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Causes of high and low potassium in urine
Last reviewed: 06.07.2025
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Reference values (norm) for potassium in urine are 25-125 meq/day (mmol/day).
The excretion of potassium by the kidneys is subject to complex regulatory systems. Potassium is not only filtered and reabsorbed in the kidneys, but also excreted by the renal tubules.
A study of potassium in urine allows, taking into account the amount of diuresis, to estimate the daily loss of this electrolyte. The results of this study are of great importance for resuscitated patients in serious condition when assessing the effectiveness of replacement therapy with potassium preparations.
Increased excretion of potassium in the urine is observed during the resorption of edema, the use of diuretics, chronic nephritis accompanied by polyuria, renal and diabetic acidosis. Increased excretion of potassium in the urine is observed during malnutrition, feverish conditions and intoxications, diabetic coma. Hyperfunction of the adrenal cortex with increased production of aldosterone is accompanied by the most pronounced excretion of potassium, which is called "potassium diabetes".
The amount of potassium in urine increases in renal hyperaminoaciduria, proximal tubular acidosis caused by a defect in the proximal tubules, metabolic acidosis, hemorrhagic fever with renal syndrome, nephropathy, pyelonephritis, acute tubular necrosis, hyperaldosteronism, Cushing's syndrome, Fanconi syndrome, alkalosis, administration of diuretics, etc.
Urinary potassium excretion decreases in glomerulonephritis, chronic pyelonephritis, extrarenal uremia, hyperaldosteronism (Addison's disease), acidosis and hypoxia.
Determination of the potassium and sodium content in urine plays an important role in the differential diagnosis of prerenal and renal forms of acute renal failure. In the prerenal form of acute renal failure, the kidneys respond to a decrease in blood perfusion by increased conservation of sodium and water. Sodium conservation is manifested by a low sodium content in the urine, as well as an increase in the K/Na coefficient in the urine by 2-2.5 times (the norm is 0.2-0.6). The opposite relationship is observed in the renal form of acute renal failure.
To diagnose hyperkalemia due to aldosterone deficiency or resistance, as well as non-renal causes, the transtubular potassium gradient (TKG) is calculated - an indicator of potassium secretion by the distal nephron: TPG = (Km / Ks ) × (Osm s / Osm m ), where Km is the concentration of potassium in the urine; Ks is the concentration of potassium in the serum; Osm s is the osmolarity of the serum; Osm m is the osmolarity of the urine. Normally, the TPG is 6-12; if it is above 10, then aldosterone deficiency or resistance to it can be excluded and a non-renal cause of hyperkalemia can be sought; a TPG value of less than 5 suggests aldosterone deficiency or resistance to it. A TPG value above 10 indicates hypoaldosteronism, the absence of TPG changes indicates a defect (resistance) of the renal tubules. Patients with this defect are resistant to any potassium-sparing diuretics.