My team was consulted for acute kidney injury (AKI) and hyperkalemia. Before we saw the patient they had already been given the standard, calcium, bicarb, and insulin/glucose cocktail. This had no effect. Potassium went from 6.4 to 6.4.
The patient was still making urine. The AKI was due to emergency surgery with an impressive estimated blood loss (translation: blood loss measured in liters). We gave a liter of NS, 80mg of IV furosemide and 0.2 mg of oral fludrocortisone. Potassium went from 6.4 to 3.4 despite a further increase in the serum creatinine.
Remember to use the kidney for treating hyperkalemia. Even in AKI you can get impressive results.
Renal clearance of potassium is entirely dependent on the cortical collecting duct, specifically the principal cells. It is a multi-step process:
- reabsorption sodium down its chemical gradient through eNaC
- The chemical gradient to allow sodium resorption is generated and maintained by the Na-K-ATPase
- Movement of sodium without an anion(or a cation going in the opposite direction creates a negative charge in the tubular fluid which pulls potassium down an electrical and chemical gradient from the cells into the tubule. This occurs through ROMK and BIGK.
That is how potassium is excreted but, how is potassium regulated? There are two primary components to regulation:
- Aldosterone stimulates the transcription of all three transporters (ENaC, Na-K-ATPase, and ROMK) as well as transcribing versions of the proteins which are more active.
- Tubular flow. Increased distal sodium delivery provides plenty of sodium to be reabsorbed into the principal cell providing the negative charge, as well as washes away any secreted potassium to maintain the chemical gradient favoring potassium excretion.
The medical management we provided takes care of both aspects of potassium regulation, the furosemide and saline makes sure there is a robust supply of sodium delivered distally and the fludrocortisone makes sure there is ample aldosterone activity to assist with potassium clearance.