Since the demise of TTKG I have had to retrain my brain to determine if hypokalemia is due to renal wasting or extra-renal potassium losses (as well as intracellular shift). The is not so important in the evaluation of hyperkalemia as persistent hyperkalemia is always due to decreased renal clearance of potassium.
There are two methods of looking at renal potassium wasting, the first is Fractional Excretion of Potassium. Super easy calculation.
The values are from this Skeleton Key group article at the Renal Fellow Network. They pulled it from this study of 84 hypokalemic individuals: Fractional excretion of potassium in normal subjects and in patients with hypokalaemia. From the abstract:
The mean FEK+ in normal subjects was 8% (range 4-16%). FEK+ was positively correlated with serum potassium (r = 0.74, p < 0.0001) and inversely with serum creatinine (r = -0.51, p < 0.001). The mean FEK+ in patients with hypokalaemia of external origin was 2.8% (range 1.5-6.4%). On the contrary, the mean FEK+ in hypokalaemic patients in whom renal potassium loss was the main aetiologic factor for the pathogenesis of hypokalaemia was 15% (range 9.5-24%).
Even though the creatinine is measured in mg/dL and the potassium is measured in mEq/L the units don’t mess you up because the serum and urine creatinine units cancel each other out.
The other way to look at hypokalemia is urine potassium creatinine ratio. Just divide the urine potassium by the urine creatinine and if it is greater than 1.5 you have renal potassium wasting. But alas this only works if the urine creatinine is measured in mmol/L. I get urine creatinines in mg/dl, so to make this conversion you need to multiply urine creatinine by 88 to get micromol/L of creatinine and then divide it by 1000 to convert to mmol/L. In one step it looks like this:
The line in the sand of 2.5 comes from this study, Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis published in JAMA Internal Medicine.
