Thyroid hormone coordinately regulates Na+-K+-ATPase alpha- and beta-subunit mRNA levels in kidney

McDonough, Alicia A.; Brown, Thomas W.; Horowitz, Burton; Chiu, Robert; Schlotterbeck, J D; Bowen, Jesse W.; Schmitt, C

doi:10.1152/ajpcell.1988.254.2.c323

Cited by 92 publications

(40 citation statements)

References 26 publications

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“…Furthermore, brain natriuretic peptide levels have correlation with free T3 and T4 levels (4). Also, it has been recently shown that T4 is known to regulate Na + /Ca 2+ channels and Na + /K + -ATPase activity in the sarcoplasmic reticulum of nephrons (5). Another important mechanism of renal dysfunction in hypothyroidism is through muscle involvement.…”

Section: Discussionmentioning

confidence: 99%

Rhabdomyolysis case based on hypothyroidism

Ateş¹

2016

EJEA

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SummaryHypothyroidism is a wide clinical spectrum disorder and only a few cases in literature show this. Rhabdomyolysis and acute renal impairment can be seen concurrently in a hypothyroid state. We report a case of severe hypothyroidism with poor drug compliance leading to rhabdomyolysis and acute kidney injury. ID: 16-0083; October 2016 DOI: 10.1530 Correspondence should be addressed to I Ates Email dr.ihsanates@hotmail.com Learning points:• Hypothyroidism is a rare cause of acute kidney injury.• In this case report, we studied a rare occurrence of acute renal impairment due to hypothyroidism with poor drug compliance, which induced rhabdomyolysis.• Our report emphasized that thyroid status should be evaluated in patients with unexplained acute renal impairment or presenting with the symptoms of muscle involvement. Case presentationA 53-year-old male was admitted to a hospital with 15 days history of dyspnoea, weakness and oliguria, and muscle pain. His medical history included pulmonary thromboembolic, hypertension and cardiac arrhythmia. He had undergone total thyroidectomy for papillary thyroid cancer two years ago. His medication consisted of metoprolol, enoxaparin and l-thyroxine with no use in the past 4 weeks. Physical examination revealed dry and pale skin and slow speech. His pulse rate was 55 beats/minute and blood pressure was 130/90 mm Hg.Electrocardiography has shown bigemine ventricular extra systole. Laboratory investigations showed the following values: creatine phosphokinase, 1560 U/L (reference range, 52-336 U/L); creatinine, 2.1 mg/dL (0.2-1.0 mg/dL); potassium, 5.3 mEq/L (3.5-5.0 mEq/L); thyroid-stimulating hormone (TSH) 43.2 µIU/mL (0.4-4.8 uIU/mL), free thyroxine (fT4) <0.3 ng/dL (1.71-2.8 ng/dL) and free triiodothyronine (fT3) 0.48 pg/mL (1.57-4.71 pg/ mL). Haematological tests showed haemoglobin 9.4 g/dL (12-16), white cell count 9000 µL and platelet counts were in normal range. His urine was bloody in appearance and urine analysis showed blood reaction with dipstick test, but no erythrocytes were found on microscopic examination. Fraction excretion of Na and urinary Na were high (2.6% and 46 mEq/L, respectively). Renal tract ultrasonography was normal. No signs suggested the presence of an associated infectious or systemic inflammatory disease. In addition, other causes resulting in rhabdomyolysis such as muscular trauma, drugs and toxins were excluded with history and laboratory investigations. His condition was diagnosed as acute kidney injury secondary to hypothyroidism-induced rhabdomyolysis. This case was also consulted with the department of cardiology physicians who started him on metoprolol 25 mg before beginning thyroid replacement therapy. Cardiac status remained stable: l-thyroxine 25 microgram/day was prescribed, then 2 weeks later it was continued with l-thyroxine 50 microgram/day. His fluid deficiency was treated aggressively. His symptoms resolved over the following 3 weeks.

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Section: Discussionmentioning

confidence: 99%

Rhabdomyolysis case based on hypothyroidism

Ateş¹

2016

EJEA

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“…Benos (1981b) (Boardman et al, 1974;Pollack et al, 1981;Edelman et al, 1985) is modulated by hormonal factors (Jorgenssen, 1972;Geheb et al, 1983;Paccolat et al, 1987;McDonough et al, 1988 (Daniel, 1964), and a decrease in overall oxidative metabolism (Benos &Balaban, 1980,1983. Other physiological studies (Benos, 1981a, b;Benos & Biggers, 1981;Benos etal, 1985) …”

Section: Free Intracellular Methionine Contentmentioning

confidence: 99%

Synthesis of Na+/K+ ATPase by the preimplantation rabbit blastocyst

Overström

Benos²,

Biggers³

1989

Reproduction

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“…The differences in these ATPase-isoforms and the other organs could make the brain more susceptible to modulation by both intrinsic and extrinsic factors, and could account for the brain's distinct response to the toxicants. The increased activity of Na + /K + ATPase in the brain of the animals induced by these treatments could, therefore, be a result of one or a combination of the following: (i) inhibition of the regulatory factor protein kinase C, resulting from an increase in intracellular sodium concentration, leading to dephosphorylation of Na + /K + ATPase and increasing its activity (Mallick et al, 2000); (ii) upregulation of the enzyme by increased cAMP (Burnier, 2008); (iii) enhanced expression of the β1 subunit of Na + /K + ATPase, the rate limiting subunit, which has been suggested to increase the enzyme activity (Sennoune et al, 2000); and (iv) hormonal modulation (McDonough et al, 1988).…”

Section: A S 3+ + D E H P C O M P a R E D W It H C O N T R O L B A Rmentioning

confidence: 99%

Combined arsenic and di-(2-ethylhexyl) phthalate exposure elicits responses in brain ATPases different from hepatic and renal activities in rats

Afolabi¹,

Ugbaja²,

Ademuyiwa³

2016

J. Toxicol. Environ. Health Sci.

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Arsenic and di-(2-ethylhexyl) phthalate (DEHP) are environmentally ubiquitous and epidemiologically important toxic agents that millions of people are currently exposed to, worldwide. Although the adverse impact due to exposure to either arsenic or DEHP are documented, the toxicological effects of co-exposure to these agents are largely unknown. In this study, exposure to these chemicals was investigated for their effects on ATPase activities in the brain, liver and kidney of rats. Male Wistar rats were exposed daily to 100 mg L -1 arsenic via drinking water and to 100 mg DEHP kg -1 body weight in corn oil either individually or concurrently for 30 days. Toxicity was assessed by evaluating changes in body and organ weights, as well as, Na + /K + -, Ca 2+ -, Mg 2+ -and total ATPase activities in the brain, liver and kidney. Exposure to either arsenic or DEHP resulted in drastic reduction in activities of the enzymes in the compartments investigated, except in the brain where Na + /K + -and Mg 2+ -ATPases had their activities significantly increased. Also, DEHP displayed no effect on the total ATPase and Ca 2+ATPase in the kidney and brain, respectively. Interestingly, co-exposure to these toxicants significantly stimulated the activities of all these enzymes in the brain. In this compartment, combined treatment resulted in an additive interaction between the toxicants and a potentiation effect of arsenic on DEHP with regards to the Na + /K + -ATPase activity and Ca 2+ -ATPase activity, respectively. Our findings demonstrate tissue specific response to combined arsenic and DEHP exposure in rats with the effect on the brain significantly different from other compartments.

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Thyroid hormone coordinately regulates Na+-K+-ATPase alpha- and beta-subunit mRNA levels in kidney

Cited by 92 publications

References 26 publications

Rhabdomyolysis case based on hypothyroidism

Rhabdomyolysis case based on hypothyroidism

Synthesis of Na+/K+ ATPase by the preimplantation rabbit blastocyst

Combined arsenic and di-(2-ethylhexyl) phthalate exposure elicits responses in brain ATPases different from hepatic and renal activities in rats

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