Diagnose HRS-AKI by ICA-ADQI 2024 criteria and treat with terlipressin and albumin; manage cardiorenal syndrome by decongestion.
At the bedside
Timed steps- 1
Cirrhosis with AKI: first steps
Day 0-2Stop diuretics, NSAIDs, beta-blockers if hypotensive, nephrotoxins; treat infection (SBP: diagnostic tap), bleeding, hypovolaemia (albumin 1 g/kg/day, max 100 g, for 2 days).
- 2
Diagnose HRS-AKI
If AKI persists (stage ≥ 1B or progressing) without shock and urine sediment is bland (protein < 500 mg/day, < 50 RBC/hpf, normal ultrasound): HRS-AKI.
- 3
Treat HRS-AKI
Terlipressin (bolus 0.5-1 mg q4-6h or infusion 2 mg/day, up-titrate to max 12 mg/day) + albumin 20-40 g/day. Noradrenaline infusion is an alternative in ICU (central line). Midodrine + octreotide is less effective.
- 4
Monitor for harm
Daily SpO2, chest exam, fluid status: terlipressin + albumin can cause pulmonary oedema and respiratory failure. Stop if SpO2 < 90%; avoid in ACLF grade 3 or creatinine ≥ 5 mg/dL.
- 5
Response and transplant
Response = creatinine fall to < 0.3 mg/dL above baseline. Refer all HRS for liver transplant assessment; RRT as bridge if transplant candidate.
- 6
Cardiorenal: decongest
Loop diuretic IV at 1-2.5x oral dose; check spot urine Na at 2 h (< 50-70 mmol/L = inadequate) and UO at 6 h (< 100-150 mL/h): double dose, add thiazide/acetazolamide. A modest creatinine rise during effective decongestion is acceptable.
- 7
Refractory cardiorenal
Inotrope if low output; ultrafiltration/RRT for diuretic-resistant congestion.
HRS-AKI vasoconstrictor
Terlipressin
- Dose
- 0.5-1 mg q4-6h, or 2 mg/24 h infusion; max 12 mg/day
- Range
- 2–12 mg/day
- Preparation
- 2 mg in 50 mL NS over 24 h = ~2 mL/h
- Worked example
- Start 2 mg/24 h infusion; creatinine fall < 25% at 48 h → increase to 4 mg/24 h
Infusion has fewer ischaemic side effects than boluses.
Volume expansion / HRS treatment
Human albumin 20%
- Dose
- Day 1-2: 1 g/kg/day (max 100 g); with terlipressin 20-40 g/day
- Worked example
- 70 kg: 70 g = 350 mL of 20% albumin on day 1
Decongestion in cardiorenal
Furosemide
- Dose
- 1-2.5x total daily oral dose as bolus; repeat/double at 6 h if poor response
- Worked example
- On oral furosemide 40 mg BD (80 mg/day): give 80-200 mg IV; urine Na at 2 h < 50 mmol/L → double dose
Calculators for this topic
References
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AKI in cirrhosis
Step 1 of ~5
Stop diuretics/nephrotoxins; treat infection, bleeding; tap ascites (SBP)
Based on Nadim MK, Kellum JA, Forni L, et al; Wong F, Pappas SC, Curry MP, et al. Educational use; follow local protocol.
Pathophysiology
In cirrhosis, splanchnic vasodilation reduces effective arterial volume, activating RAAS, sympathetic system and vasopressin, causing intense renal vasoconstriction (HRS). Systemic inflammation from infection is a frequent trigger. In cardiorenal syndrome, raised venous pressure transmitted to the kidney (renal congestion) reduces GFR more than low forward flow.
Evidence
- CONFIRM (300 patients): terlipressin + albumin increased HRS reversal (32% vs 17%) but caused more respiratory failure deaths [Wong 2021].
- ICA-ADQI 2024 consensus updated definitions of AKI and HRS-AKI in cirrhosis [Nadim 2024].
- HFA 2019 position statement: natriuresis-guided diuretic titration in congestion [Mullens 2019].
Controversies
- Terlipressin infusion vs bolus; noradrenaline vs terlipressin in ICU (similar efficacy in small trials, including Indian RCTs).
- Acceptable creatinine rise during decongestion ('permissive worsening renal function').
🇮🇳 India notes
- Terlipressin is affordable and widely used in India; many Indian RCTs (e.g. from ILBS Delhi) compared terlipressin and noradrenaline in HRS.
- Alcohol-related and hepatitis B/C cirrhosis predominate; consider ACLF triggers (alcoholic hepatitis, hepatitis E/A superinfection).
References
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Test yourself
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Educational reference for trained clinicians. Check doses against your hospital protocol and the patient in front of you.