A 58-year-old man with hypertension and chronic kidney disease (eGFR 35 mL/min/1.73m²) presents with ankle edema and dyspnea on exertion. His current medications include lisinopril and amlodipine. On examination, BP is 158/96 mmHg, JVP elevated, and bilateral ankle edema present. Serum K⁺ is 5.8 mEq/L, Na⁺ is 138 mEq/L, and Cr is 2.1 mg/dL. Which diuretic is most appropriate to initiate for fluid overload management in this patient?

## Clinical Context This patient has: - **Chronic kidney disease (CKD stage 3b)** with eGFR 35 - **Hyperkalemia** (K⁺ 5.8 mEq/L) — already on ACE inhibitor - **Fluid overload** (edema, dyspnea, elevated JVP) - **Hypertension** inadequately controlled ## Why Furosemide Is Correct **Key Point:** Loop diuretics (furosemide) are the diuretics of choice in moderate-to-advanced CKD with fluid overload, because they: 1. Remain effective even at low GFR (secreted into tubular lumen via organic anion transporter) 2. Produce potent natriuresis and diuresis 3. Do NOT worsen hyperkalemia (actually promote K⁺ excretion) 4. Can be used safely in CKD stage 3–5 **High-Yield:** Loop diuretics work in CKD because they are actively secreted into the proximal tubule, bypassing the need for glomerular filtration. Thiazides become ineffective when GFR < 30. **Clinical Pearl:** In this patient, furosemide will relieve fluid overload AND help lower serum K⁺ by increasing urinary potassium excretion — a dual benefit. ## Why Other Agents Fail | Diuretic | Problem in This Patient | | --- | --- | | **Spironolactone** | **Potassium-sparing agent** — contraindicated in hyperkalemia; will worsen K⁺ further. | | **Hydrochlorothiazide** | Thiazides lose efficacy at eGFR < 30; ineffective in this stage of CKD. Also worsens hyperkalemia and hyperglycemia. | | **Acetazolamide** | Carbonic anhydrase inhibitor; weak diuretic, causes metabolic acidosis, and worsens hyperkalemia. Not used for fluid overload. | **Mnemonic: LOOP in CKD** — Loop diuretics work in CKD; thiazides don't. ## Mechanism Furosemide inhibits the Na⁺-K⁺-2Cl⁻ cotransporter in the thick ascending limb, causing: - Massive Na⁺ and Cl⁻ loss → diuresis - Increased K⁺ secretion in collecting duct → lowers serum K⁺ - Reduced renal vascular resistance → maintains renal perfusion even in CKD [cite:KD Tripathi 8e Ch 18]