NEPHRO 17: CKD Hyperkalemia

Learning Objective 1: Pathophysiology and Incidence of Hyperkalemia in CKD

1. What is Potassium and Why Does it Matter?

   • Potassium (K⁺): A key mineral your body uses to help muscles (including the heart) contract and nerves send signals.

   • Where is it? About 98% of potassium is inside your cells, mainly in muscles, while 2% is in the blood.

   • Balance is Everything: The balance of potassium inside and outside the cells affects how muscles and nerves work (resting membrane potential).

2. How Does the Body Handle Potassium?

   • Intake: You get potassium from food, and it’s absorbed in your intestines.

   • Excretion: Most potassium is removed by your kidneys (in the urine). A small amount (~10%) is removed through the colon, but this becomes more important if the kidneys don’t work well.

3. What Happens in CKD?

   • In chronic kidney disease (CKD), the kidneys lose the ability to excrete potassium properly, leading to hyperkalemia (high potassium levels).

   • CKD patients adapt by increasing potassium elimination through the gut and using hormones (like aldosterone) to shift potassium into cells.

4. Incidence in CKD:

   • Hyperkalemia is common in CKD patients. About 21-37% of hemodialysis (HD) patients and 10-36% of peritoneal dialysis (PD) patients have potassium >5.5 mmol/L.

   • Hyperkalemia increases the risk of cardiovascular complications (e.g., arrhythmias) and mortality.

Learning Objective 2: Special Considerations for CKD Patients with Hyperkalemia

1. Causes of Hyperkalemia:

   • Medications: ACE inhibitors, ARBs, potassium-sparing diuretics (like spironolactone), and potassium supplements can worsen hyperkalemia.

   • Other Factors:

     • Acidosis: When blood becomes too acidic, potassium shifts out of cells into the blood.

     • Diabetes: Insulin helps move potassium into cells. Poor blood sugar control can worsen hyperkalemia.

2. Symptoms of Hyperkalemia:

   • Mild hyperkalemia often has no symptoms, but severe cases can cause:

     • Muscle weakness or paralysis.

     • Heart issues: Arrhythmias, slowed conduction (seen on ECG as peaked T waves, widened QRS, or sine wave pattern).

3. Adaptive Mechanisms in CKD:

   • CKD patients may develop cardiac tissue adaptations (e.g., reduced sensitivity to potassium-induced arrhythmias).

   • The body increases potassium elimination through the gut, shifts potassium into cells using hormones, and produces more aldosterone.

Learning Objective 3: Therapeutic Plan for Hyperkalemia in CKD

Treatment of Acute Hyperkalemia

1. Stabilize the Heart:

   • IV Calcium (e.g., calcium gluconate): Protects the heart from dangerous arrhythmias for ~30–60 minutes.

2. Shift Potassium into Cells:

   • Insulin with Dextrose: Moves potassium into cells within 10-20 minutes. Lasts 4–6 hours.

   • Beta-agonists (e.g., salbutamol): Also shift potassium into cells (less common).

3. Remove Potassium:

   • Diuretics: Help the kidneys excrete potassium if kidney function is still present.

   • Potassium Binders: Bind potassium in the gut and remove it through stool. Examples include sodium polystyrene sulfonate (SPS), patiromer, and sodium zirconium cyclosilicate (Lokelma).

   • Dialysis: Most efficient for removing potassium in severe cases.

4. Address the Cause:

   • Treat issues like acidosis, hyperglycemia, or medication changes contributing to hyperkalemia.

Treatment of Chronic Hyperkalemia

• Step 1: Identify Causes:

  • Review medications (e.g., ACEi/ARB) and adjust doses.

  • Look for diet issues (e.g., high potassium foods like bananas, potatoes).

• Step 2: Correct Reversible Factors:

  • Manage blood sugar (in diabetes).

  • Treat metabolic acidosis with bicarbonate.

• Step 3: Potassium Binders for Long-term Control:

  • Newer binders like patiromer and Lokelma are safer and more effective for chronic hyperkalemia than older options like SPS.

• Step 4: Regular Monitoring:

  • Check potassium levels and adjust treatment as needed.