concentrating mechanism have been examined and compared with euthyroid animals. These components during fluid deprivation include release of the antidiuretic hormone, arginine vasopressin (AVP), and upregulation of the abundance of aquaporin-2 (AQP2) water channels in the principal cells of the collecting duct. Activation of the countercurrent concentrating mechanism, which is initiated by increased sodium-potassium-2 chloride (Na-K-2Cl) co-transporter in the water impermeable ascending limb, creates the osmotic driving force for passive water reabsorption across the collecting duct. There are also roles for other water channels, including aquaporins 1, 3, and 4, and for urea transporters in urinary concentration. The present study was undertaken to define the effect of hypothyroidism on these various molecular events during fluid deprivation in the rat. Materials and Methods Animal ModelThe study protocol was approved by the University of Colorado Institutional Animal Ca...

show abstract

mentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Western Blot Analysesmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Urinary Concentrating Defect in Hypothyroid Rats

Cadnapaphornchai¹,

Kim²,

Gurevich³

et al. 2003

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…While somereports have postulated inappropriate secretion of antidiuretic hormone (ADH)as being causative (2,3), others have implicated a relative deficiency of adrenal cortical hormone (4) or changes in renal function (5,6).…”

Section: Introductionmentioning

confidence: 99%

Hyponatremia with Increased Plasma Antidiuretic Hormone in a Case of Hypothyroidism.

et al. 2000

View full text Add to dashboard Cite

Wereport a 70-year-old womanwith hypothyroidism and severe hyponatremia. Her plasma antidiuretic hormone (ADH) level was inappropriately high for her low plasma osmolality. Her low serum sodium level was gradually corrected by water restriction and sodium supplementation prior to the initiation of thyroid hormone replacement. After a diagnosis of Hashimoto's thyroiditis had been made, the patient was treated with levothyroxine. Following this treatment, the patient's serum sodium level increased drastically. It is suggested that the elevated plasma ADHlevel played an important role in the development of hyponatremia in this case.

show abstract

Clinical Disorders of Urine Concentration and Dilution

Harrington¹

1973

Arch Intern Med

View full text Add to dashboard Cite

Effects of myxedema on the renal diluting and concentrating mechanism

Cited by 93 publications

References 25 publications

Urinary Concentrating Defect in Hypothyroid Rats

Urinary Concentrating Defect in Hypothyroid Rats

Hyponatremia with Increased Plasma Antidiuretic Hormone in a Case of Hypothyroidism.

Clinical Disorders of Urine Concentration and Dilution

Contact Info

Product

Resources

About