# Situation: A 64-year-old man with chronic atrial fibrillation and hypertension takes digoxin 0.125 mg and hydrochlorothiazide 25 mg orally every morning. He has no heart failure or kidney disease. He is admitted with generalized weakness, leg cramps, and palpitations. His serum potassium is 2.9 mEq/L (3.5–5.0 mEq/L). The hydrochlorothiazide is held, and he has a peripheral intravenous (IV) catheter in his forearm. On day 3 he has received 120 mEq of potassium chloride, and the hydrochlorothiazide has stayed on hold since admission. His results are: Potassium: 3.1 mEq/L (3.5–5.0 mEq/L) Magnesium: 1.2 mg/dL (1.7–2.2 mg/dL) Sodium: 137 mEq/L (135–145 mEq/L) Calcium: 9.0 mg/dL (8.6–10.2 mg/dL) What is the MOST likely reason his potassium remains low?

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## 문제

Situation: A 64-year-old man with chronic atrial fibrillation and hypertension takes digoxin 0.125 mg and hydrochlorothiazide 25 mg orally every morning. He has no heart failure or kidney disease. He is admitted with generalized weakness, leg cramps, and palpitations. His serum potassium is 2.9 mEq/L (3.5–5.0 mEq/L). The hydrochlorothiazide is held, and he has a peripheral intravenous (IV) catheter in his forearm.

On day 3 he has received 120 mEq of potassium chloride, and the hydrochlorothiazide has stayed on hold since admission. His results are:
Potassium: 3.1 mEq/L (3.5–5.0 mEq/L)
Magnesium: 1.2 mg/dL (1.7–2.2 mg/dL)
Sodium: 137 mEq/L (135–145 mEq/L)
Calcium: 9.0 mg/dL (8.6–10.2 mg/dL)
What is the MOST likely reason his potassium remains low?

## 보기

1. The held thiazide is still causing potassium loss in the urine
2. Digoxin is moving potassium out of his blood and into his cells
3. Low magnesium is causing continued potassium loss in the urine **✔ 정답**
4. The 0.9% sodium chloride carrier is diluting his serum potassium

**정답: 3**

## 해설

His magnesium is low (1.2 mg/dL), and hypomagnesemia makes hypokalemia resistant to treatment because the kidneys keep wasting potassium until magnesium is replaced. The thiazide has been held for 3 days, so its effect has worn off. Magnesium replacement is needed for the potassium to correct.

## 심화 해설

Why the potassium stays low
This patient’s serum magnesium is 1.2 mg/dL (reference 1.7–2.2 mg/dL), which is the key to the persistent hypokalemia. Hypomagnesemia causes the kidneys to continue wasting potassium in the urine, so potassium replacement alone cannot correct the serum potassium until magnesium is repleted. Even after 120 mEq of potassium chloride over three days, the potassium rose only from 2.9 mEq/L to 3.1 mEq/L because the renal potassium leak remained active.

Mechanism linking magnesium and potassium
In the distal nephron, potassium secretion through the renal outer medullary potassium (ROMK) channel is normally inhibited by intracellular magnesium. When magnesium is depleted, this magnesium-dependent inhibition is lost, and ROMK channels remain open, allowing ongoing urinary potassium excretion. The result is refractory hypokalemia: potassium given intravenously is rapidly excreted in the urine rather than retained. This is why hypomagnesemia is a well-recognized cause of potassium wasting that does not respond to potassium supplementation alone.

Why the other options are less likely
Watch out! The thiazide diuretic was held on admission and has remained held for three days. Thiazide-induced kaliuresis resolves within that timeframe, so ongoing drug effect is not a plausible explanation for the persistently low potassium on day 3. Digoxin inhibits the Na⁺/K⁺-ATPase pump, which can raise extracellular potassium slightly; it does not cause hypokalemia by shifting potassium into cells. A 0.9% sodium chloride carrier does not dilute serum potassium enough to explain a value of 3.1 mEq/L after aggressive replacement.

Clinical application for the licensure exam
Key point! Whenever hypokalemia does not correct despite adequate potassium replacement, check the serum magnesium. The sequence of correction is important: magnesium replacement should be given first or concurrently, because repleting magnesium restores the kidney’s ability to retain potassium. This principle appears across electrolyte imbalance, diuretic therapy, and arrhythmia-related questions.

| Finding | Value | Interpretation |
| --- | --- | --- |
| Serum potassium | 3.1 mEq/L | Still low despite 120 mEq KCl |
| Serum magnesium | 1.2 mg/dL | Hypomagnesemia driving renal K⁺ wasting |
| Serum sodium | 137 mEq/L | Normal |
| Serum calcium | 9.0 mg/dL | Normal |

Connecting to the evidence
The case reports describe patients with refractory hypokalemia accompanied by hypomagnesemia, where potassium levels remained low until the underlying renal magnesium and potassium wasting was addressed [1][2][3][4]. Although these reports focus on Gitelman syndrome, they illustrate the same physiologic principle seen in this patient: persistent renal potassium loss in the setting of hypomagnesemia makes potassium replacement ineffective until magnesium is corrected. In this patient, the combination of chronic diuretic use and hypomagnesemia created a similar state of renal potassium wasting, and the low magnesium on day 3 is the most direct explanation for the failure of potassium to normalize.References (research sources)

- [1]Long-Standing Hypokalemia and Hypomagnesemia in a 61 Year-Old Woman: A Delayed Diagnosis of Gitelman Syndrome.Research articleLee SY, Han SW, Lee J, Yu MY. (2026) · DOI: 10.5049/ebp.2026.24.e14

- [2]Symptomatic heterozygous Gitelman syndrome in a professional baseball player: a case report.Case reportDougherty JJ, Medina AC, Dougherty JJ, Hoover CJ. (2026) · DOI: 10.1515/jom-2025-0185

- [3]Gitelman Syndrome.Research articleMustafa QU, Haroon ZH, Ijaz A, Sajid MT, Ayyub M (2017)

- [4]Chronic Musculoskeletal Pain as an Initial Presentation of Gitelman Syndrome in Adulthood: A Case Report.Case reportNair S, Michel M L, Kumar K, Fathima NM, Jacob HR. (2026) · DOI: 10.7759/cureus.110572

## 임상 시나리오

Refractory Hypokalemia: Check Magnesium FirstPotassium will not correct until magnesium is repleted
When hypokalemia persists despite adequate potassium replacement, always check serum magnesium. Hypomagnesemia causes ongoing renal potassium wasting by removing magnesium-dependent inhibition of ROMK channels in the distal nephron.

In this patient, potassium rose only from 2.9 mEq/L to 3.1 mEq/L after 120 mEq of potassium chloride because magnesium was 1.2 mg/dL (low). The kidneys continued excreting potassium in the urine.

CautionDo not attribute persistent hypokalemia to a held thiazide after 3 days—its kaliuretic effect has resolved. Replace magnesium first, then reassess potassium.

## 핵심 개념

- **Refractory hypokalemia** — Hypokalemia that does not correct with potassium replacement alone because an underlying cause, such as hypomagnesemia, continues to drive potassium loss.
- **ROMK channel** — Renal outer medullary potassium channel in the distal nephron that secretes potassium; normally inhibited by intracellular magnesium.
- **Hypomagnesemia** — Low serum magnesium level (below 1.7 mg/dL) that impairs magnesium-dependent inhibition of ROMK, leading to renal potassium wasting.
- **Kaliuresis** — Increased urinary excretion of potassium, often caused by diuretics or mineralocorticoid excess.
- **Thiazide diuretic** — A class of diuretics that inhibits sodium-chloride cotransport in the distal tubule, causing potassium loss; effect resolves within days of discontinuation.

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