A 42-year-old woman with systemic lupus erythematosus on mycophenolate mofetil presents with fatigue and muscle cramps. Laboratory findings: serum potassium 6.8 mEq/L, eGFR 35 mL/min/1.73m², serum bicarbonate 18 mEq/L, and serum creatinine 1.9 mg/dL. ECG shows normal sinus rhythm with no peaked T waves. She is haemodynamically stable and denies chest pain. What is the most appropriate next step in management?

Explanation

## Clinical Assessment This patient has **asymptomatic hyperkalemia without ECG changes** in the setting of **CKD stage 3b with metabolic acidosis**. The absence of cardiac membrane instability changes the management priority from emergency cardioprotection to **identification of the cause and initiation of K⁺-lowering therapy**. ## Hyperkalemia: Symptomatic vs Asymptomatic Management | Feature | Symptomatic + ECG Changes | Asymptomatic or Normal ECG | |---|---|---| | **Immediate priority** | Cardiac stabilization (calcium) | Identify cause; lower K⁺ | | **First intervention** | IV calcium gluconate | Address underlying cause | | **Potassium-lowering agents** | Insulin, β₂-agonist, bicarbonate | Diuretics, binders, dialysis | | **Urgency of dialysis** | Within hours | Within 24–48 hours if eGFR < 15 | ## Diagnostic Approach to Hyperkalemia ```mermaid flowchart TD A[Hyperkalemia K+ > 5.5]:::outcome --> B{ECG changes?}:::decision B -->|Yes| C[Cardiac instability]:::urgent C --> D[IV Calcium gluconate]:::action B -->|No| E[Assess cause]:::decision E -->|Medication-induced<br/>ACE-I/ARB/NSAID/K-sparing| F[Discontinue offending agent]:::action E -->|Acidosis| G[Correct pH with bicarbonate]:::action E -->|Volume depletion| H[IV saline + diuretic]:::action E -->|Renal insufficiency| I[Dialysis if eGFR < 15]:::action F --> J[Add K+-lowering agent:<br/>Loop diuretic + binder]:::action G --> J H --> J I --> J ``` ## Management of This Patient **Key Point:** This patient has **three treatable causes of hyperkalemia:** 1. **Metabolic acidosis** (HCO₃⁻ = 18) — shifts K⁺ out of cells 2. **CKD stage 3b** (eGFR 35) — reduced renal K⁺ excretion 3. **Likely ACE inhibitor or ARB use** (common in SLE with renal involvement) — reduces aldosterone-mediated K⁺ secretion **High-Yield:** In asymptomatic hyperkalemia, the **first step is to identify and address the underlying cause**, not to rush into dialysis. ### Immediate Actions: 1. **Review medications:** Discontinue ACE inhibitor, ARB, NSAIDs, potassium-sparing diuretics, or trimethoprim if present 2. **Initiate loop diuretic** (e.g., furosemide 40 mg IV) — increases renal K⁺ excretion 3. **Start sodium polystyrene sulfonate** (Kayexalate) 15 g three times daily — binds K⁺ in the GI tract 4. **Correct metabolic acidosis** — sodium bicarbonate or optimise renal function 5. **Repeat serum potassium in 4–6 hours** to assess response 6. **Arrange haemodialysis within 24 hours** if K⁺ remains > 6.5 despite above measures or eGFR < 15 **Clinical Pearl:** Mycophenolate mofetil itself does not directly cause hyperkalemia, but SLE patients on MMF often also receive ACE inhibitors or ARBs for lupus nephritis — this is the likely culprit. **Mnemonic: CAKD for Hyperkalemia Causes** - **C** = Cellular shift (acidosis, insulin deficiency, β-blocker use) - **A** = Addison's disease, ACE-I/ARB - **K** = Kidney disease (CKD, AKI) - **D** = Drugs (NSAIDs, K-sparing diuretics, trimethoprim) [cite:Harrison 21e Ch 280]