{
  "schemaVersion": 2,
  "eyebrow": "Hepatology",
  "title": "Hepatorenal Syndrome",
  "summary": "Hepatorenal syndrome–acute kidney injury is a time-sensitive, exclusionary diagnosis in decompensated cirrhosis. Rapidly identify infection, hypovolemia, acute tubular injury, obstruction, and venous congestion before selecting albumin plus vasoconstrictor therapy and pursuing liver transplantation.",
  "seoDescription": "Point-of-care diagnosis and management of hepatorenal syndrome–acute kidney injury in cirrhosis, including exclusion of mimics and terlipressin safety.",
  "clinicalQuestion": "How should physicians diagnose, phenotype, and treat hepatorenal syndrome–acute kidney injury in patients with cirrhosis?",
  "specialty": "Hepatology and Nephrology",
  "audience": "U.S. physicians and medical trainees",
  "tags": [
    "hepatorenal syndrome",
    "HRS-AKI",
    "cirrhosis",
    "acute kidney injury",
    "terlipressin",
    "albumin",
    "acute tubular injury",
    "liver transplantation"
  ],
  "keyTakeaways": [
    "In cirrhosis with ascites, AKI is a serum creatinine increase of at least 0.3 mg/dL within 48 hours or at least 50% within 7 days; HRS-AKI is considered only after hypovolemia, shock, nephrotoxins, and structural kidney disease are excluded. [22][24]",
    "Treat reversible precipitants immediately, particularly infection, gastrointestinal fluid loss, overdiuresis, nephrotoxin exposure, and post-paracentesis circulatory dysfunction; do not delay etiologic evaluation while awaiting an albumin response. [11][14][24]",
    "Urinary NGAL, IL-18, KIM-1, and L-FABP are higher in acute tubular necrosis than in functional AKI phenotypes and can support a structural injury branch when standard clinical assessment is indeterminate. [10][12][13]",
    "Terlipressin is FDA-approved to improve kidney function in adults with HRS and rapidly declining kidney function, but requires baseline and continuous oxygen-saturation monitoring and discontinuation for SpO2 below 90% or worsening hypoxia. [1]",
    "Avoid terlipressin in ACLF grade 3 and use particular caution with volume overload, because respiratory failure and ischemia can jeopardize liver-transplant eligibility. [1][20]",
    "Liver transplantation is the definitive treatment pathway; vasoconstrictor therapy is principally a bridge while renal function and transplant candidacy are reassessed. [20][21]"
  ],
  "sections": [
    {
      "id": "recognize-and-stabilize-aki",
      "eyebrow": "First hours",
      "heading": "Recognize AKI and address immediately reversible threats",
      "intro": "Manage AKI in decompensated cirrhosis as a diagnostic emergency rather than presuming HRS.",
      "paragraphs": [
        "Use an AKI threshold of serum creatinine increase of at least 0.3 mg/dL within 48 hours or at least 50% from baseline within 7 days. AKI occurs in approximately 27% to 53% of hospitalized patients with cirrhosis and ascites; prerenal azotemia and acute tubular necrosis are the most common etiologies. [22][24]",
        "At presentation, identify and reverse hemodynamic or nephrotoxic triggers: shock, infection, gastrointestinal hemorrhage or fluid loss, excess diuresis, nephrotoxic exposure, and recent large-volume paracentesis without appropriate albumin replacement. HRS-AKI should not be assigned until hypovolemia or shock, nephrotoxins, intrinsic kidney disease, and obstructive disease have been actively excluded. [14][22][24]",
        "Obtain urinalysis with urine microscopy, urine protein assessment, and renal ultrasonography while evaluating volume status and infection. Hematuria, pyuria, substantial proteinuria, casts suggestive of tubular injury, or urinary obstruction should redirect management toward intrinsic or postrenal AKI rather than a purely functional HRS phenotype. [11][14][17]",
        "Use point-of-care ultrasound as an adjunct when physical examination and routine laboratory indices do not resolve volume status. In one reported cohort, 62% of patients clinically labeled HRS had high cardiac filling pressures on right-heart catheterization and improved creatinine after volume expansion was stopped and diuretics were started; congestive physiology should therefore prevent reflexive albumin escalation. [16]"
      ],
      "bullets": [
        "Measure serial serum creatinine and assess urine output during the initial evaluation; a rising creatinine despite correction of an identified precipitant increases concern for HRS-AKI or acute tubular injury. [11][15]",
        "Perform diagnostic evaluation for infection early, especially spontaneous bacterial peritonitis, because infection is a common setting for HRS-AKI and may coexist with other renal insults. [14][24]",
        "For spontaneous bacterial peritonitis with increased or rising creatinine, administer albumin 1.5 g/kg within 6 hours of diagnosis, then 1 g/kg on day 3. [2]"
      ],
      "subsections": [],
      "table": {
        "caption": "Initial etiologic branches for AKI in cirrhosis and the management consequence. [10][11][14][16][24]",
        "columns": [
          "AKI branch",
          "Findings that shift probability",
          "Immediate next action"
        ],
        "rows": [
          [
            "Hypovolemic prerenal AKI",
            "Volume loss, gastrointestinal bleeding, overdiuresis, or another reversible reduction in effective circulating volume; renal function improves after correction. [11][14]",
            "Correct the precipitant and reassess creatinine response before labeling HRS-AKI. [11][14]"
          ],
          [
            "HRS-AKI",
            "Cirrhosis with ascites and prerenal AKI after exclusion of shock, nephrotoxins, structural renal disease, and obstruction; no standalone diagnostic test confirms HRS. [13][17][24]",
            "Use albumin-based volume assessment and initiate a vasoconstrictor strategy when the functional phenotype persists. [11][20]"
          ],
          [
            "Acute tubular injury or necrosis",
            "Urine injury biomarkers including NGAL, IL-18, KIM-1, and L-FABP are higher than in HRS or prerenal azotemia; tubular injury may coexist with hemodynamic AKI. [10][12][4]",
            "Treat the underlying tubular insult and avoid assuming response to HRS-directed vasoconstriction. [10][13]"
          ],
          [
            "Venous congestion or cardiorenal physiology",
            "POCUS or invasive hemodynamics demonstrate high filling pressures; creatinine may improve when albumin is stopped and diuresis is initiated. [16]",
            "Avoid indiscriminate volume expansion; tailor diuretic and fluid management to congestion. [16]"
          ],
          [
            "Postrenal or glomerular disease",
            "Hydronephrosis on ultrasonography, or active urine sediment and proteinuria suggesting structural renal disease. [11][14]",
            "Treat obstruction or pursue nephrology-directed intrinsic renal evaluation rather than HRS-only therapy. [11][14]"
          ]
        ]
      }
    },
    {
      "id": "establish-hrs-aki",
      "eyebrow": "Diagnostic branch",
      "heading": "Establish HRS-AKI only after competing renal phenotypes are addressed",
      "intro": "HRS-AKI is an exclusionary clinical syndrome in advanced cirrhosis, not a urine sodium or creatinine threshold diagnosis.",
      "paragraphs": [
        "Current AKI-era terminology replaces HRS type 1 with HRS-AKI and recognizes HRS-NAKI for the former type 2 phenotype. HRS-AKI occurs in advanced cirrhosis with portal-hypertensive vasodilation and inflammatory activation, but the clinical diagnosis remains dependent on excluding prerenal, intrinsic, and obstructive causes. [17][4][13]",
        "Do not wait for an arbitrary creatinine concentration before acting. AKI-based HRS criteria were designed to identify clinically meaningful renal deterioration earlier than historical creatinine-threshold definitions, and earlier terlipressin initiation at lower creatinine has been associated with greater treatment effectiveness. [15][20]",
        "A conventional approach is to withhold obvious precipitants and give intravenous albumin-based volume expansion for up to 48 hours before designating HRS-AKI. This remains a useful diagnostic maneuver when hypovolemia is plausible, but it must be balanced against pulmonary edema and venous congestion, especially when ultrasound suggests high filling pressures. [11][16]",
        "Interpret urine indices cautiously. Fractional excretion of sodium and urine sodium are included among tools used to phenotype AKI in cirrhosis, but structural biomarkers may add greater discrimination when acute tubular injury remains a serious alternative. Urinary NGAL, IL-18, KIM-1, and L-FABP were significantly higher in adjudicated acute tubular necrosis than in other AKI etiologies in cirrhosis. [10][11][12]"
      ],
      "bullets": [
        "Favors a functional HRS-AKI pathway: cirrhosis with ascites, persistent prerenal physiology after correction of reversible causes, and no convincing evidence of structural renal injury or obstruction. [14][17][24]",
        "Favors acute tubular injury: a compatible ischemic, septic, toxic, or inflammatory insult plus elevated structural urine injury biomarkers. [4][10][12]",
        "Favors a mixed phenotype: severe infection, ACLF, bile-acid or endotoxin-mediated injury, or prolonged renal hypoperfusion; functional and structural mechanisms can coexist. [4][8][9]",
        "Escalate to hepatology and nephrology when active urinary sediment, proteinuria, obstructive findings, unresolved volume status, or failure of an initially plausible HRS-directed strategy makes the phenotype uncertain. [11][14][16]"
      ],
      "subsections": [],
      "table": {
        "caption": "Tests that refine the HRS-AKI differential when clinical examination alone is insufficient. [10][11][16]",
        "columns": [
          "Test",
          "Interpretation",
          "Decision consequence"
        ],
        "rows": [
          [
            "Urinalysis and microscopy",
            "Red or white blood cells, casts, or other active sediment support a structural or infectious renal process rather than uncomplicated functional HRS. [11]",
            "Investigate intrinsic renal disease or infection and do not rely on vasoconstrictor therapy alone. [11][14]"
          ],
          [
            "Urine protein assessment",
            "Proteinuria increases concern for structural kidney disease. [11][14]",
            "Obtain nephrology input and consider disease-specific evaluation. [11][14]"
          ],
          [
            "Renal ultrasonography",
            "Hydronephrosis or other obstruction excludes a pure HRS-AKI explanation. [11][14]",
            "Relieve or otherwise manage obstruction. [14]"
          ],
          [
            "Urinary NGAL, IL-18, KIM-1, L-FABP",
            "Higher concentrations support acute tubular necrosis over HRS or prerenal azotemia. [10][12]",
            "Prioritize tubular-injury management and reassess expected benefit of HRS-directed vasoconstriction. [10][13]"
          ],
          [
            "POCUS assessment of congestion",
            "High filling pressures may identify albumin-intolerant venous congestion despite a clinical HRS label. [16]",
            "Stop further volume expansion and consider diuresis when congestion is demonstrated. [16]"
          ]
        ]
      }
    },
    {
      "id": "albumin-and-vasoconstrictors",
      "eyebrow": "Medical treatment",
      "heading": "Use albumin and vasoconstrictors selectively for persistent HRS-AKI",
      "intro": "Treatment aims to reverse functional renal vasoconstriction while avoiding respiratory and ischemic complications.",
      "paragraphs": [
        "For patients meeting a persistent HRS-AKI phenotype after correction of reversible causes, combine vasoconstrictor therapy with albumin-based management. Vasoconstrictors including terlipressin, norepinephrine, and midodrine plus octreotide act on the splanchnic circulation to improve renal function; terlipressin has the strongest evidence base and is more effective than albumin alone for HRS kidney-injury reversal. [20][21]",
        "In the United States, terlipressin is FDA-approved to improve kidney function in adults with HRS accompanied by rapid reduction in kidney function. The FDA label states that patients with serum creatinine above 5 mg/dL are unlikely to benefit, making delayed initiation a poor-value strategy when the diagnosis is established. [1]",
        "Terlipressin requires respiratory-risk stratification before the first dose. Obtain baseline SpO2, monitor continuously by pulse oximetry during therapy, and discontinue terlipressin if SpO2 falls below 90% or if hypoxia or respiratory symptoms develop. Fluid overload increases respiratory-failure risk; reduce or discontinue albumin and other fluids and use diuretics judiciously until volume status improves. [1]",
        "Avoid terlipressin in ACLF grade 3 because of substantial respiratory-failure risk. Also assess for ischemic risk and transplant implications: terlipressin-related respiratory failure or ischemia can render a listed patient ineligible for transplantation, so a patient with worsening oxygenation or volume overload should have treatment interrupted rather than continued solely to pursue creatinine improvement. [1][20]",
        "Norepinephrine plus albumin is an alternative vasoconstrictor strategy, particularly where close hemodynamic monitoring is available. Midodrine plus octreotide is used off label in the United States but is less effective than terlipressin in comparative evidence and should not be considered equivalent therapy when terlipressin is appropriate and available. [20][21]"
      ],
      "bullets": [
        "Before terlipressin: document baseline SpO2, assess respiratory symptoms and volume status, and identify ACLF grade 3 as a major safety exclusion. [1]",
        "During terlipressin: use continuous pulse oximetry and regular clinical respiratory assessments; stop therapy for SpO2 below 90%, hypoxia, or worsening respiratory symptoms. [1]",
        "With fluid overload: reduce or stop albumin and other fluids, use diuretics judiciously, and temporarily interrupt, reduce, or discontinue terlipressin until volume status improves. [1]",
        "With serum creatinine above 5 mg/dL: reassess expected benefit, as FDA labeling identifies these patients as unlikely to benefit from terlipressin. [1]"
      ],
      "subsections": [],
      "table": {
        "caption": "Vasoconstrictor selection and safety considerations in HRS-AKI. [1][20][21]",
        "columns": [
          "Strategy",
          "Role",
          "Key constraint"
        ],
        "rows": [
          [
            "Terlipressin plus albumin",
            "FDA-approved therapy to improve kidney function in adults with HRS and rapidly declining kidney function; most effective medical option described for HRS-AKI reversal. [1][20]",
            "Continuous SpO2 monitoring; discontinue for SpO2 below 90% or hypoxia; avoid ACLF grade 3; benefit is unlikely when creatinine exceeds 5 mg/dL. [1]"
          ],
          [
            "Norepinephrine plus albumin",
            "Alternative vasoconstrictor approach with efficacy similar to or potentially lower than terlipressin in head-to-head evidence. [20][21]",
            "Requires a setting capable of close hemodynamic monitoring. [20]"
          ],
          [
            "Midodrine plus octreotide plus albumin",
            "Off-label U.S. approach sometimes used outside intensive monitoring settings. [20][21]",
            "Inferior efficacy to terlipressin; do not substitute when a patient is eligible for terlipressin. [20]"
          ]
        ]
      }
    },
    {
      "id": "albumin-context-and-procedures",
      "eyebrow": "Precipitant prevention",
      "heading": "Prevent paracentesis- and infection-associated renal deterioration",
      "intro": "Albumin use is indication-specific; excessive administration can worsen congestion and terlipressin-associated respiratory risk.",
      "paragraphs": [
        "After paracentesis exceeding 5 L, infuse 20% or 25% albumin at 8 g per liter of ascites removed. For paracentesis below 5 L, the same dose can be considered in ACLF or in patients at high risk for post-paracentesis AKI. [2][3]",
        "In spontaneous bacterial peritonitis with increased or rising serum creatinine, administer albumin 1.5 g/kg within 6 hours of diagnosis and 1 g/kg on day 3. This is a renal-protective adjunct to infection management and should occur before persistent renal dysfunction is attributed solely to HRS-AKI. [2]",
        "For refractory ascites, consider transjugular intrahepatic portosystemic shunt in appropriately selected patients. In contrast, automated low-flow ascites pumps should be restricted to special circumstances with robust clinical governance, audit, or research arrangements because survival benefit has not been demonstrated. [2][3]"
      ],
      "bullets": [
        "Large-volume paracentesis greater than 5 L: albumin 8 g/L removed after completion. [3]",
        "Paracentesis below 5 L with ACLF or high post-paracentesis AKI risk: consider albumin 8 g/L removed. [2]",
        "SBP plus increased or rising creatinine: albumin 1.5 g/kg within 6 hours, then 1 g/kg on day 3. [2]",
        "Refractory ascites: evaluate candidacy for TIPS rather than repeated escalation of unsupported device-based drainage strategies. [2][3]"
      ],
      "subsections": [],
      "table": {
        "caption": "Albumin indications relevant to AKI and HRS risk in cirrhosis. [2][3]",
        "columns": [
          "Clinical setting",
          "Albumin regimen",
          "Decision point"
        ],
        "rows": [
          [
            "Paracentesis greater than 5 L",
            "20% or 25% albumin, 8 g/L of ascites removed after the procedure. [3]",
            "Use routinely to reduce post-paracentesis circulatory and renal risk. [3]"
          ],
          [
            "Paracentesis below 5 L with ACLF or high AKI risk",
            "Consider 20% or 25% albumin, 8 g/L removed. [2]",
            "Individualize because recommendation strength and evidence certainty are lower. [2]"
          ],
          [
            "SBP with increased or rising creatinine",
            "1.5 g/kg within 6 hours of diagnosis, then 1 g/kg on day 3. [2]",
            "Administer promptly as part of infection-associated renal dysfunction management. [2]"
          ],
          [
            "Suspected HRS-AKI with congestion",
            "Do not automatically escalate albumin; reduce or stop albumin and other fluids when volume overload is present. [1][16]",
            "Protect oxygenation and reassess the hemodynamic phenotype. [1][16]"
          ]
        ]
      }
    },
    {
      "id": "transplant-and-monitoring",
      "eyebrow": "Definitive pathway",
      "heading": "Treat HRS-AKI as a liver-transplant urgency and monitor for treatment harm",
      "intro": "Renal reversal is clinically valuable, but definitive management depends on liver-transplant assessment.",
      "paragraphs": [
        "Initiate or expedite liver-transplant evaluation when HRS-AKI is identified. Liver transplantation is the definitive treatment for HRS-AKI and other advanced cirrhosis complications; terlipressin-based treatment is commonly used as a bridge while transplant candidacy, renal trajectory, and need for renal replacement therapy are reassessed. [20][21]",
        "Follow serum creatinine trajectory, oxygenation, respiratory examination, and volume status during vasoconstrictor therapy. A fall in creatinine supports response, whereas progressive AKI should prompt renewed evaluation for acute tubular injury, occult infection, persistent hypovolemia, venous congestion, or another unrecognized structural process rather than automatic continuation of an ineffective HRS-directed course. [10][11][16]",
        "Respond to terlipressin toxicity immediately. Discontinue the drug for SpO2 below 90%; interrupt, reduce, or discontinue treatment during volume overload until improvement; and reassess for ischemic complications. These events matter both for short-term safety and because respiratory failure or ischemia may affect transplant eligibility. [1]",
        "Renal replacement therapy may be needed for selected patients with severe renal dysfunction as a bridge in the transplant pathway. Terlipressin treatment has been associated with less renal replacement therapy use and better post-transplant kidney function in reported analyses, but it does not replace definitive transplant planning. [20][21]"
      ],
      "bullets": [
        "Monitor oxygenation continuously during terlipressin treatment and stop therapy for SpO2 below 90%. [1]",
        "Reassess volume status repeatedly; new edema, pulmonary symptoms, or ultrasound evidence of congestion should trigger reduction of fluids and reconsideration of albumin exposure. [1][16]",
        "If creatinine fails to improve, revisit the AKI phenotype with urine microscopy, structural injury biomarkers when available, renal imaging, infection assessment, and hemodynamic evaluation. [10][11][14][16]",
        "Coordinate transplant evaluation early because a serious terlipressin adverse event can compromise eligibility. [1][20]"
      ],
      "subsections": [],
      "table": {
        "caption": "Monitoring triggers that should change HRS-AKI management. [1][10][11][16][20]",
        "columns": [
          "Monitoring finding",
          "Interpretation",
          "Action"
        ],
        "rows": [
          [
            "SpO2 below 90% during terlipressin",
            "Terlipressin-associated hypoxia risk. [1]",
            "Discontinue terlipressin. [1]"
          ],
          [
            "New fluid overload or worsening respiratory symptoms",
            "Higher risk for respiratory failure during terlipressin and albumin exposure. [1]",
            "Reduce or stop albumin and other fluids, use diuretics judiciously, and interrupt or modify terlipressin until volume status improves. [1]"
          ],
          [
            "Persistent or worsening creatinine despite presumed HRS therapy",
            "May represent acute tubular injury, mixed injury, persistent infection, occult hypovolemia, or congestion. [4][10][16]",
            "Repeat etiologic assessment rather than assuming refractory functional HRS alone. [10][11][16]"
          ],
          [
            "Creatinine above 5 mg/dL before terlipressin",
            "Low likelihood of benefit according to FDA labeling. [1]",
            "Reassess treatment value and prioritize transplant-pathway planning and supportive renal management. [1][20]"
          ]
        ]
      }
    }
  ],
  "faq": [],
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    {
      "number": 23,
      "title": "Renal Effects of Angiotensin‐Converting Enzyme Inhibitors ...",
      "detail": "www.ccjm.org",
      "url": "https://www.ccjm.org/lookup/external-ref?access_num=",
      "authors": "www.ccjm.org",
      "host": "www.ccjm.org"
    },
    {
      "number": 24,
      "title": "Diagnosis and management of ascites, spontaneous ...",
      "detail": "www.ccjm.org",
      "url": "https://www.ccjm.org/content/90/4/209",
      "authors": "www.ccjm.org",
      "host": "www.ccjm.org"
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  ],
  "editorialNote": "Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.",
  "citations": [
    {
      "number": 1,
      "title": "022231Orig1s000 - accessdata.fda.gov",
      "detail": "www.accessdata.fda.gov",
      "url": "https://www.accessdata.fda.gov/drugsatfda_docs/nda/2022/022231Orig1s000lbl.pdf",
      "authors": "www.accessdata.fda.gov",
      "host": "www.accessdata.fda.gov",
      "snippet": "Contraindications (4)]. Monitor patients for changes in respiratory status using continuous pulse oximetry and regular clinical assessments. Discontinue TERLIVAZ in patients experiencing hypoxia or increased respiratory symptoms. Patients with fluid overload may be at increased risk of respiratory f",
      "score": 0.7009158
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    {
      "number": 2,
      "title": "Guidelines on the management of ascites in cirrhosis - Gut",
      "detail": "gut.bmj.com",
      "url": "https://gut.bmj.com/content/70/1/9",
      "authors": "gut.bmj.com",
      "host": "gut.bmj.com",
      "snippet": "### Recommendation\n\nAutomated low-flow ascites pump should be considered only in special circumstances with robust arrangements of clinical governance, audit or research. (Quality of evidence: low; Recommendation: weak)\n\n### Hepatorenal syndrome\n\nPatients with cirrhosis and ascites can develop a spe",
      "score": 0.68697983
    },
    {
      "number": 3,
      "title": "Guidelines on the management of ascites in cirrhosis",
      "detail": "gut.bmj.com",
      "url": "https://gut.bmj.com/content/gutjnl/early/2020/10/15/gutjnl-2020-321790.full.pdf",
      "authors": "gut.bmj.com",
      "host": "gut.bmj.com",
      "snippet": "by guest on March 9, 2026  Downloaded from 16 October 2020. 10.1136/gutjnl-2020-321790 on Gut: first published as 18 Aithal GP, et al. Gut 2020;0:1–21. doi:10.1136/gutjnl-2020-321790 Guidelines 61 Fernández J, Navasa M, Planas R, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays",
      "score": 0.6757865
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    {
      "number": 4,
      "title": "Reappraising the spectrum of AKI and hepatorenal syndrome in patients with cirrhosis | Nature Reviews Nephrology",
      "detail": "www.nature.com",
      "url": "https://www.nature.com/articles/s41581-019-0218-4",
      "authors": "www.nature.com",
      "host": "www.nature.com",
      "snippet": "Title: Reappraising the spectrum of AKI and hepatorenal syndrome in patients with cirrhosis | Nature Reviews Nephrology\n# Reappraising the spectrum of AKI and hepatorenal syndrome in patients with cirrhosis. The occurrence of acute kidney injury (AKI) in patients with end-stage liver disease constit",
      "score": 0.6739866
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    {
      "number": 5,
      "title": "Management of hepatorenal syndrome in patients with cirrhosis | Nature Reviews Nephrology",
      "detail": "www.nature.com",
      "url": "https://www.nature.com/articles/nrneph.2011.96",
      "authors": "www.nature.com",
      "host": "www.nature.com",
      "snippet": "Title: Management of hepatorenal syndrome in patients with cirrhosis | Nature Reviews Nephrology\n# Management of hepatorenal syndrome in patients with cirrhosis. In patients with advanced cirrhosis, these processes culminate in renal vasoconstriction and type 2 hepatorenal syndrome (HRS), which is c",
      "score": 0.72605723
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    {
      "number": 6,
      "title": "Cardio-Pulmonary-Renal Interactions: A Multidisciplinary Approach",
      "detail": "www.jacc.org",
      "url": "https://www.jacc.org/doi/10.1016/j.jacc.2015.04.024",
      "authors": "www.jacc.org",
      "host": "www.jacc.org",
      "snippet": "could be cardiovascular disease outcomes in these forms of CRS. Finally, CRS type 5 describes a systemic insult to both the heart and the kidneys, such as sepsis, where both organs are injured simultaneously in persons with previously normal heart and kidney function at baseline. Pulmonary-renal syn",
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    {
      "number": 7,
      "title": "Advances in the management of complications from cirrhosis",
      "detail": "academic.oup.com",
      "url": "https://academic.oup.com/gastro/article/doi/10.1093/gastro/goae072/7727525",
      "authors": "academic.oup.com",
      "host": "academic.oup.com",
      "snippet": "by J Singh · 2024 · Cited by 13 — The approval of terlipressin for the treatment of hepatorenal syndrome (HRS) AASLD practice guidance on portal hypertensive. Acute kidney",
      "score": 0.6158511
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    {
      "number": 8,
      "title": "Hepatorenal syndrome in acute-on-chronic liver failure with acute ...",
      "detail": "academic.oup.com",
      "url": "https://academic.oup.com/gastro/article-pdf/9/6/505/41794381/goab040.pdf",
      "authors": "academic.oup.com",
      "host": "academic.oup.com",
      "snippet": "In cirrhosis with ascites, hepatorenal syndrome (HRS) is a specific prerenal dysfunction unresponsive to fluid volume ex- pansion. Acute-on-chronic liver",
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    {
      "number": 9,
      "title": "Hepatorenal syndrome in acute-on-chronic liver failure with ...",
      "detail": "academic.oup.com",
      "url": "https://academic.oup.com/gastro/article/9/6/505/6375168",
      "authors": "academic.oup.com",
      "host": "academic.oup.com",
      "snippet": "by S Liu · 2021 · Cited by 17 — Hepatorenal syndrome (HRS) is a complication of advanced cirrhosis characterized by an abrupt deterioration in renal function. It is unresponsive to fluid",
      "score": 0.46147847
    },
    {
      "number": 10,
      "title": "Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury - Belcher - 2014 - Hepatology - Wiley Online Library",
      "detail": "onlinelibrary.wiley.com",
      "url": "https://onlinelibrary.wiley.com/doi/full/10.1002/hep.26980",
      "authors": "onlinelibrary.wiley.com",
      "host": "onlinelibrary.wiley.com",
      "snippet": "Median values for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), liver-type fatty acid binding protein (L-FABP), and albumin differed between etiologies and were significantly higher in patients adjudicated with ATN. *Conclusion*: Urinary",
      "score": 0.8098936
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    {
      "number": 11,
      "title": "Hepatorenal Syndrome Type 1: From Diagnosis Ascertainment... : Kidney360",
      "detail": "journals.lww.com",
      "url": "https://journals.lww.com/kidney360/fulltext/2022/02000/hepatorenal_syndrome_type_1__from_diagnosis.26.aspx",
      "authors": "journals.lww.com",
      "host": "journals.lww.com",
      "snippet": "Title: Hepatorenal Syndrome Type 1: From Diagnosis Ascertainment... : Kidney360\n**Approach to diagnosis of AKI in cirrhosis.** The conventional approach to determine the etiology of AKI in individuals with cirrhosis has been centered in the possibility of three primary causes: prerenal azotemia (Pre",
      "score": 0.7420672
    },
    {
      "number": 12,
      "title": "Kidney biomarkers and differential diagnosis of patients ...",
      "detail": "onlinelibrary.wiley.com",
      "url": "https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/hep.26980",
      "authors": "onlinelibrary.wiley.com",
      "host": "onlinelibrary.wiley.com",
      "snippet": "by JM Belcher · 2014 · Cited by 405 — hepatorenal syndrome (HRS). Urinary biomarkers of kidney injury distinguish AKI etiology. FENa, fractional excretion of sodium; HRS, hepatorenal syndrome;",
      "score": 0.7309246
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    {
      "number": 13,
      "title": "Hepatorenal Syndrome Type 1: Diagnosis and Treatment",
      "detail": "www.sciencedirect.com",
      "url": "https://www.sciencedirect.com/science/article/abs/pii/S2949813923000575",
      "authors": "www.sciencedirect.com",
      "host": "www.sciencedirect.com",
      "snippet": "Hepatorenal syndrome (HRS)is a feared complication in patients with advanced cirrhosis and is associated with significant morbidity and mortality. While recognized as a distinct physiologic condition for well over one hundred years, a lack of objective diagnostic tests has made the diagnosis one of ",
      "score": 0.7213709
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    {
      "number": 14,
      "title": "Hepatorenal Syndrome–Acute Kidney Injury in Liver Transplantation",
      "detail": "www.sciencedirect.com",
      "url": "https://www.sciencedirect.com/science/article/pii/S1542356523004949",
      "authors": "www.sciencedirect.com",
      "host": "www.sciencedirect.com",
      "snippet": "Hepatorenal syndrome (HRS) is a serious complication of cirrhosis. HRS nomenclature has recently changed to HRS-AKI (acute kidney injury). HRS is a complex response to chronic vasodilatory changes brought about by portal hypertension and exacerbated by inflammatory responses that portends poor progn",
      "score": 0.71113056
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    {
      "number": 15,
      "title": "Hepatorenal syndrome in the era of acute kidney injury - Solé",
      "detail": "onlinelibrary.wiley.com",
      "url": "https://onlinelibrary.wiley.com/doi/full/10.1111/liv.13893",
      "authors": "onlinelibrary.wiley.com",
      "host": "onlinelibrary.wiley.com",
      "snippet": "by C Solé · 2018 · Cited by 63 — The new diagnostic criteria are based on AKI stages and there is no need to reach a specific serum creatinine threshold. According to these new",
      "score": 0.6826801
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    {
      "number": 16,
      "title": "Acute kidney injury and point-of-care ultrasound in liver cirrhosis: redefining hepatorenal syndrome | Clinical Kidney Journal | Oxford Academic",
      "detail": "academic.oup.com",
      "url": "https://academic.oup.com/ckj/article/17/5/sfae112/7646085",
      "authors": "academic.oup.com",
      "host": "academic.oup.com",
      "snippet": "# Acute kidney injury and point-of-care ultrasound in liver cirrhosis: redefining hepatorenal syndrome *Open Access*. Eduardo Josué Banegas-Deras, Jaime Mazón-Ruiz, Gregorio Romero-González, Juan Carlos Ruiz-Cobo, Clara Sanz-García, Mara Serrano-Soto, Emilio Sánchez, Eduardo R Argaiz, Acute kidney i",
      "score": 0.666736
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    {
      "number": 17,
      "title": "Renal damage in Hepatorenal Syndrome: A still unsolved issue - ScienceDirect",
      "detail": "www.sciencedirect.com",
      "url": "https://www.sciencedirect.com/science/article/abs/pii/S2210740123001031",
      "authors": "www.sciencedirect.com",
      "host": "www.sciencedirect.com",
      "snippet": "Acute kidney injury (AKI) is a common complication of cirrhosis, burdened by high morbidity and mortality rates and progression to chronic kidney disease. HRS diagnosis is still clinical, once pre-renal azotemia and intrinsic kidney damage have been excluded by applying well-established and internat",
      "score": 0.6664756
    },
    {
      "number": 18,
      "title": "Ascites, Renal Dysfunction and Hepatorenal Syndrome",
      "detail": "onlinelibrary.wiley.com",
      "url": "https://onlinelibrary.wiley.com/doi/full/10.1002/hep.27493",
      "authors": "onlinelibrary.wiley.com",
      "host": "onlinelibrary.wiley.com",
      "snippet": "... urine sodium or albumin are associated with changes in creatinine. For subjects receiving less than or equal to 0.5 g/kg of albumin BID,",
      "score": 0.61057013
    },
    {
      "number": 19,
      "title": "Terlipressin and the Treatment of Hepatorenal Syndrome: How the CONFIRM Trial Moves the Story Forward - ScienceDirect",
      "detail": "www.sciencedirect.com",
      "url": "https://www.sciencedirect.com/science/article/pii/S0272638621008908",
      "authors": "www.sciencedirect.com",
      "host": "www.sciencedirect.com",
      "snippet": "# Perspective Terlipressin and the Treatment of Hepatorenal Syndrome: How the CONFIRM Trial Moves the Story Forward. ### Diagnosis, treatment and survival of patients with hepatorenal syndrome: a survey on daily medical practice. ### Terlipressin, a vasoactive prodrug recommended in hepatorenal synd",
      "score": 0.49626526
    },
    {
      "number": 20,
      "title": "Use of Terlipressin in AKI Associated with Hepatorenal... : Kidney360",
      "detail": "journals.lww.com",
      "url": "https://journals.lww.com/kidney360/fulltext/2024/06000/use_of_terlipressin_in_aki_associated_with.5.aspx",
      "authors": "journals.lww.com",
      "host": "journals.lww.com",
      "snippet": "Title: Use of Terlipressin in AKI Associated with Hepatorenal... : Kidney360\n# Use of Terlipressin in AKI Associated with Hepatorenal Syndrome: COMMENTARY. Terlipressin, a V1a receptor agonist with a longer half-life than its analogue vasopressin, is more effective at reversing the kidney injury of ",
      "score": 0.8446273
    },
    {
      "number": 21,
      "title": "Safety and efficacy of continuous terlipressin... : Liver Transplantation",
      "detail": "journals.lww.com",
      "url": "https://journals.lww.com/lt/fulltext/2024/10000/safety_and_efficacy_of_continuous_terlipressin.7.aspx",
      "authors": "journals.lww.com",
      "host": "journals.lww.com",
      "snippet": "Weinberg EM, Wong F, Vargas HE, Curry MP, Jamil K, Pappas SC, et al. Pretransplant terlipressin treatment for hepatorenal syndrome decreases the need for renal replacement therapy both pre- and posttransplant: A 12-month follow-up analysis of the CONFIRM Trial. Abstract. Hepatology. 2022;76(S1):S145",
      "score": 0.71305263
    },
    {
      "number": 22,
      "title": "Print Article | Cleveland Clinic Journal of medicine",
      "detail": "www.ccjm.org",
      "url": "https://www.ccjm.org/custom-print/80137",
      "authors": "www.ccjm.org",
      "host": "www.ccjm.org",
      "snippet": "## ABSTRACT\n\nAscites is the most common decompensation-associated complication of cirrhosis leading to reduced survival. Following significant development of antimicrobial resistance and studies comparing therapeutic options, the American Association for the Study of Liver Diseases released a new gu",
      "score": 0.66229486
    },
    {
      "number": 23,
      "title": "Renal Effects of Angiotensin‐Converting Enzyme Inhibitors ...",
      "detail": "www.ccjm.org",
      "url": "https://www.ccjm.org/lookup/external-ref?access_num=",
      "authors": "www.ccjm.org",
      "host": "www.ccjm.org",
      "snippet": "EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis,",
      "score": 0.6466616
    },
    {
      "number": 24,
      "title": "Diagnosis and management of ascites, spontaneous ...",
      "detail": "www.ccjm.org",
      "url": "https://www.ccjm.org/content/90/4/209",
      "authors": "www.ccjm.org",
      "host": "www.ccjm.org",
      "snippet": "## ABSTRACT\n\nAscites is the most common decompensation-associated complication of cirrhosis leading to reduced survival. Following significant development of antimicrobial resistance and studies comparing therapeutic options, the American Association for the Study of Liver Diseases released a new gu",
      "score": 0.63939893
    }
  ],
  "publishedAt": "2026-08-24T17:27:04.962091+00:00",
  "updatedAt": "2026-08-24T17:27:04.962091+00:00",
  "readingMinutes": 7,
  "slug": "hepatorenal-syndrome"
}