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Hepatorenal Syndrome (HRS-AKI) in Hospitalized Patients: Navigating the Razor-Thin Margin of Survival in Cirrhosis—New Guidelines, Albumin, and the Transplant Bridge
In this episode of Hospital Medicine Unplugged, we sprint through hepatorenal syndrome–AKI (HRS-AKI)—exclude look-alikes fast, start albumin + vasoconstrictor early, watch the lungs, and loop in transplant.
We open with the do-firsts: clinical diagnosis by exclusion—rule out hypovolemia, nephrotoxins, structural kidney disease. Pull diuretics/ACEi/NSAIDs, check UA/sediment (should be bland), kidney US (should look normal), and hunt triggers (SBP, GI bleed, overdiuresis). Albumin challenge (≈1 g/kg/day, max 100 g for 24–48 h): no renal improvement → HRS-AKI. Urine biomarkers (e.g., NGAL) may help ATN vs HRS but aren’t ready for routine.
Call AKI early using ICA criteria: ↑Cr ≥0.3 mg/dL/48 h or ≥1.5× baseline/7 d and/or low urine output. Don’t chase urine Na/FeNa alone (diuretics confound). Treat the precipitant (especially SBP: antibiotics + albumin).
Treatment—build the hemodynamic fix:
• Albumin is adjunct, not a cure: after the initial challenge, continue 20–40 g/day with vasoconstrictor.
• First-line vasoconstrictor: terlipressin (now FDA-approved) + albumin. Dosing: 0.5–2 mg IV q6h or continuous infusion; up to 14 days. Stop early if <25% Cr fall by day 4 at max tolerated dose.
• Safety watch: respiratory failure/pulmonary edema risk—avoid large albumin loads, hold if SpO₂ <90%, be cautious in advanced ACLF or cardiopulmonary disease.
• Validated alternative: norepinephrine (ICU, central line). Evidence supports noninferior HRS reversal and sometimes fewer AEs—great in shock or when terlipressin is contraindicated.
• If IV agents unavailable: midodrine + octreotide + albumin (inferior; use only as a fallback).
Special plays & edge cases:
• ACLF: higher grade → lower response, higher risk—expedite transplant evaluation.
• Volume overload on therapy: down-titrate/hold albumin, reassess with POCUS (IVC/B-lines), pause terlipressin if hypoxemia.
• SBP: treat and give albumin (1.5 g/kg day 1, 1 g/kg day 2) to prevent kidney failure.
• RRT: bridge to liver transplant or for life-threatening indications; limited benefit in non-candidates—align with goals of care.
• Transplant is the only definitive cure; consider SLK in persistent renal dysfunction.
Monitoring that matters:
• Daily Cr, UOP, weights, electrolytes, oxygenation; infection surveillance.
• Track congestion (exam + POCUS), and de-escalate albumin if lungs load up.
• Define response (Cr to near-baseline); nonresponse by day 4 → switch strategies.
Medication pitfalls you don’t want to meet:
• Over-infusing albumin → pulmonary edema.
• Delaying vasoconstrictors waiting for full “workup.”
• Using midodrine/octreotide first when IV options exist.
• Stopping early despite improving Cr; or continuing blindly past day-4 nonresponse.
We close with the HRS bundle that sticks: (1) Exclude hypovolemia/nephrotoxins/structural disease fast; (2) Albumin challenge (24–48 h) → if no improvement, start vasoconstrictor + albumin; (3) Prefer terlipressin, use norepinephrine in ICU/shock or contraindications; (4) Hard stop/check at day 4 for response; (5) Prevent/ treat SBP (antibiotics + albumin); (6) Protect the lungs—watch SpO₂, CXR/POCUS, adjust albumin; (7) Early transplant activation ± RRT as bridge; (8) Multidisciplinary liver–kidney–ICU collaboration.
Bottom line: HRS-AKI is a race against time—diagnose by exclusion, pair albumin with the right vasoconstrictor, watch for respiratory hits, and escalate to transplant pathways early.
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By Roger Musa, MDIn this episode of Hospital Medicine Unplugged, we sprint through hepatorenal syndrome–AKI (HRS-AKI)—exclude look-alikes fast, start albumin + vasoconstrictor early, watch the lungs, and loop in transplant.
We open with the do-firsts: clinical diagnosis by exclusion—rule out hypovolemia, nephrotoxins, structural kidney disease. Pull diuretics/ACEi/NSAIDs, check UA/sediment (should be bland), kidney US (should look normal), and hunt triggers (SBP, GI bleed, overdiuresis). Albumin challenge (≈1 g/kg/day, max 100 g for 24–48 h): no renal improvement → HRS-AKI. Urine biomarkers (e.g., NGAL) may help ATN vs HRS but aren’t ready for routine.
Call AKI early using ICA criteria: ↑Cr ≥0.3 mg/dL/48 h or ≥1.5× baseline/7 d and/or low urine output. Don’t chase urine Na/FeNa alone (diuretics confound). Treat the precipitant (especially SBP: antibiotics + albumin).
Treatment—build the hemodynamic fix:
• Albumin is adjunct, not a cure: after the initial challenge, continue 20–40 g/day with vasoconstrictor.
• First-line vasoconstrictor: terlipressin (now FDA-approved) + albumin. Dosing: 0.5–2 mg IV q6h or continuous infusion; up to 14 days. Stop early if <25% Cr fall by day 4 at max tolerated dose.
• Safety watch: respiratory failure/pulmonary edema risk—avoid large albumin loads, hold if SpO₂ <90%, be cautious in advanced ACLF or cardiopulmonary disease.
• Validated alternative: norepinephrine (ICU, central line). Evidence supports noninferior HRS reversal and sometimes fewer AEs—great in shock or when terlipressin is contraindicated.
• If IV agents unavailable: midodrine + octreotide + albumin (inferior; use only as a fallback).
Special plays & edge cases:
• ACLF: higher grade → lower response, higher risk—expedite transplant evaluation.
• Volume overload on therapy: down-titrate/hold albumin, reassess with POCUS (IVC/B-lines), pause terlipressin if hypoxemia.
• SBP: treat and give albumin (1.5 g/kg day 1, 1 g/kg day 2) to prevent kidney failure.
• RRT: bridge to liver transplant or for life-threatening indications; limited benefit in non-candidates—align with goals of care.
• Transplant is the only definitive cure; consider SLK in persistent renal dysfunction.
Monitoring that matters:
• Daily Cr, UOP, weights, electrolytes, oxygenation; infection surveillance.
• Track congestion (exam + POCUS), and de-escalate albumin if lungs load up.
• Define response (Cr to near-baseline); nonresponse by day 4 → switch strategies.
Medication pitfalls you don’t want to meet:
• Over-infusing albumin → pulmonary edema.
• Delaying vasoconstrictors waiting for full “workup.”
• Using midodrine/octreotide first when IV options exist.
• Stopping early despite improving Cr; or continuing blindly past day-4 nonresponse.
We close with the HRS bundle that sticks: (1) Exclude hypovolemia/nephrotoxins/structural disease fast; (2) Albumin challenge (24–48 h) → if no improvement, start vasoconstrictor + albumin; (3) Prefer terlipressin, use norepinephrine in ICU/shock or contraindications; (4) Hard stop/check at day 4 for response; (5) Prevent/ treat SBP (antibiotics + albumin); (6) Protect the lungs—watch SpO₂, CXR/POCUS, adjust albumin; (7) Early transplant activation ± RRT as bridge; (8) Multidisciplinary liver–kidney–ICU collaboration.
Bottom line: HRS-AKI is a race against time—diagnose by exclusion, pair albumin with the right vasoconstrictor, watch for respiratory hits, and escalate to transplant pathways early.