Diuretic Therapy in Critically Ill

Source: Saengngammongkhol P. Ramathibodi Hospital 2025 + KDIGO AKI 2026 + ESC HF 2021 + ESICM Fluid Therapy 2025 (ICM 2025;51:1749–1763)


🪴 Part 1: Basic Renal Physiology — Sodium Handling

SegmentNa reabsorbTransporterกลไก
PCT60–70%NHE3, SGLT2, NaHCO₃ cotransporterParacellular + glucose/AA cotransport; volume-status dependent
TALH25–30%NKCC2ROMK recycles K⁺ → lumen+ → paracellular Ca²⁺/Mg²⁺ (claudin-16/19)
DCT10%NCC↑Ca²⁺ reabsorption (thiazide-sensitive)
Collecting duct10%ENaC • Na⁺/K⁺-ATPaseAldosterone-dependent; ADH → AQP2 (free water)

PCT reabsorption เพิ่มขึ้นใน edematous states (HF, cirrhosis) → ให้ diuretic ที่ออกฤทธิ์ downstream มีประสิทธิภาพลดลง — เหตุผลหลักของ diuretic resistance


💊 Part 2: Diuretic Classification & Pharmacology

แบ่ง 3 กลุ่ม:

  • Natriuretics: ลด Na⁺ reabsorption ที่ different tubular sites — Carbonic anhydrase inhibitor, Loop diuretic, Thiazide, K-sparing
  • Aquaretics: ยับยั้ง vasopressin receptor → ลด free water reabsorption (ไม่ใช่ natriuresis)
  • Osmotic diuretics: สร้าง osmotic force ใน tubule

2.1 Carbonic Anhydrase Inhibitor (Acetazolamide)

ยับยั้ง CA II (cytoplasm, 95%) และ CA IV (luminal border) → ขัดขวาง bicarbonate reclamation → HCO₃⁻ คั่งใน lumen → alkaline diuresis + Na⁺/K⁺ excretion

  • Dose: Oral 250–375 mg; IV 500 mg (ไม่มีในไทย); FENa ~4%
Clinical IndicationAdverse Effect
Idiopathic intracranial hypertensionAbnormal taste, GI distress
GlaucomaHypokalemia (ถ้าใช้นาน เสริม NaHCO₃)
Mountain sicknessProximal RTA (type 2)
Prophylaxis hypokalemic periodic paralysis type IPoor efficacy long-term: Braking phenomenon — Ca II absorb HCO₃⁻ 1/3, Na⁺ still reabsorb distally, metabolic acidosis → ↓filtered HCO₃⁻, TGF activation
Metabolic alkalosis จาก loop diuretic (ICU use)

2.2 Loop Diuretics

OOK ฤทธิ์โดย inhibit NKCC2 ที่ TALH (reabsorb 25–30% filtered Na⁺) → Natriuresis; ↓lumen+ potential → calciuresis/magnesiuresis; disrupts countercurrent multiplication → ↓medullary osmotic gradient → dilute urine (loss Na + free water) → risk of hyponatremia ต่ำกว่า thiazide

Loop diuretics ต้อง deliver ผ่าน OAT1/3 ที่ PCT-S2:

  • Competitors: Probenecid, Beta-lactam, Uremic organic anions
  • Hypoalbuminemia: ↑Vd, ↓diuretic delivery, albuminuria → ↓free drug ใน lumen
  • NSAIDs: ↓PGE2 → ลด loop diuretic action ที่ TALH
FurosemideBumetanideTorsemide
Oral bioavailability64% (variable)80–100%80–100%
Onset IV~5 min~5 min~5 min
2h1–1.5h3–6h
FENa%20–25%

Ceiling Doses Loop Diuretics:

ConditionFurosemide IVFurosemide POBumetanideTorsemide
GFR 20–5080–160 mg160 mg6 mg50 mg
GFR <20200 mg240 mg10 mg100 mg
Nephrotic (normal GFR)120 mg240 mg3 mg50 mg
Cirrhosis40–80 mg80–160 mg1 mg20 mg
Heart failure40–80 mg80–160 mg1 mg20 mg

2.3 Thiazide and Thiazide-like Diuretics

Inhibit NCC ที่ DCT → Natriuresis; ต่างจาก loop diuretics: ↑Ca²⁺ reabsorption (hypercalcemia); ↓Ca²⁺ excretion

HTCZ eGFR adjusted dose:

  • eGFR >50: 25 mg; eGFR 20–50: 50 mg; eGFR <20: 100 mg (เพิ่ม dose ตาม renal impairment)

ADR: Volume depletion/azotemia, Hypokalemia, Hypomagnesemia, Metabolic alkalosis, Hypercalcemia, Hyperuricemia, Hyperglycemia, Hyperlipidemia

Thiazide-induced Hyponatremia mechanisms:

  1. Reduced distal filtrate delivery (↓GFR, ↑PT reabsorption)
  2. Inhibition of NCC → impairs maximal dilution
  3. ↑Collecting duct water permeability: ADH-dependent (volume depletion → ↑ADH) + ADH-independent (↑luminal PGE2 จาก ↓PGT activity; SLCO2A1 variant)

Risk: Female, old age, low body mass, SLCO2A1 variant, excessive water intake


2.4 K-sparing Diuretics

Inhibit ENaC ที่ late distal tubule/collecting duct — 2 กลุ่ม:

  • ENaC inhibitors: Amiloride, Triamterene (direct channel block)
  • MRA: Spironolactone, Eplerenone, Finerenone (nonsteroidal MRA)

Block ENaC → ↓lumen negative potential → ↓K⁺ secretion (ROMK) + ↓H⁺ secretion (H⁺-ATPase) → Hyperkalemia + Type 4 RTA

DrugDoseIndication
Spironolactone25–50 mg PO16.5hCirrhotic ascites + loop (ratio 100:40), HFrEF, Resistant HTN
Eplerenone25–50 mg3–6hHFrEF (ลด gynecomastia)
FinerenoneNonsteroidal MRADiabetic nephropathy (ลด CV events, CKD progression)

ADR: Hyperkalemia (major), Gynecomastia (spironolactone>>eplerenone)


2.5 Vasopressin Receptor Antagonist (Aquaretics/Vaptans)

Inhibit V2 receptor ที่ cortical collecting duct → block vasopressin-stimulated AQP2 insertion → ↓free water reabsorption → electrolyte-free water excretion (ไม่เพิ่ม Na⁺ excretion — จึงเป็น aquaretic ไม่ใช่ natriuretic)

  • Indications: SIAD, Hypervolemic hyponatremia (ADHF, Cirrhosis, ใช้เฉพาะ Na <135), ADPKD
  • ADR: Hypernatremia (ถ้า monitor ไม่ดี), Transaminitis (tolvaptan)

2.6 Osmotic Diuretics

Free filtrated แต่ poorly reabsorbed → osmotic force ตลอดทั้ง nephron → ↓passive reabsorption

  • Drugs: Mannitol, Sorbitol, Glycerol
  • Indications: Cerebral edema (hepatic encephalopathy, severe head injury), Dialysis disequilibrium syndrome
  • ADR: Hypertonic hyponatremia (translocation) → hypernatremic dehydration; AKI (renal vasoconstriction); Osmotic nephrosis (tubular necrosis)

2.7 Pharmacology Comparison (ESC Heart Fail 2019)

AcetazolamideLoopThiazide-likeMRAAmiloride
SiteProximalTALHEarly DCTLate distal/CDLate distal/CD
Onset PO1h0.5–1h1–2.5h48–72h2h
FENa%4%20–25%5–8%2%2%
Oral bioavailabilityDose-dependentFurosemide 64%65–75%~90%30–90%

🔄 Part 3: Ultrafiltration (UF)

Principles

Convection ขับเคลื่อนด้วย transmembrane pressure (TMP) → solutes ถูก “dragged” ไปพร้อม water (solvent drag) เหมาะสำหรับ middle molecules (cytokines, β2-microglobulin); ต่างจาก diffusion ที่ขึ้นกับ concentration gradient (small solutes)

Modalities

ModalityBlood flow (mL/min)Fluid removal (mL/h)Notes
Intermittent UF250–4000–2000Widely available; hemodynamic instability risk
Continuous UF (SCUF/CVVH)50–1000–300Hemodynamically stable; CVVH allows Na/water dissociation
Peritoneal dialysisN/A0–500No venous access; hemostable; paediatrics
HD intermittent250–4000–2000Adds solute clearance
HD continuous50–1000–300Hemostable + solute clearance

UF Rate in CKRT

U-shaped relationship ระหว่าง UF rate กับ mortality (Nat Rev Nephrol 2021):

  • UF rate ต่ำเกินไป → organ oedema
  • UF rate สูงเกินไป → organ ischaemia
  • “Zone of safe UF”: 1–1.75 mL/kg/h = lowest mortality risk

Loop Diuretic vs Isolated UF

Loop DiureticsIsolated UF
NeurohormonalDirect RAAS/SNS activationNo neurohormonal activation
UrineHypotonicIsotonic plasma water removal
Na/water controlUnpredictablePrecise
ResistanceDevelops with timeRestores diuretic responsiveness
Electrolytes↓K⁺, ↓Mg²⁺No effect
Anticoagulationไม่ต้องการต้องการ

UF Trials (ESICM 2025)

ESICM 2025: Suggest AGAINST routine UF/extracorporeal fluid removal หลัง acute resuscitation phase without other RRT indication (Conditional, low certainty)

TrialnKey Finding
RAPID-CHF40NS; trend toward higher weight loss ใน UF
UNLOAD200UF>DT weight loss; NS renal function
CARRESS-HF188Sig ↑SCr ใน UF arm; Higher SAEs
CUORE56Sig ↑SCr ใน DT at 6mo
AVOID-HF224Higher SAEs in UF arm

🚧 Part 4: Diuretic Resistance

Definition

Inadequate clearance of edema despite adequate doses — ก่อน label ว่า resistant: exclude incorrect diagnosis, poor compliance, high sodium intake

Adaptation Mechanisms

Humoral/neuronal changes: ↑RAAS, ↑Sympathetic, ↑ADH, ↓PGE2 (PGE2 ปกติ inhibit NKCC2)

Short-term: Post-diuresis salt retention — ↓volume → ↑RAAS/SNS → enhanced Na⁺ reabsorption inter-dose (Braking Phenomenon graph)

Long-term — Nephron Remodeling:

  • DCT: ↑NCC expression
  • Principal cell: ↑ENaC expression
  • Intercalated cell: ↑Pendrin → ↑Na⁺/Cl⁻ reabsorption

Mechanisms of Diuretic Resistance

กลุ่มกลไก
PK limitationsGut edema → ↓absorption; Hypoalbuminemia → ↓delivery; OAT competition (CKD, probenecid, beta-lactam, uremic anions); Low CO/↑CVP → ↓renal perfusion
Tubular adaptation↑Distal NCC (DCT hypertrophy), ↑ENaC, Chloride-dependent WNK activation
Neurohormonal activationBasal sodium avidity, Braking, Vasoconstriction → ↓eGFR

Phenotype-specific Resistance

  • Right HF: ↑CVP → venous congestion → ↓RV output → impaired drug delivery
  • Advanced CKD: Metabolic alkalosis, chronic sodium avidity, ↓tubular secretion, ↑uremic toxins (OAT competition)
  • Obesity HFpEF: Adipokines → RAAS; ↑intraabdominal pressure; RV overload
  • Elderly/Frail: ↓Renal reserve, altered PK/PD, ↑AKI risk

Albumin + Furosemide ใน Hypoalbuminemia (Meta-analysis PLoS One 2021; 13 studies, n=422):

  • ↑urine output MD 31.45 mL (19.30–43.59)
  • Subgroup albumin <2.5 g/dL: MD 60.68 mL (24.38–96.98)
  • Albumin dose ≥30 g: MD 58.77 mL (27.56–89.97)
  • → พิจารณา albumin + furosemide ถ้า albumin <2.5 g/dL และมี diuretic resistance

🏥 Part 5: Clinical Application

5.1 Acute Heart Failure (AHF) — ESC 2021

IV Loop diuretics (Class I, Level C):

  • Diuretic-naive: Furosemide 20–40 mg IV
  • Chronic use: At least equivalent to daily oral dose
  • Combination + thiazide-type for resistant oedema (Class IIa, Level B)

Diuretic Response Assessment (ESC 2021):

  • Urinary spot Na⁺ ≥50–70 mEq/L หลัง 2 ชม.
  • Urine output ≥100–150 mL/h หลัง 6 ชม.
  • ถ้าไม่ตอบสนอง → Double dose IV → Sequential nephron blockade → ตรวจ SCr/electrolytes ทุก 24h → UF/RRT

DOSE Trial (NEJM 2011; n=308) — 2×2 factorial ADHF:

  • Bolus vs Continuous: ไม่ต่างกัน VAS score หรือ SCr change
  • High dose (2.5× oral): ↑↑ net fluid loss ที่ 72h (4899 vs 3575 mL, p=0.001)
  • Post-hoc DOSE (J Card Fail 2016): WRF ที่ 72h → ↓ risk composite death/rehospitalization ที่ 60d — acceptable renal stress
  • Cochrane 2024 (7 RCT, n=681): ไม่ต่างกัน LOS/readmission/AKI; continuous → +0.86 kg weight loss (very low certainty)

Sequential Nephron Blockade — Key Trials:

TrialInterventionOutcome
ADVOR (NEJM 2022; n=519)Acetazolamide 500mg IV + FurosemideSig decongestion 72h (RR 1.46, p<0.001); No diff mortality/rehospitalization
EMPULSE (Nat Med 2022; n=530)Empagliflozin 10mg for 90d + loopSig composite HF outcome at 90d; early eGFR dip (<2wk), no sig at 90d
CLOROTIC (EHJ 2023; n=230)Oral HCTZ (eGFR-adjusted) + FurosemideSig BW + dyspnea at 72h; HCTZ: more hypokalemia + renal impairment
SECRETs of CHF (JACC 2017; n=250)Tolvaptan 30mg + FurosemideNo sig dyspnea; Sig BW decrease
ATHENA-HF (JAMA 2017; n=360)Spironolactone 100mg/d for 96h + FurosemideNo sig NTproBNP, dyspnea, or UO

Diuretic Strategy Algorithm (ESC 2021):

  1. Loop diuretic IV (naive → 20–40mg; chronic → 1–2× oral dose)
  2. Check Urinary Na ±2h, UO ±6h
  3. ถ้าตอบสนอง → repeat similar dose q12h
  4. ถ้าไม่ตอบสนอง → double dose until maximum IV → Sequential blockade (CAI, HTCZ, SGLT2i, MRA, V2RA) → UF/RRT

Notes:

Hyponat → tolvaptan

Met alkalo → acetazolamide

Hypernat → thiazide

Inpatient HF → SGLT2i


5.2 Acute Kidney Injury (AKI) — KDIGO Evolution

KDIGO 2012 → 2026 — Major Shift:

KDIGO 2012KDIGO 2026
Preventionไม่แนะนำ diuretic prevent AKI (1B)
Treatmentไม่แนะนำ diuretic treat AKI ยกเว้น volume overload (2C)Suggest diuretics for significant volume overload in AKI/AKD (2B)
UF vs DiureticRecommend initial diuretics OVER extracorporeal removal ใน AKI + volume overload ไม่มี other RRT indication (1C)
Role ใน ICUDiuretic = marker of AKI risk prediction + marker of KRT discontinuation

ESICM 2025 Evidence (ICM 2025;51:1749–1763): Protocolized diuretics vs usual care:

  • Mortality: RR 0.90 (trend benefit)
  • ICU-free days: MD +2.2 days
  • Ventilator-free days: MD +2.53 days
  • Need for RRT: RR 0.72 (significant)

De-Resuscitation — REDUCE Trial (Crit Care 2025; n=100):

  • P: Adult circulatory shock, stabilized >12h
  • Protocol: Fluid restriction + Diuretic หาก I>O 500 mL + KRT หาก I>O 1000 mL for 48h แม้ได้ diuretic
  • Result: No sig 30d mortality; ↓ ICU LOS (7 vs 10d, p=0.006); ↓ Hospital LOS (16 vs 22d, p=0.006)
  • 7-day cumulative fluid balance: −2353 vs +793 mL (p<0.001)

ROSE framework (R-O-S-E phases):

  • Resuscitation: CLASSIC/CLOVER → no benefit of fluid restriction
  • Optimization/Stabilization: → Active de-resuscitation? (REDUCE trial)
  • Evacuation: Active negative fluid balance (LGFR)

5.3 KDIGO 2026 Diuretic Strategy in AKI — Escalation Pathway

StepDoseGoal
AssessmentFurosemide 1.0 mg/kg IV (1.5 mg/kg ถ้าเคยใช้ diuretic)UO >200 mL/2h → continue scheduled dosing
EscalationDouble dose (160–200 mg IV) q6–12hMax bolus 200 mg ก่อน switch infusion
SynergismAdd thiazide-like (metolazone 5–10 mg PO หรือ chlorothiazide 500 mg IV)ให้ 30–60 นาทีก่อน loop diuretic
IntensifySwitch continuous infusion 5–10 mg/hrTitrate to 20 mg/hr
FailureRe-evaluate for RRTไม่ได้ negative balance แม้ max therapy หรือ K⁺/pH deranged

KDIGO 2026 Practice Point 3.3.1: Intermittent boluses preferred over continuous infusion เป็น initial strategy ใน AKI/AKD


5.4 Furosemide Stress Test (FST)

Dynamic test of tubular reserve — ต้องอาศัย intact renal perfusion + proximal tubular secretion + viable nephron mass

  • No prior loop diuretic: Furosemide 1.0 mg/kg IV
  • Prior loop diuretic: 1.5 mg/kg IV
ResponseInterpretation
UO ≥200 mL/2hLikely reversible AKI
UO <200 mL/2hHigh risk AKI stage 3 progression → Consider early RRT planning (ไม่ใช่ indication ทันที)

KDIGO 2026 Recommendation 2.3.1 (2C adults, 2B children): Suggest FST to assess risk of progression to Stage 3 AKI/RRT ใน Stage 1–2 AKI, euvolemic/hypervolemic

Meta-analysis (11 studies, n=1366; Crit Care 2020):

  • KRT prediction: Sensitivity 0.84, Specificity 0.77
  • AKI progression: Sensitivity 0.81, Specificity 0.88

5.5 Discontinue KRT (KDIGO 2026)

Practice Point 5.9.3: UO >450 mL/24h without diuretics หรือ >2300 mL/24h with diuretics + 2-hour timed CrCl ≥23 mL/min → predict successful RRT discontinuation

Practice Point 5.9.4: Diuretics ก่อน/หลัง RRT discontinuation ใช้ augment UO และ fluid balance ได้ แต่ไม่ proven ว่า facilitate AKI resolution

TrialUO without diureticUO with diuretic
ELAIN (2016)>400 mL/24h>2100 mL/24h
AKIKI / IDEAL-ICU / AKIKI-2>1000 mL/24h>2000 mL/24h

📌 Part 6: Take-Home Messages (ICM 2024;50:1331–1334)

1. Prescription of Loop Diuretics:

  • Furosemide IV 40 mg (เพิ่มถ้า reduced kidney function) หรือ infusion 2–10 mg/hr
  • Bumetanide 1 mg IV bolus หรือ 0.5 mg/hr; Torsemide 20 mg IV
  • T½ prolonged ใน hepatic/renal failure + heart failure

2. Managing Diuretic Resistance (Step-wise):

  1. ↑ dose (consider doubling) → optimize delivery
  2. Add Acetazolamide 250–500 mg IV daily หรือ HCTZ 50 mg/d หรือ SGLT2i (HF)
  3. Correct hypoalbuminemia (Albumin + Furosemide ถ้า albumin <2.5 g/dL)
  4. Consider RRT

3. Monitoring for Adverse Effects:

↓ ลง↑ ขึ้น
Na⁺ (thiazide)Na⁺ (loop diuretics)
K⁺, PO₄⁻, Mg²⁺, Cl⁻pH / Metabolic alkalosis (loop + thiazide)
pH (acetazolamide)Uric acid (loop diuretics)
Cardiac output, BP, GFR

📚 Landmark Trials Summary

TrialYearnสรุป
DOSENEJM 2011308Bolus = Continuous efficacy/safety; High dose → ↑fluid loss; WRF ≠ worse outcomes
Cochrane loop diuretic2024681Bolus = Continuous clinical outcomes; continuous → slightly more weight loss
ADVORNEJM 2022519Acetazolamide + furosemide → Sig decongestion RR 1.46; no mortality benefit
EMPULSENat Med 2022530Empagliflozin → Sig composite HF outcomes at 90d; early eGFR dip
CLOROTICEHJ 2023230HCTZ + furosemide → Sig BW + dyspnea; ↑hypokalemia + renal impairment
ATHENA-HFJAMA 2017360High-dose spironolactone → No sig benefit
REDUCECrit Care 2025100Protocolized restrictive fluid → ↓ICU LOS (7 vs 10d), ↓hospital LOS (16 vs 22d)
FST meta-analysisCrit Care 20201,366Sensitivity 0.84/Specificity 0.77 สำหรับ KRT prediction; KDIGO 2026 (2C)

Guidelines

  • ESC HF 2021 — Eur Heart J 2021;42(36)
  • KDIGO AKI 2026 — Intensive Care Med 2025;51(10):1749–1763
  • ESICM Fluid Therapy Part 3 2025 — ICM 2025;51:1749–1763