Diuretics

Core Concepts

A quick nephron map

The nephron is the kidney's functional unit; each segment reabsorbs different solutes:

1. Proximal convoluted tubule (PCT) — reabsorbs the bulk of filtered sodium and water.
2. Loop of Henle — thick ascending limb — reabsorbs sodium, potassium, and chloride together via a Na-K-2Cl cotransporter and builds the gradient that concentrates urine.
3. Distal convoluted tubule (DCT) — reabsorbs sodium and chloride via a Na-Cl cotransporter.
4. Collecting duct — fine-tunes sodium and water; aldosterone acts here (mineralocorticoid receptors) to retain sodium and excrete potassium, and the epithelial sodium channel (ENaC) is the final sodium entry point.

Each diuretic class blocks reabsorption at one of these sites.

Loop diuretics: the heavy hitters

Loop diuretics (e.g., furosemide, torsemide, bumetanide — verify the formulary) block the Na-K-2Cl cotransporter in the thick ascending limb. Because that site handles a large sodium load, they are the most potent class and the mainstay for acute congestion. Their "high ceiling" means the effect keeps rising with dose (up to a point) rather than plateauing quickly.

Consequences that follow from the mechanism:

• Electrolyte losses: potassium, sodium, magnesium, and calcium (calcium excretion increases — opposite of thiazides).
• Volume depletion: vigorous diuresis can drop blood pressure and worsen kidney function if fluid is removed faster than the circulation tolerates.
• Other effects to monitor: increased uric acid (gout flares), blood-sugar effects in people with diabetes (verify current labeling), and ototoxicity (hearing disturbance) linked to rapid administration or high doses — a reason these drugs are given carefully per orders.

Thiazide diuretics: the steady workhorses

Thiazide-type diuretics block the Na-Cl cotransporter in the distal convoluted tubule. They are less potent — a "low ceiling" class whose effect plateaus at modest doses — and are classic antihypertensives (Chapter 18). In heart failure they are used for milder congestion or, in resistant cases, combined with a loop diuretic for "sequential nephron blockade": blocking two sites in series makes the kidney excrete far more sodium than either drug alone.

Electrolyte signature — the mirror image of loop diuretics in one key way:

• Hypokalemia and hyponatremia are risks (like loop diuretics).
• *Calcium reabsorption* increases** — thiazides raise calcium, the opposite of loop diuretics. A classic exam point.
• Uric acid and blood sugar effects resemble loop diuretics; thiazides are classically described as less effective when kidney function is severely reduced — verify current guidance rather than applying an absolute rule.

Potassium-sparing diuretics: weak diuresis, strong electrolyte effects

Potassium-sparing diuretics act in the collecting duct, which handles only a small fraction of sodium — so their diuretic effect is weak and their value is in what they don't do: waste potassium. Two mechanisms:

• ENaC blockers (e.g., amiloride, triamterene) block the epithelial sodium channel directly, so less sodium is reabsorbed and less potassium is traded for it.
• Mineralocorticoid receptor antagonists (MRAs) (spironolactone, eplerenone) block aldosterone's action (Topic 2). In HFrEF they are used not for diuresis but for their mortality benefit and remodeling effects.

The shared risk is hyperkalemia — especially with ACE inhibitors/ARBs, kidney impairment, or potassium supplements. The mirror-image point: loop and thiazide diuretics tend to lower potassium; potassium-sparing diuretics can raise it.

Nursing monitoring and teaching

• Daily weight is the monitor of monitors. Same time, same scale, same clothing; rapid gain signals fluid accumulation and is reported per orders — the single most valuable home habit.
• Intake and output in acute settings quantifies the response to therapy.
• Orthostatic vital signs: dizziness on standing suggests volume depletion; hypotension may require prescriber review.
• Labs per orders: potassium, sodium, kidney function, sometimes magnesium; the expected pattern depends on the class (loop/thiazide → hypokalemia risk; potassium-sparing → hyperkalemia risk).
• Signs to report: dizziness, weakness, muscle cramps, palpitations, severe thirst, decreased urine output, or rapid weight change — either direction.
• Teaching: take the drug as scheduled; discuss potassium supplements and salt substitutes (some contain potassium) with the provider or pharmacist; report illness with poor intake; never adjust the dose on your own.

Common Confusions