Letter to the Editor Published online: May 27, 2014
Blood Purif 2014;37:188 DOI: 10.1159/000360274
Hypokalemia in Thyrotoxic Periodic Paralysis: Implication for Nephrology Practice Ugo Vertolli a Agostino Naso a Camilla Rubini a Rosa Carmello b Lorenzo A. Calò a a
Department of Medicine, Nephrology and Internal Medicine and b Emergency Department, University Hospital of Padua, Padua, Italy
Dear Editor, Thyrotoxic periodic paralysis (TPP) has been widely reported in Asian populations, in which the incidence among patients with hyperthyroidism is approximately 2% [1]. This contrasts with the much lower incidence of TPP in non-Asian populations, which among individuals with hyperthyroidism is 0.1–0.2%. Polynesians are also at higher risk for TPP compared to the risk of those of European descent [2]. Despite a higher incidence of hyperthyroidism in women, over 95% of the TPP cases occur in men [3], which have a particularly high incidence among Asian men with thyrotoxicosis (8.7–13%) [4]. Individuals who are susceptible to TPP may have an ion channel defect, which, in the normal thyroid state, is not sufficient to raise symptoms [5]. Indeed, it has been shown that patients with TPP have a mutation in the gene encoding Kir2.6, an inwardly rectifying potassium channel, expressed in skeletal muscle, transcriptionally regulated by the thyroid hormone [6]. We report a case of a female patient with TPP as an example of unusual hypokalemia, which could turn up in a nephrology practice of a Western country. A 22-year-old woman presented in the emergency room of Padua University Hospital complaining of transient sensations of burns and weakness in the proximal muscles of her arms and legs. Clinical examination was unremarkable; ECG showed sinus tachycardia and blood pressure was 123/78 mm Hg. Routine blood tests were normal with the exception of severe hypokalemia (2.2 mmol/l). Her clinical history ruled out the
common causes of hypokalemia, including vomiting, diarrhea and use of diuretics. Plasma potassium was normalized by intravenous infusion of 1 liter of saline supplemented with 40 mmol of potassium chloride, and the patient was referred to the Padua Nephrology Clinic for a diagnostic workup for hypokalemia of apparent unknown origin. Hypokalemia following tubular acidosis was ruled out by the normal blood and urinary pH (7.39 and 7.0, respectively), and by urinary bicarbonate that was normal as well (22.7 mmol). Tubular function abnormalities were ruled out by the normal values of urinary potassium (20 mmol/l) and sodium fractional excretion (3%). Finally, plasma renin activity and aldosterone concentration were found in the normal range [plasma renin activity: 2.31 μg/l/h (n.v.: 0.20– 3.30); aldosterone: 381 pmol/l (n.v.: 21– 415)]. Due to the fact that in our nephrology clinic evaluation of thyroid function is part of starting laboratory workup for the new admissions, very high levels of FT4 and FT3 were found [66.50 pmol (n.v.
Blood Purif 2014;37:188 DOI: 10.1159/000360274
Hypokalemia in Thyrotoxic Periodic Paralysis: Implication for Nephrology Practice Ugo Vertolli a Agostino Naso a Camilla Rubini a Rosa Carmello b Lorenzo A. Calò a a
Department of Medicine, Nephrology and Internal Medicine and b Emergency Department, University Hospital of Padua, Padua, Italy
Dear Editor, Thyrotoxic periodic paralysis (TPP) has been widely reported in Asian populations, in which the incidence among patients with hyperthyroidism is approximately 2% [1]. This contrasts with the much lower incidence of TPP in non-Asian populations, which among individuals with hyperthyroidism is 0.1–0.2%. Polynesians are also at higher risk for TPP compared to the risk of those of European descent [2]. Despite a higher incidence of hyperthyroidism in women, over 95% of the TPP cases occur in men [3], which have a particularly high incidence among Asian men with thyrotoxicosis (8.7–13%) [4]. Individuals who are susceptible to TPP may have an ion channel defect, which, in the normal thyroid state, is not sufficient to raise symptoms [5]. Indeed, it has been shown that patients with TPP have a mutation in the gene encoding Kir2.6, an inwardly rectifying potassium channel, expressed in skeletal muscle, transcriptionally regulated by the thyroid hormone [6]. We report a case of a female patient with TPP as an example of unusual hypokalemia, which could turn up in a nephrology practice of a Western country. A 22-year-old woman presented in the emergency room of Padua University Hospital complaining of transient sensations of burns and weakness in the proximal muscles of her arms and legs. Clinical examination was unremarkable; ECG showed sinus tachycardia and blood pressure was 123/78 mm Hg. Routine blood tests were normal with the exception of severe hypokalemia (2.2 mmol/l). Her clinical history ruled out the
common causes of hypokalemia, including vomiting, diarrhea and use of diuretics. Plasma potassium was normalized by intravenous infusion of 1 liter of saline supplemented with 40 mmol of potassium chloride, and the patient was referred to the Padua Nephrology Clinic for a diagnostic workup for hypokalemia of apparent unknown origin. Hypokalemia following tubular acidosis was ruled out by the normal blood and urinary pH (7.39 and 7.0, respectively), and by urinary bicarbonate that was normal as well (22.7 mmol). Tubular function abnormalities were ruled out by the normal values of urinary potassium (20 mmol/l) and sodium fractional excretion (3%). Finally, plasma renin activity and aldosterone concentration were found in the normal range [plasma renin activity: 2.31 μg/l/h (n.v.: 0.20– 3.30); aldosterone: 381 pmol/l (n.v.: 21– 415)]. Due to the fact that in our nephrology clinic evaluation of thyroid function is part of starting laboratory workup for the new admissions, very high levels of FT4 and FT3 were found [66.50 pmol (n.v.
