Diuretics

Key Points

  • Four diuretic classes: loop (most potent), thiazide (first-line for HTN), potassium-sparing, and osmotic
  • Each class acts on a different nephron segment to inhibit sodium/water reabsorption
  • Loop diuretics cause hypokalemia (potassium loss); potassium-sparing diuretics risk hyperkalemia (potassium retention)
  • Monitor daily weights (1 kg ≈ 1 liter fluid), electrolytes, and intake & output
  • Loop diuretics IV rapid push → ototoxicity risk
  • In pediatric congenital-cardiac pathways, diuretics are used to reduce pulmonary congestion/fluid overload with close kidney-function and electrolyte surveillance.

Drug Class Overview

Diuretics increase urinary output to treat edema, hypertension, heart failure, cirrhosis, and renal disease. All diuretics inhibit sodium and water reabsorption at specific nephron segments. Different classes are often used in combination for complementary effects.

Diuretic Classes

Loop Diuretics — Most Potent

Mechanism: Inhibit Na-K-2Cl (NKCC2) cotransporters in the thick ascending loop of Henle → loss of sodium, potassium, chloride, calcium, and magnesium → significant diuresis.

Agents: Furosemide (Lasix) — prototype; torsemide; bumetanide.

Key Dosing (Furosemide):

  • Edema: 20–80 mg orally daily; max 600 mg
  • IV/IM: 20–40 mg, may repeat in 2 hours
  • Acute pulmonary edema: 40 mg IV stat
  • Half-life: 1.5–2 hours; bioavailability oral ~50%

Indications: Heart failure, cirrhosis, renal disease, nephrotic syndrome, acute pulmonary edema, hypertension (combined with other agents).

Adverse Effects:

  • Hypokalemia (most common electrolyte imbalance) → cardiac dysrhythmia risk, digoxin toxicity
  • Hyponatremia, hypomagnesemia, hypocalcemia
  • Ototoxicity — especially with rapid IV infusion
  • Postural hypotension, dizziness
  • Hyperglycemia, metabolic alkalosis

Ototoxicity Risk

Furosemide administered as rapid IV push can cause permanent hearing loss. Administer IV furosemide no faster than 4 mg/minute (some sources: no more than 20 mg/min). Report tinnitus or hearing changes immediately.

Thiazide Diuretics — First-Line for Hypertension

Mechanism: Inhibit Na-Cl cotransporters in the distal convoluted tubule → sodium, chloride, and water excretion. Unlike loop diuretics, thiazides increase calcium reabsorption → useful adjunct for osteoporosis prevention, but can cause hypercalcemia.

Agents: Hydrochlorothiazide (HCTZ) — most common; chlorthalidone (48–72h duration); metolazone.

Key Dosing (Hydrochlorothiazide):

  • Hypertension: 25 mg orally daily; may increase to 50 mg/day
  • Edema: 25–100 mg orally daily

Indications: First-line antihypertensive; edema from heart failure, cirrhosis, renal disease; nephrolithiasis (calcium-containing stones — calcium reabsorption decreases urinary calcium).

Adverse Effects:

  • Hypokalemia → increases risk of digoxin toxicity
  • Hyperuricemia → gout exacerbations
  • Hyperglycemia (impaired insulin release)
  • Hyponatremia, hypercalcemia
  • Photosensitivity reactions, possible skin cancer risk with long-term use
  • Sodium-wasting pattern can produce hypovolemic/isotonic hyponatremia when sodium and water are both depleted.

Contraindication: Sulfonamide allergy (cross-reactivity possible).

Potassium-Sparing Diuretics — Weakest, Often Combined

Mechanism: Inhibit sodium reabsorption in collecting tubule while decreasing potassium and hydrogen ion secretion → sodium and water excreted, potassium retained.

Agents:

  • Spironolactone (Aldactone): Also blocks aldosterone (mineralocorticoid) receptors; heart failure; cirrhosis; resistant hypertension. RALES trial: 30% reduction in all-cause mortality in heart failure.
  • Eplerenone: More selective aldosterone antagonist; fewer hormonal side effects than spironolactone.
  • Amiloride, triamterene: Block sodium transporters directly (not aldosterone-dependent).

Key Dosing (Spironolactone):

  • Heart failure: 25–50 mg orally once daily (potassium <5 mEq/L required; creatinine clearance >30 mL/hr)
  • Hypertension: 25–100 mg/day
  • Edema: 100–200 mg/day

Indications: Combined with loop or thiazide diuretics to prevent hypokalemia; heart failure (NYHA II–IV); hyperaldosteronism.

Adverse Effects:

  • Hyperkalemia — most dangerous; fatal if severe
  • Spironolactone: gynecomastia, menstrual irregularities, impotence (androgen blockade side effects)
  • FDA Black Box Warning: Spironolactone may cause tumor development at high doses exceeding recommendations

Hyperkalemia Risk with Potassium-Sparing Diuretics

Avoid concurrent ACE inhibitors, ARBs, potassium supplements, or NSAID use. Avoid potassium-rich foods (bananas, oranges, avocado, potatoes) and potassium-based salt substitutes.

Osmotic Diuretics

Mechanism: Non-reabsorbable solutes (mannitol) pull water into the tubular lumen via osmosis → increased urinary output.

Indications: Increased intracranial pressure, increased intraocular pressure, acute oliguria, and prevention of acute kidney injury.

Route: IV infusion only (oral forms not effective for diuresis).

Nursing Assessment

Before Administration:

  • Verify current serum electrolytes (especially potassium — normal 3.5–5.0 mEq/L)
  • Obtain baseline weight; auscultate breath sounds (crackles = fluid overload)
  • Review renal function (BUN, creatinine) — impaired renal function reduces diuretic effectiveness
  • Check current medications for interactions: digoxin (loop/thiazide increase toxicity), ACE inhibitors/ARBs (potassium-sparing → hyperkalemia risk), NSAIDs (reduce diuretic effectiveness)

Ongoing Monitoring:

  • Daily weight at same time, same scale, same clothing — weight change >1–2 kg in 24h is clinically significant
  • Strict intake and output
  • Serum electrolytes (potassium, sodium, magnesium)
  • Blood pressure (orthostatic changes with aggressive diuresis)
  • Signs of electrolyte imbalance: muscle cramps (hypokalemia), palpitations, weakness
  • In pediatric CHD/heart-failure use, monitor weight and urine-output trends closely to evaluate preload reduction while avoiding renal hypoperfusion.

Patient Education:

  • Rise slowly from seated/lying position to avoid orthostatic hypotension
  • Loop/thiazide diuretics: increase dietary potassium (bananas, oranges, leafy greens, potatoes)
  • Potassium-sparing diuretics: avoid potassium supplements and potassium-rich foods
  • Report muscle cramps, excessive thirst, decreased urination, palpitations
  • Take in morning to avoid nocturia disrupting sleep

Self-Check

  1. Which diuretic class is most potent? Where in the nephron does it act?
  2. A patient taking furosemide also takes digoxin. What electrolyte imbalance increases digoxin toxicity risk?
  3. Which class of diuretics should NOT be combined with potassium supplements, and why?