Investigating hypokalaemia
BMJ 2013; 347 doi: https://doi.org/10.1136/bmj.f5137 (Published 24 September 2013) Cite this as: BMJ 2013;347:f5137
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Oram and his colleagues ( BMJ 2013;347:f5137) propose a random urine potassium concentration alone, rather than 24 hour collections of urine, as the most practical way to assess renal potassium loss to assess the cause of hypokalaemia. They discuss, but do not stress enough, the merits of urinary potassium measurement as a first response - whenever there is uncertainty about the reason for hypokalaemia. A simultaneous urinary potassium and creatinine measurement, with a repeat serum potassium value (to confirm the hypokalaemia), provides an immediate indication of whether urinary potassium loss is still present or urinary potassium conservation is active. When inappropriate renal excretion is not present, i.e. the kidneys are conserving potassium, either non-renal loss, usually secondary to a gastrointestinal cause, is probable or the cause of past renal loss is no longer active, usually diuretics already having been ceased. The availability of measurements of potassium from early in the assessment of hypokalaemia greatly facilitates making a diagnosis. In several decades of providing nephrological consultations I have found that these measurements are often not done, or done only after replacement of potassium deficit is well advanced, when they are of limited or no value.
The measurement of potassium/creatinine ratio (KCR) in “spot” urine collected before potassium replacement is given, as they suggest, with a urine KCR of 2.5 mmol/mmol used as cut-off, merits further evaluation as an improvement on using just the urine potassium concentration in a “spot” urine, or to waiting for a 24 hour collection - which will often be difficult to interpret due to potassium replacement. Measurement of serum bicarbonate (or/and blood gas analysis), serum magnesium and chloride should be part of the initial evaluation as they also assist in the early identification of cause in some patients and also modify management strategies.
Appropriate investigations in primary care or in the Emergency Department before potassium replacement has the potential to minimise the need for or the duration of hospitalisation, by expediting the diagnosis and by assisting management.
Competing interests: No competing interests
The authors did mention that in primary hyperaldosteronism the patient presents with hypertension with unexplained hypokalaemia(1). However dietary potassium intake may also have this picture.
Among dietary factors playing an important role in the pathogenesis and management of essential hypertension, [2] K + is known to modulate the pressor effect of dietary NaCl. In fact, both normal and hypertensive subjects, ingesting a low K + diet may exhibit lower sodium excretion than that observed during normal K + intake; [3],[4] consequently, it has been concluded that Na + retention may contribute to blood pressure elevation during K + depletion. Dietary K + restriction increases blood pressure in patients with essential hypertension. Both Na + retention and Ca 2+ depletion may contribute to the increase in blood pressure during K + depletion. [4] K + depletion may exacerbate essential hypertension and not only Na + restriction, but also K + and Ca 2+ supplementation, could be particularly advisable in salt-sensitive hypertensive patients. [4]
References:
1. BMJ 2013;347:f5137
2. Dustan HP. Nutrition and hypertension. Ann Intern Med 1983;98:660-2.
3. Krishna GG, Chusid P, Hoeldtke RD. Mild potassium depletion provokes renal sodium retention. J Lab Clin Med 1987;109:724-30.
4. Krishna GG, Kapoor SC. Potassium depletion exacerbates essential hypertension. Ann Intern Med 1991;115:77-83.
5. Coruzzi P, Brambilla L, Brambilla V, Gualerzi M, Rossi M, Parati G, et al. Potassium depletion and salt sensitivity in essential hypertension. J Clin Endocrinol Metab 2001;86:2857-62.
Competing interests: No competing interests
Re: Investigating hypokalaemia
The report on investigating hypokalaemia by Oram et al (1) provides an excellent basis for the investigation and management of this potentially life threatening condition. However, although Cushing’s disease is mentioned as a cause there is little specific mention of therapeutically used glucocorticoid steroids as significant cause of hypokalaemia. Thus long term glucocorticoid steroid treatment should be borne in mind as an iatrogenic cause of hypokalaemia. This may complicate not only prolonged oral and parenteral therapy (2,3) but may also occur acutely in conditions such as asthma (4). It is also vitally important for clinicians to be mindful of ectopic ACTH secreting tumours (5) which can cause a profound and life threatening hypercorticolism and hypokalaemia (6). Moreover, the hypokalaemia in Cushing’s disease can be associated with a prolonged QT interval in males predisposing to torsade de pointe (7) and predisposing to unpredictable ventricular fibrillation.
1. Oram RA, McDonald TJ, Vaidya B. Investigating hypokalaemia. BMJ. 2013; 347: 35-37.
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Sugiyama E, Minoshima A, Tanabe Y, Akasaka K, Kawabe J, Kawamura Y, Doi A, Hasebe N. Three cases of corticosteroid therapy triggering ventricular fibrillation in
J-wave syndromes. Heart Vessels. 2013 Nov 27. [Epub ahead of print]
3. Tamez-Pérez HE, Cisneros-Pérez V, Cedillo-Rodríguez JA, Diaz-De-León-González E, Torres-Valenzuela M, Tamez-Peña AL, Forsbach-Sánchez G, Gutiérrez-Hermosillo H. [Prevalence of hypokalemia in patients with methylprednisolone pulse therapy]. Rev Invest Clin. 2009;61(3):194-7.
4. Tsai WS, Wu CP, Hsu YJ, Lin SH. Life-threatening hypokalemia in an asthmatic patient treated with high-dose hydrocortisone. Am J Med Sci. 2004;327(3):152-5.
5. Doi M, Sugiyama T, Izumiyama H, Yoshimoto T, Hirata Y. Clinical features and management of ectopic ACTH syndrome at a single institute in Japan. Endocr J. 2010;57(12):1061-9.
6. Lutgers HL, Vergragt J, Dong PV, de Vries J, Dullaart RP, van den Berg G,
Ligtenberg JJ. Severe hypercortisolism: a medical emergency requiring urgent intervention. Crit Care Med. 2010;38(7):1598-601.
7. Pecori Giraldi F, Toja PM, Michailidis G, Metinidou A, De Martin M, Scacchi M,
Stramba-Badiale M, Cavagnini F. High prevalence of prolonged QT interval duration in male patients with Cushing's disease. Exp Clin Endocrinol Diabetes. 2011;119(4):221-4.
Competing interests: No competing interests