Maiko Alejandro Tavera Díaz1* Annia Aguilar Loayza2 Juan Fernando Mamani Ochoa3
1Department of Internal medicine and Nephrology, Univalle Hospital, Elizabeth Seton Hospital, Cochabamba, Bolivia*Corresponding author: Maiko Alejandro Tavera Díaz, Department of internal medicine and Nephrology, Univalle Hospital, Elizabeth Seton Hospital, Cochabamba, Bolivia, E-mail: taveradiaz@gmail.com
A 69-year-old patient with multiple comorbidities including diabetes mellitus, hypertension, congestive heart failure (CHF), cor pulmonale, severe pulmonary hypertension, stage IV chronic kidney disease, type II cardiorenal syndrome, and sick sinus syndrome with pacemaker presented with worsening dyspnea, orthopnea, and progressive lower limb edema over 72 hours.
Initial examination revealed hypotension, pulmonary hypoventilation, tricuspid systolic murmur, jugular engorgement, and bilateral pitting edema. Diagnostic imaging showed pulmonary edema, pleural effusion, and cardiomegaly. Laboratory tests indicated hyperazotemia, hypertransaminasemia, and hyperbilirubinemia, with an ALT/LDH ratio of 0.3. VEXUS protocol ultrasound confirmed moderate to severe congestion, while echocardiogram demonstrated right chamber dilation and severe pulmonary hypertension.
The patient was diagnosed with cardiogenic shock, acute liver injury due to ischemic hepatitis secondary to decompensated CHF, acute-on-chronic kidney disease, and type II cardiorenal syndrome. Due to clinical deterioration, including refractory oliguria and worsening edema, the patient was admitted to ICU for vasoactive support and Continuous Renal Replacement Therapy (CRRT).
Treatment with VVHDF achieved a significant negative fluid balance over 72 hours, leading to gradual improvement in hemodynamics and venous congestion. The patient was transitioned to intermittent dialysis and eventually discharged on Dapagliflozin, Spironolactone, and Valsartan. Two months post-discharge, improved renal function allowed discontinuation of dialysis.
This case highlights the complex management of cardiorenal syndrome complicated by ischemic hepatitis, emphasizing the importance of early recognition and aggressive management of congestion through diuretics and, when necessary, renal replacement therapy.
The successful outcome demonstrates the effectiveness of a comprehensive treatment approach in managing multiple organ dysfunction.
Ischemic Hepatitis; Cardiorenal Síndrome; Heart Failure
Ischemic hepatitis is caused by insufficient blood volume delivery to the liver to maintain the metabolic demands of hepatocytes, which enter an anaerobic condition reflected in elevated transaminases exceeding more than 10 times their normal value and acute increase in lactate dehydrogenase (LDH) exceeding the transaminase values by up to 20 times, a finding that allows calculation of the ALT/LDH ratio with a result <1.5 which is characteristic [1]. It is uncommon and should be suspected as a complication especially in patients with decompensated heart failure and cardiorenal syndrome [2]. Mortality increases during hospitalization, therefore it is important to correct the hemodynamic alteration by improving cardiac output, tissue perfusion, and achieving adequate decongestion to prevent the perpetuation of acute liver injury [1].
A 69-year-old patient with a history of diabetes mellitus, arterial hypertension, Congestive Heart Failure (CHF), cor pulmonale, severe pulmonary hypertension, stage IV chronic kidney disease, type II cardiorenal syndrome, and sick sinus syndrome with pacemaker. The patient presents to nephrology consultation with clinical symptoms of 72 hours evolution characterized by progression of dyspnea from functional class II to IV, orthopnea, asthenia, adynamia, hyperoxia, and progressive symmetrical edema in lower limbs. Upon admission, BP 100/60 mmHg, hypoventilation in pulmonary bases, grade III/IV systolic murmur in tricuspid focus, jugular engorgement 2/3 without collapse with positive hepatojugular reflux, lower extremities with bilateral edema, symmetrical pitting edema (++). Chest X-ray shows evidence of pulmonary edema, right hemithorax pleural effusion, and grade I-II cardiomegaly at the expense of right chambers. Laboratory tests: hyperazotemia; hypertransaminasemia; ALT/LDH ratio 0.3; hyperbilirubinemia (Figure 1). During hospitalization, ultrasound according to VEXUS protocol was also requested, which confirms moderate to severe grade 2-3 congestion. Transthoracic echocardiogram shows significant dilation of right chambers and left atrium; left ventricular remodeling; LVEF of 69%; moderate tricuspid insufficiency; severe pulmonary hypertension PASP 100 mmHg.
Figure 1: Temporal evolution of laboratory tests during hospitalization and subsequent follow-ups and VEXUS (Venous Excess Ultrasound Score): Dilated suprahepatic and left hepatic veins with S wave lower than D wave, dilated inferior vena cava and abnormal flow pattern indicating moderate to severe grade 2-3 congestion.
Diagnoses include cardiogenic shock, acute liver injury due to ischemic hepatitis secondary to decompensated CHF, acute-onchronic kidney disease, type II cardiorenal syndrome.
Patient evolves with hypotension 80/50 mmHg, oliguria refractory to diuretics (120 mg Furosemide and 3% hypertonic solution), painful hepatomegaly 5 cm below costal margin, lower limbs with increased pitting edema (+++). In this clinical context, admitted to Intensive Care Unit with initiation of vasoactive and inotropic agents and Continuous Renal Replacement Therapy (CRRT) in Venovenous Hemodiafiltration Mode (VVHDF), with 5000 ml ultrafiltration in the first 24 hours, continuing CRRT for 72 hours, achieving a cumulative negative balance of 11 liters. In the first week, patient responds with gradual reduction of vasoactive and inotropic agents, decreased venous congestion while maintaining elevated azotemia, thus continuing with Intermittent Renal Replacement Therapy. Due to clinical improvement, hospital discharge was granted for outpatient follow-up with Dapagliflozin, Spironolactone, Valsartan, and two months later, progressive decrease in azotemia was evident (Figure 1), leading to discontinuation of dialytic treatment and continuing outpatient follow-up.
Ischemic hepatitis is a rare complication with an incidence between 0.16% and 0.5%, being more frequent in the elderly population [3].
Ischemic hepatitis represents acute deterioration of liver function characterized by increased transaminases and LDH, a finding that allows calculation of ALT/LDH ratio <1.5 characteristic of ischemic hepatitis [1]. Another finding is that initially AST exceeds ALT and subsequently there is a reversal of the AST/ALT ratio [4]; our patient exhibited all three parameters. It occurs through a dual mechanism: first, hepatic congestion produces increased hydrostatic pressure and hepatocyte hypertrophy. Subsequently, after acute exacerbation, sustained hypotension occurs, leading to hypoperfusion and cellular hypoxia, causing hepatic cytolysis [5]. Cellular damage leads to intracellular oxidative stress due to anaerobiosis, releasing reactive oxygen species and pro inflammatory cytokines such as TNF-α, IL-1, and interferon-γ [6].
Management involves controlling cardiac and renal triggers, hemodynamic stabilization with vasopressors and inotropics. Additionally, it’s important to treat congestion, making high-dose diuretics fundamental, either alone or in combination with other diuretics, or the use of multisegmental diuretic therapy. In case of diuretic resistance, Continuous Renal Replacement Therapy is an alternative [7-9]. Statin use may be protective against developing ischemic hepatitis through improvement of hepatic microcirculation and endothelial function, reduction of platelet recruitment, decrease in systemic vascular inflammation, therefore patients with comorbidities might benefit from such medication [5,6].
Ischemic hepatitis secondary to cardiorenal syndrome is associated with higher mortality. Venous congestion has a deleterious impact on renal and hepatic function, characterized by ischemia, where the ALT/ LDH ratio is greatly helpful in diagnosis. Achieving hemodynamic stability in these patients is important; one of the fundamental pillars is the use of diuretics. In case of diuretic resistance, an alternative is Extracorporeal Support Therapy in SCUF mode when renal function is preserved, and in those with renal deterioration and hemodynamic instability, CKRT in VVHDF or VVHF mode is an alternative.
This work has not received specific funding from public sector agencies, commercial sector, or non-profit organizations. The authors declare no conflicts of interest and have obtained authorization or informed consent from those involved in this case.
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Article Type: CASE REPORT
Citation: Tavera Díaz MA, Loayza AA, Mamani Ochoa JF (2025) Hepato-Cardio-Renal Failure. Int J Nephrol Kidney Fail 11(1): dx.doi.org/10.16966/2380- 5498.248
Copyright: ©2025 Tavera Díaz MA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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