RENAL FUNCTION AND PLASMA RENIN ACTIVITY AS POTENTIAL FACTORS CAUSING HYPERKALEMIA IN PATIENTS WITH THYROID CARCINOMA UNDERGOING THYROID HORMONE WITHDRAWAL FOR RADIOACTIVE IODINE THERAPY

2020 ◽  
Vol 26 (2) ◽  
pp. 197-206
Author(s):  
Tetsuro Niri ◽  
Ichiro Horie ◽  
Takao Ando ◽  
Hiromi Kawahara ◽  
Mayu Ueda ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Plasma Renin Activity ◽  
Serum Potassium ◽  
Adrenocorticotropic Hormone ◽  
Radioactive Iodine ◽  
Estimated Glomerular Filtration Rate ◽  
Serum Potassium Level ◽  
Plasma Renin ◽  
Renin Activity ◽  
Acute Hypothyroidism

Objective: Hypothyroidism is not commonly considered a cause of hyperkalemia. We previously reported that hyperkalemia was observed mainly in elderly patients treated with renin-angiotensin-aldosterone system (RAS) inhibitors when levothyroxine treatment was withdrawn for the thyroidectomized patients with thyroid carcinoma to undergo radioactive iodine treatment. Here, we investigated whether acute hypothyroidism causes hyperkalemia in patients who were not treated with RAS inhibitors. We also investigated factors influencing potassium metabolism in hypothyroid patients. Methods: We conducted a single-center, prospective cohort study of 46 Japanese patients with thyroid carcinoma undergoing levothyroxine withdrawal prior to radioiodine therapy. All patients were normokalemic before levothyroxine withdrawal. Blood samples were analyzed 3 times: before, and at 3 and 4 weeks after levothyroxine withdrawal. We investigated factors that may be associated with the elevation of serum potassium levels from a euthyroid state to a hypothyroid state. Results: None of the patients developed symptomatic hyperkalemia. The mean serum potassium level was significantly higher at 4 weeks after levothyroxine withdrawal compared to baseline. The serum sodium levels, the estimated glomerular filtration rate (eGFR), and the plasma renin activity (PRA) decreased significantly as hypothyroidism advanced. In contrast, the plasma levels of adrenocorticotropic hormone, cortisol, aldosterone, and antidiuretic hormone were not changed, while serum thyroid hormone decreased. At 4 weeks after their levothyroxine withdrawal, the patients' serum potassium values were significantly correlated with the eGFR and the PRA. Conclusion: Acute hypothyroidism can cause a significant increase in the serum potassium level, which may be associated with a decreased eGFR and decreased circulating RAS. Abbreviations: ACTH = adrenocorticotropic hormone; ADH = antidiuretic hormone; ATPase = adenosine triphosphatase; eGFR = estimated glomerular filtration rate; HbA1c = glycated hemoglobin; K+ = potassium; Na+ = sodium; PRA = plasma renin activity; RAS = renin-angiotensin-aldosterone system; T4 = thyroxine; TSH = thyroid-stimulating hormone

Effect of ovariectomy on vasopressin, ACTH, and renin activity responses to hypotension

1991 ◽  
Vol 261 (1) ◽  
pp. R223-R230 ◽  
Author(s):  
M. Keller-Wood ◽  
C. E. Wood
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Acth ◽  
Blood Samples

The gonadal axis is thought to modulate adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and plasma renin activity (PRA) responses to stimuli in several species. These experiments were designed to compare the responses to hypotension in chronically ovariectomized ewes and intact ewes. The ewes were infused with nitroprusside at rates of 5, 10, or 15 micrograms.kg-1.min-1 or infused with vehicle for 10 min. The response to 15 micrograms.kg-1.min-1 was also tested with or without treatment with 10 mg of dexamethasone 2 h before nitroprusside. Blood samples were collected before and at 5, 10, 15, 20, and 30 min after the start of the infusion for measurement of plasma ACTH, AVP, and PRA. In both groups of animals there were significant responses to hypotension. There was a significant effect of ovariectomy on ACTH, AVP, and PRA responses. ACTH and PRA responses were lower in the ovariectomized ewes; AVP responses were increased in the ovariectomized ewes. Administration of dexamethasone inhibited ACTH responses and did not inhibit PRA responses in both groups of ewes. Administration of dexamethasone did not inhibit the AVP response in the intact ewes but did reduce the response in the ovariectomized ewes.

Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Aldosterone Secretion ◽  
Atrial Natriuretic

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

Letters to the Editor

PEDIATRICS ◽  
1981 ◽  
Vol 67 (2) ◽  
pp. 310-310
Author(s):  
Clarence E. Grim
Keyword(s):  
Plasma Renin Activity ◽  
Serum Potassium ◽  
Potassium Level ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin I ◽  
Letters To The Editor

The comments by Dr Walson raise some worthwhile points. The level of serum potassium in each patient was measured on nine separate days. In only one patient (the youngest) was a single potassium level of less than 3.6 mEq/liter obtained. Thus, in 26 of 27 measurements, potassium was normal (96% of the time). In contrast, plasma renin activity (PRA) was always less than 0.5 ng of angiotensin I (AI) per ml per 3 hr in 17 of 17 samples collected (100%) on each patient.

Progesterone-cortisol interaction in control of renin activity but not aldosterone

1990 ◽  
Vol 259 (2) ◽  
pp. R350-R356 ◽  
Author(s):  
M. Keller-Wood ◽  
J. Silbiger ◽  
C. E. Wood
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Nitroprusside ◽  
Adrenocorticotropic Hormone ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Acth Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
K Concentration

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.

Sign in / Sign up

Export Citation Format

Share Document