Renal Function and Electrolyte Levels in Hyperthyroidism: Urinary Protein Excretion and the Plasma Concentrations of Urea, Creatinine, Uric Acid, Hydrogen Ion and Electrolytes

Ford, Henry C.; Lim, W.Chew; Chisnall, Wayne N.; Pearce, J. M.

doi:10.1111/j.1365-2265.1989.tb02238.x

Cited by 46 publications

(27 citation statements)

References 33 publications

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“…These findings are comparable with the plasma creatinine changes observed in humans (40) and cats (41). The reduction in serum creatinine concentration in hyperthyroidism may be due to decreased production by a reduced muscle mass (12), whereas the increase observed in hypothyroidism is caused by a creatinine generation from possible myopathy and rhabdomyolysis (37). Moreover, these changes in plasma creatinine may in part be explained by volume expansion and dilution and by volume depletion in hyper-and hypothyroid rats, respectively, as suggested by the plasma protein levels.…”

Section: E285supporting

confidence: 86%

“…Proteinuria is often present in hyperthyroid humans (12) and rats (27,34) without being related to reninangiotensin system activity, BP levels (34), or oxidative stress (27). Proteinuria was aggravated by the increased sodium intake in hyperthyroid rats.…”

Section: E285mentioning

confidence: 99%

“…When tubular cells are damaged, they release tubular enzymes into the ultrafiltrate, increasing urinary enzyme activities. Urinary markers of tubular damage (33), such as retinol-binding protein or N-acetyl-␤-glucosaminidase, are elevated in hyperthyroid humans (12,29) and cats (42). In this paper, we analyzed the urinary excretion of GluAP, AlaAP, CysAp, and AspAp as possible biomarkers of tubular dysfunction in thyroid disorders and after an increased saline intake.…”

Section: E285mentioning

confidence: 99%

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Salt sensitivity in experimental thyroid disorders in rats

Pérez-Abud

Rodríguez-Gómez

Villarejo

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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This study assessed salt sensitivity, analyzing the effects of an increased saline intake on hemodynamic, morphological, and oxidative stress and renal variables in experimental thyroid disorders. Six groups of male Wistar rats were used: control, hypothyroid, hyperthyroid, and the same groups treated with salt (8% via food intake). Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 6 wk. Finally, BP and HR were recorded directly, and morphological, metabolic, plasma, and renal variables were measured. High-salt intake increased BP in thyroxine-treated rats but not in control or hypothyroid rats. High-salt intake increased cardiac mass in all groups, with a greater increase in hyperthyroid rats. Urinary isoprostanes and H 2O2 were higher in hyperthyroid rats and were augmented by high-salt intake in all groups, especially in hyperthyroid rats. High-salt intake reduced plasma thyroid hormone levels in hyperthyroid rats. Proteinuria was increased in hyperthyroid rats and aggravated by high-salt intake. Urinary levels of aminopeptidases (glutamyl-, alanyl-, aspartyl-, and cystinylaminopeptidase) were increased in hyperthyroid rats. All aminopeptidases were increased by salt intake in hyperthyroid rats but not in hypothyroid rats. In summary, hyperthyroid rats have enhanced salt sensitivity, and high-salt intake produces increased BP, cardiac hypertrophy, oxidative stress, and signs of renal injury. In contrast, hypothyroid rats are resistant to salt-induced BP elevation and renal injury signs. Urinary aminopeptidases are suitable biomarkers of renal injury. salt intake; hyperthyroidism; hypothyroidism; aminopeptidases; blood pressure RENAL FUNCTION AND SALT AND water metabolism can be considerably impaired by thyroid disorders (3, 46). Some authors reported that hypothyroid rats have a lesser ability to concentrate urine and show increased natriuresis after salt or water loading (10,18,25,39) and have a reduced capacity to conserve sodium, which produces a negative sodium balance and death when subjected to dietary sodium restriction (13). However, our group did not observe increased sodium excretion in hypothyroid methimazole-treated rats under some of the above conditions (44) or in pressure-diuresis-natriuresis studies (43). On the other hand, thyroxine (T 4 )-treated rats showed changes in renal hemodynamics and sodium resorption (46), increased blood volume (34), polydipsia/polyuria (15), reduced ability to excrete sodium after hypertonic saline loading (44), and a blunted pressure-diuresis-natriuresis response (43).These data indicate that thyroid disorders are accompanied by major changes in renal sodium handling.Hypothyroidism reduces blood pressure (BP) and prevents experimental hypertension (46), whereas T 4 administration to rats increases BP (6) and accelerates the course of hypertension (46). Although numerous systems can influence BP over the short term, long-term BP regulation depends on the renal excretion of sodium (22). An increased BP in response to dietary sodium (sal...

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Section: E285supporting

confidence: 86%

Section: E285mentioning

confidence: 99%

Section: E285mentioning

confidence: 99%

See 1 more Smart Citation

Salt sensitivity in experimental thyroid disorders in rats

Pérez-Abud

Rodríguez-Gómez

Villarejo

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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“…This observation is in accordance with previous findings indicating that erythrocyte ion transport is altered in hyperthyroidism. Changes in sodium metabolism in hyperthyroidism have been discussed extensively by several groups [22][23][24][25]. Although their clinical significance is not known, they indicate pathophysiological responses to high plasma thyroid levels.…”

Section: Discussionmentioning

confidence: 99%

Magnesium Metabolism in Hyperthyroidism.

et al. 1996

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“…Proteinuria is often present in hyperthyroid humans 45 and rats. 46,47 Proteinuria was attenuated by a low sodium intake in the T 4 -treated rats.…”

Section: Discussionmentioning

confidence: 99%

Dietary salt restriction in hyperthyroid rats. Differential influence on left and right ventricular mass

Wangensteen

Rodríguez-Gómez

Pérez-Abud

et al. 2014

Exp Biol Med (Maywood)

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This study assessed the impact of salt restriction on cardiac morphology and biochemistry and its effects on hemodynamic and renal variables in experimental hyperthyroidism. Four groups of male Wistar rats were used: control, hyperthyroid, and the same groups under low salt intake. Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 4 weeks. Morphologic, metabolic, plasma, cardiac, and renal variables were also measured. Low salt intake decreased BP in T 4 -treated rats but not in controls. Low salt intake reduced relative left ventricular mass but increased absolute right ventricular weight and right ventricular weight/BW ratio in both control and hyperthyroid groups. Low salt intake increased Naprotein abundance in both ventricles in normal rats but not in hyperthyroid rats, independently of its effect on ventricular mass. Mammalian target of rapamycin (mTOR) protein abundance was not related to left or right ventricular mass in hyperthyroid or controls rats under normal or low salt conditions. Proteinuria was increased in hyperthyroid rats and attenuated by low salt intake. In this study, low salt intake produced an increase in right ventricular mass in normal and hyperthyroid rats. Changes in the left or right ventricular mass of control and hyperthyroid rats under low salt intake were not explained by the NHE-1 or mTOR protein abundance values observed. In hyperthyroid rats, low salt intake also slightly reduced BP and decreased HR, proteinuria, and water and sodium balances.

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Renal Function and Electrolyte Levels in Hyperthyroidism: Urinary Protein Excretion and the Plasma Concentrations of Urea, Creatinine, Uric Acid, Hydrogen Ion and Electrolytes

Cited by 46 publications

References 33 publications

Salt sensitivity in experimental thyroid disorders in rats

Salt sensitivity in experimental thyroid disorders in rats

Magnesium Metabolism in Hyperthyroidism.

Dietary salt restriction in hyperthyroid rats. Differential influence on left and right ventricular mass

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