Diuretics

A deliberately narrow role: volume overload in the oliguric phase, typically high-dose IV furosemide. Diuretics do not treat the kidney injury and have no role in converting oliguric to non-oliguric AKI — and remember that over-diuresis is itself a cause of pre-renal AKI, diuretic use worsens prognosis, and diuretics confound FENa. Overload refractory to diuretics means dialysis, not more diuretic.

The answer to CKD’s salt-and-water retention: many patients benefit from a loop diuretic before escalating other antihypertensives (per StatPearls) — one drug hitting both the volume overload and the hypertension it causes. Its limit defines the endgame: fluid overload refractory to diuretics is an indication for dialysis.

Ascites is aldosterone’s disease: splanchnic vasodilation fools the kidneys into RAAS activation, so therapy is spironolactone-based — the aldosterone antagonist is the foundation, with furosemide added in a 100 mg : 40 mg ratio. First-line together with the 2,000 mg sodium restriction. Monitor weight, electrolytes (K⁺ moves both ways), BUN/creatinine — because over-diuresis dehydrates the patient into encephalopathy.

The double-edged class of this chapter: diuretics are a leading cause of hypokalemia, hyponatremia, and hypomagnesemia — and simultaneously a treatment used to promote renal excretion of potassium in hyperkalemia and magnesium in hypermagnesemia (with saline). Every diuretic order implies an electrolyte-monitoring order.

The loop diuretic is the first pharmacologic step for the volume overload that drives the hypertension, not an afterthought to it. "Loop diuretics may be administered to excrete excess sodium and water retained in the body," and the sequencing rule is explicit: antihypertensives are added only for blood pressure that stays elevated "despite dietary salt, fluid restriction, and loop diuretics." That ordering is the whole logic of nephritic hypertension — the pressure is a volume problem first, so removing the volume is the first-line treatment. The same applies in post-streptococcal disease, where "restriction of dietary sodium intake and loop diuretics may be used to manage hypervolemia and hypertension," with calcium channel blockers added for additional control. Watch the electrolytes as the diuresis proceeds, since hyperkalemia, hyperphosphatemia and hypocalcemia are already listed complications of the underlying disease.

Acetazolamide (a carbonic anhydrase inhibitor) — narrow role. StatPearls: it "decreases CSF secretion by the choroid plexus and hence used in the treatment of hydrocephalus. It is mostly used in pseudotumor cerebri." In NPH, "Carbonic anhydrase inhibitors and serial drainage lumbar punctures have a role only in nonsurgical candidates." Surgery, not medicine, is the main treatment. No doses here.

The osmotic arm: mannitol raises plasma tonicity, and because it cannot cross the intact blood–brain barrier, it draws water out of the brain parenchyma into the vessels for renal excretion — FDA-approved for cerebral edema, first-line alongside hypertonic saline for refractory intracranial hypertension and impending herniation. ICP dosing 0.25–1 g/kg IV, onset 5–10 min, lasting ~6 h. Check osmolality every 4–6 h and hold at ≥ 320 mOsm; watch for hypovolemia, AKI, and rebound cerebral edema with repeated dosing; contraindicated in anuria, severe dehydration, pulmonary edema, and active intracranial bleeding.

[Ménière’s] NIDCD: "Limiting dietary salt to 1,500-2,000 milligrams per day and taking a diuretic" may help control symptoms. (This is NIDCD’s diet target, not a drug dose.)

Symptom control, not disease control — loop diuretics are the primary agents for the edema and they do nothing about the protein leak. The disorder-specific trap is that the drug cannot work without oncotic pressure to pull the fluid back into the vessel: achieving satisfactory diuresis is hard once serum albumin falls below 1.5 g/dL, and an albumin infusion is sometimes given alongside. The second trap is direction of error — because volume status in nephrotic syndrome may be low or high, over-diuresis is a named precipitant of acute kidney injury, so doses need continual reassessment as albumin and volume shift.

Diuretics appear in this disorder pair in two opposite and counter-intuitive roles. In SIADH, a loop diuretic — furosemide 20 mg twice daily — is added for persistent hyponatremia specifically when urine osmolality is above 500 mOsm/kg, that is, when the urine is too concentrated for fluid restriction alone to work; it blunts the medullary concentrating gradient so free water is lost alongside the sodium. In AVP-R (nephrogenic DI), the paradox runs the other way: a thiazide diuretic reduces urine output. It induces mild hypovolemia that enhances proximal sodium and water reabsorption, so less water is delivered distally to the collecting duct where ADH cannot act anyway. The counter-warning belongs here too — thiazides are themselves a common cause of hyponatremia, and diuretic use is one of the reasons a urine sodium can exceed 30 mEq/L, so a high urine sodium in a patient on a thiazide must not be read as SIADH.

Timing. Diuretics can cause or worsen leaks; Open RN: "scheduling prescribed diuretic medication in the morning or early afternoon" helps.

Symptom relief for the congestion every lesion eventually produces — pulmonary venous congestion and peripheral edema in MS, heart-failure symptoms in AS, AR, and MR. They are not disease-modifying: no diuretic changes a valve. In aortic stenosis avoid excessive volume depletion — the thick, stiff, preload-dependent LV needs filling pressure to push blood through the fixed valve, and over-diuresis drops cardiac output and blood pressure.

Slow heart rate & lower BP by blocking β-adrenergic receptors. Watch for bradycardia.

Lower BP by blocking angiotensin conversion. Classic dry cough & angioedema risk.

Lower LDL cholesterol via HMG-CoA reductase inhibition. Monitor for myopathy.

Injectable antibodies that protect the liver’s LDL receptors, cutting LDL cholesterol by about half and lowering cardiovascular events. Given subcutaneously every 2–4 weeks.

PPAR-α agonists that mainly lower triglycerides — used with diet for severe hypertriglyceridemia — with muscle, gallbladder, liver and kidney risks, highest for gemfibrozil combined with a statin.

Non-absorbed resins that trap bile acids in the gut, forcing the liver to use cholesterol and pull LDL from the blood. Constipation, drug binding and rising triglycerides are the issues to manage.