Hypokalaemia (Low Potassium) Cause Interpreter
Hypokalaemia (Low Potassium) Cause Interpreter
Find the cause of a low potassium. Enter the urine potassium — a spot potassium-to-creatinine ratio, or a 24-hour urine potassium — to decide whether the kidney is losing potassium or conserving it, then let the bicarbonate, the blood pressure and the urine chloride split the causes: diuretics, vomiting, mineralocorticoid excess, renal tubular acidosis, Bartter and Gitelman syndromes, magnesium depletion, diarrhoea, or a shift into cells.
Why is the potassium low?
Urine potassium + acid-base + blood pressure → causeA 48-year-old man with resistant hypertension has a potassium of 2.9 mmol/L and a bicarbonate of 31 mmol/L. Spot urine K:creatinine 4.2 mmol/mmol; urine chloride 45 mmol/L; no diuretic; magnesium normal.
Two questions, in order
2. If it is: diuretic acting? → acid-base → blood pressure → urine chloride → magnesium
- 1.5 mmol/mmol
- the ceiling expected when the kidney responds appropriately to hypokalaemia (Halperin 2017); 13 mmol/g is the same threshold rounded in the other unit
- 15 and 20 mmol/day
- two published 24-hour cut-offs; the band between them is shown as a disagreement
- TTKG
- the older transtubular potassium gradient, abandoned by its originators
Worked example
A 48-year-old man with resistant hypertension has a potassium of 2.9 mmol/L and a bicarbonate of 31 mmol/L. Spot urine K:creatinine 4.2 mmol/mmol; urine chloride 45 mmol/L; no diuretic; magnesium normal.
Ratio 4.2 mmol/mmol is well above 1.5 → the kidney is losing potassium
No diuretic acting, so the loss is not explained by a drug
Bicarbonate 31 → metabolic alkalosis
Hypertension with renal potassium loss and alkalosis → mineralocorticoid excess; measure renin and aldosterone
Is the kidney losing potassium?
| Test | Kidney conserving | Renal loss | Source |
|---|---|---|---|
| Spot K:creatinine, mmol/mmol | Below 1.5 | 1.5 or more | Halperin 2017 |
| Spot K:creatinine, mmol/g | Below 13 | 13 or more | Leiva-Murillo 2025, citing Palmer and Clegg 2019 |
| 24-hour urine K | Below 15 mmol/day | 20 mmol/day or more | Leiva-Murillo 2025; Medscape workup (20) |
Renal potassium loss: splitting the causes
| Acid-base | Blood pressure / urine chloride | Think of |
|---|---|---|
| Acidosis | Any | Renal tubular acidosis, ketoacidosis, acetazolamide |
| Alkalosis | High blood pressure | Primary aldosteronism, renovascular disease, Cushing’s, liquorice, Liddle |
| Alkalosis | Normal BP, urine chloride low | Vomiting, gastric drainage |
| Alkalosis | Normal BP, urine chloride high | Diuretics, Bartter, Gitelman, magnesium depletion |
Why this page does not use the TTKG
A low potassium (hypokalaemia, or hypokalemia in US spelling) has three mechanisms: potassium lost through the kidney, potassium lost through the gut or never taken in, and potassium that has simply moved into cells. The treatment differs for each, so the first question is always what the kidney is doing. A spot urine potassium-to-creatinine ratio answers it in one sample; dividing by creatinine cancels out how concentrated the urine happens to be. A ratio below 1.5 mmol/mmol — 13 mmol per gram of creatinine, the same threshold rounded in the other unit — means the kidney is conserving as it should. A 24-hour urine potassium does the same job more slowly; below 15 mmol a day is conservation on every reading, and sources place the renal-loss threshold between 15 and 20.
The transtubular potassium gradient was the standard tool for this for twenty years, and its own originators have disowned it. The TTKG assumes that little solute is reabsorbed after the cortical collecting duct, so that urine osmolality can correct for water removal. Kamel and Halperin showed in 2011 that a large amount of urea is reabsorbed in the medullary collecting duct and recycled, which invalidates that assumption, and in 2017 Halperin wrote plainly: “We now recommend the use of the K+/creatinine ratio.” The site’s TTKG calculator says the same, and this page works from the urine potassium-to-creatinine ratio calculator.
Once renal loss is established, the bicarbonate and the blood pressure do most of the sorting. Acidosis means renal tubular acidosis or ketoacidosis. Alkalosis with hypertension means too much mineralocorticoid. Alkalosis with a normal blood pressure is vomiting if the urine chloride is low, and diuretics, Bartter or Gitelman syndrome or magnesium depletion if it is high. Redistribution is a separate branch: insulin, β2-agonists, refeeding and periodic paralysis lower the potassium with a conserving kidney, and replacement can overshoot when the potassium comes back out of cells.
Two traps. A diuretic taken in the last day or two makes every urine test show renal loss. And a very high white cell count can lower a potassium in the tube (pseudohypokalaemia) if the sample stands. This page supports clinical judgement and does not replace it.
Frequently asked questions
What urine potassium level means renal potassium loss?
A spot potassium-to-creatinine ratio of 1.5 mmol/mmol or more (13 mmol/g or more), or a 24-hour urine potassium above about 15 to 20 mmol/day, in a patient who is hypokalaemic. Sources differ on the exact 24-hour figure.
Is the TTKG still used?
It should not be. Its originators, Kamel and Halperin, showed that urea recycling in the medullary collecting duct invalidates its central assumption, and Halperin now recommends the urine potassium-to-creatinine ratio instead.
Is a spot urine or a 24-hour urine better for hypokalaemia?
The spot potassium-to-creatinine ratio is preferred for speed and performs nearly as well as the 24-hour collection, which is slower and often incomplete.
Why check magnesium in hypokalaemia?
Low magnesium increases renal potassium loss, and the potassium will not stay corrected until the magnesium is replaced.
Related calculators
References
- Halperin ML. Assessing the renal response in patients with potassium disorders: a shift in emphasis from the TTKG to the urine K+/creatinine ratio. Afr J Nephrol. 2017;20(1):22–24. doi:10.21804/20-1-2453.
- Kamel KS, Halperin ML. Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: an hypothesis with clinical implications. Curr Opin Nephrol Hypertens. 2011;20(5):547–554.
- Leiva-Murillo EA, Bechtold-Javier E, Candela-Parrilla P, Matas-García A. Finding the cause of severe hypokalemia: a 4-step approach. Cleve Clin J Med. 2025;92(12):748–756.
- Palmer BF, Clegg DJ. The use of selected urine chemistries in the diagnosis of kidney disorders. Clin J Am Soc Nephrol. 2019;14(2):306–316.
- Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a KDIGO Controversies Conference. Kidney Int. 2020;97(1):42–61.
- Medscape Reference. Hypokalemia workup: urine potassium and other electrolytes. Accessed September 2026.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.