Urine Potassium-Creatinine Ratio Calculator
Urine Potassium-Creatinine Ratio Calculator
Work out the spot urine potassium-creatinine ratio in mmol/mmol and mmol/g, and read it against the 13 mmol/g threshold that separates renal potassium wasting from gut losses and transcellular shift.
Urine Potassium-Creatinine Ratio
Potassium ÷ creatinineUrine potassium 54 mmol/L, urine creatinine 8 mmol/L
Formula
Ratio (mmol/g) = ratio (mmol/mmol) × 8.84
Renal potassium wasting: > 13 mmol/g, which is > 1.5 mmol/mmol
- × 8.84
- converts per-mmol to per-gram of creatinine, because 1 g of creatinine is 1000 ÷ 113.12 = 8.84 mmol. The two thresholds quoted in the literature — 1.5 mmol/mmol and 13 mmol/g — are the same number in different clothes, not two competing cutoffs
- why divide at all
- a spot urine potassium of 15 mmol/L means renal conservation in a concentrated sample and renal wasting in a dilute one. Creatinine is excreted at a near-constant rate, so dividing by it removes the water and leaves the excretion
- 13 mmol/g
- the threshold above which renal potassium loss is inappropriate in a hypokalaemic patient (1.5 mmol/mmol; Halperin 2017). The 2020 KDIGO controversies conference used a higher figure, above 2.5 mmol/mmol (22 mmol/g), in its hypokalaemia algorithm to point to a tubulopathy, which is why this page bands the space between them as equivocal rather than picking a winner
- what it cannot do
- distinguish a diuretic from hyperaldosteronism from Gitelman syndrome. It tells you which side of the gut wall the potassium is going, and nothing more. The blood pressure, the bicarbonate and the magnesium do the rest
- 24-hour equivalent
- more than 30 mmol of potassium per day in the face of hypokalaemia is inappropriate renal loss. The ratio exists because that collection is rarely available when the decision has to be made
Worked example
Urine potassium 54 mmol/L, urine creatinine 8 mmol/L
54 ÷ 8 = 6.75 mmol/mmol
6.75 × 8.84 = 60 mmol per gram of creatinine
Far above 1.5 mmol/mmol (13 mmol/g) → renal potassium wasting
Next: blood pressure, bicarbonate, magnesium and a diuretic history — the ratio has done all it can
Reading the ratio in a hypokalaemic patient
| Ratio | Per gram | Reading | Where to look next |
|---|---|---|---|
| < 1.5 mmol/mmol | < 13 mmol/g | Appropriate conservation | Gut losses, poor intake, or a transcellular shift — insulin, beta-2 agonists, refeeding, periodic paralysis |
| 1.5 – 2.5 mmol/mmol | 13 – 22 mmol/g | Equivocal | Do not decide on the ratio. Acid-base, blood pressure, magnesium, drug history; a 24-hour potassium if it matters |
| > 2.5 mmol/mmol | > 22 mmol/g | Renal wasting | Diuretics, vomiting, hyperaldosteronism, renal tubular acidosis, Bartter or Gitelman syndrome, magnesium depletion |
Splitting renal potassium wasting once the ratio is high
| Blood pressure | Acid-base | Likely cause |
|---|---|---|
| Normal or low | Metabolic alkalosis | Diuretics, vomiting (urine chloride low), Bartter or Gitelman syndrome, magnesium depletion |
| Normal or low | Metabolic acidosis | Renal tubular acidosis type 1 or type 2, amphotericin, toluene |
| Raised | Metabolic alkalosis | Primary hyperaldosteronism, renal artery stenosis, Cushing syndrome, liquorice, Liddle syndrome, apparent mineralocorticoid excess |
| Any | Normal | Recovering acute tubular injury, post-obstructive diuresis, osmotic diuresis |
Which side of the gut wall is the potassium going?
Hypokalaemia has three mechanisms — potassium lost through the kidney, potassium lost through the gut, and potassium that has simply moved inside cells — and the treatment differs for each. The spot urine potassium-creatinine ratio answers the first part of that question in one sample. Dividing by creatinine is what makes a spot sample interpretable: a urine concentration on its own says as much about how much the patient drank as about what the kidney did. A urine potassium of 15 mmol/L in a patient passing 400 mL a day is avid conservation; the same 15 mmol/L in a patient passing 4 litres is substantial loss. Creatinine, excreted at a near-constant rate, is the denominator that cancels the water out.
The threshold most often quoted is 13 mmol per gram of creatinine, above which renal potassium loss is inappropriate in a hypokalaemic patient. Because one gram of creatinine is 8.84 mmol, that is the same as 1.5 mmol/mmol — the two figures in the literature are one threshold expressed two ways, and a ratio of 1.5 mistaken for the 13 looks like tight conservation when it is in fact the cutoff. A second, more demanding figure of 2.5 mmol/mmol (22 mmol/g) is the one the 2020 KDIGO controversies conference used, in its hypokalaemia algorithm, to point to a tubulopathy in a normotensive patient with no obvious cause, so this page treats the space between them as genuinely equivocal rather than declaring a winner.
A low ratio in a hypokalaemic patient moves the search outside the kidney: diarrhoea, laxatives, a high-output stoma, poor intake, or a transcellular shift driven by insulin, a beta-2 agonist, refeeding or periodic paralysis. The shift group matters disproportionately, because total body potassium may be normal and enthusiastic replacement will overshoot when the potassium returns to the extracellular space. A high ratio says the kidney is the route, and then the ratio has finished its work: blood pressure, serum bicarbonate, urine chloride and a drug history separate a thiazide from primary hyperaldosteronism from Gitelman syndrome, and none of those can be read off the ratio itself.
Two practical traps. First, the ratio is uninterpretable during or shortly after a diuretic dose, which is itself the commonest cause of renal potassium wasting — the test then confirms the drug rather than finding a disease. Second, check the magnesium before chasing anything exotic: hypomagnesaemia causes renal potassium wasting directly, and the potassium will not stay up until the magnesium is replaced. This calculator supports a clinician’s assessment and does not replace it.
Frequently asked questions
What urine potassium-creatinine ratio indicates renal potassium wasting?
More than 13 mmol per gram of creatinine, which is more than 1.5 mmol/mmol, is the threshold quoted in most reviews for inappropriate renal potassium loss in a hypokalaemic patient. The 2020 KDIGO controversies conference used above 2.5 mmol/mmol (22 mmol/g) to point to a tubulopathy, so values between the two are best treated as equivocal.
How do I convert the ratio between mmol/mmol and mmol/g?
Multiply mmol/mmol by 8.84 to get mmol per gram of creatinine, because one gram of creatinine is 1000 ÷ 113.12 = 8.84 mmol. So 1.5 mmol/mmol is 13 mmol/g. The two thresholds in the literature are the same number in different units, not two different cutoffs.
Why not just measure the urine potassium concentration?
Because a urine potassium concentration tells you as much about the patient’s fluid intake as about the kidney. Fifteen mmol/L is conservation in a concentrated urine and wasting in a dilute one. Creatinine is excreted at a near-constant rate, so dividing by it removes the dilution effect.
Is the ratio better than the transtubular potassium gradient?
For most purposes yes. The transtubular potassium gradient depends on assumptions about water reabsorption in the medullary collecting duct that do not reliably hold, and it needs paired osmolalities. The potassium-creatinine ratio needs one urine sample and is less sensitive to urine concentration.
Can the ratio be interpreted in a patient on diuretics?
Only with caution. A diuretic causes renal potassium wasting by design, so a high ratio confirms the drug rather than uncovering a disease. If a tubulopathy is genuinely suspected, the question usually needs the diuretic stopped, alongside magnesium, bicarbonate, urine chloride and blood pressure.
Related calculators
References
- Palmer BF, Clegg DJ. Physiology and pathophysiology of potassium homeostasis: core curriculum 2019. Am J Kidney Dis. 2019;74(5):682–695.
- 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. — source of the 1.5 mmol/mmol figure.
- 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. — Figure 3, source of the 2.5 mmol/mmol tubulopathy figure.
- Kardalas E, Paschou SA, Anagnostis P, et al. Hypokalemia: a clinical update. Endocr Connect. 2018;7(4):R135–R146.
- Viera AJ, Wouk N. Potassium disorders: hypokalemia and hyperkalemia. Am Fam Physician. 2015;92(6):487–495.
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.