scholarly journals Hepatorenal Syndrome Type 1: From Diagnosis Ascertainment to Goal-Oriented Pharmacotherapy

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0006722021
Author(s):  
Juan Carlos Q. Velez

Hepatorenal syndrome type 1 (HRS-1) is a serious form of acute kidney injury (AKI) that affects individuals with advanced cirrhosis with ascites. Prompt and accurate diagnosis is essential for effective implementation of therapeutic measures that can favorably alter its clinical course. Despite decades of investigation, HRS-1 continues to be primarily a diagnosis of exclusion. While the diagnostic criteria dictated by the International Club of Ascites (ICA) provide a useful framework to approach the diagnosis of HRS-1, they do not fully reflect the complexity of clinical scenarios that is often encountered in patients with cirrhosis and AKI. Thus, diagnostic uncertainty is often faced. In particular, the distinction between HRS-1 and acute tubular injury (ATI) is challenging with the currently available clinical tools. Because treatment of HRS-1 differs from that of ATI, distinguishing these 2 causes of AKI has direct implications in management. Therefore, the use if the ICA criteria should be enhanced with a more individualized approach and attention to the other phenotypic aspects of HRS-1 and other types of AKI. Liver transplantation is the most effective treatment for HRS-1 but it is only available to a small fraction of the affected patients worldwide. Thus, pharmacological therapy is necessary. Vasoconstrictors aimed to increase mean arterial pressure constitute the most effective approach. Administration of intravenous albumin is an established co-adjuvant therapy. However, the risk for fluid overload in patients with cirrhosis with AKI is not negligible and interventions intended to expand or remove volume should be tailored to the specific needs of the patient. Norepinephrine and terlipressin are the most effective vasoconstrictors and their use should be determined by availability, ease of administration and attention to optimal risk/benefit balance for each clinical scenario.

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii451-iii451 ◽  
Author(s):  
Florence Wong ◽  
Thomas D Boyer ◽  
Arun J Sanyal ◽  
Lakhmir S Chawla ◽  
Stephen Chris Pappas ◽  
...  

Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P364
Author(s):  
W Vandenberghe ◽  
S Gevaert ◽  
H Peperstraete ◽  
I Herck ◽  
J Decruyenaere ◽  
...  

2002 ◽  
Vol 36 ◽  
pp. 256 ◽  
Author(s):  
Peter Jarcuska ◽  
Tomas Hildebrand ◽  
Luboslav Bena ◽  
Beata Grejtovska ◽  
Robert Roland ◽  
...  

2021 ◽  
Vol 3 (2) ◽  
pp. 1-7
Author(s):  
. Rendy ◽  
. Febyan ◽  
Krisnhaliani Wetarini

The hepatorenal syndrome is one of various potential causes of acute kidney injury in patients with decompensated liver disease. Hepatorenal syndrome is diagnosed based on reducing kidney function without any evidence of intrinsic kidney disease, including proteinuria, hematuria, or abnormal kidney ultrasonography. Clinically, hepatorenal syndrome is divided into two types named type 1 and type 2. The most favorable therapy for HRS cases is liver transplantation; however, only a few undergo this procedure due to the high mortality. Other modalities for hepatorenal syndrome therapy are pharmacology and non-pharmacology approaches. The purpose of management HRS is to optimize and stabilize the patient until an organ transplant available. This review aims to discuss the underlying pathophysiology and demonstrate the diagnostic approach of hepatorenal syndrome to determine the most appropriate therapeutic measures in clinical practice. The clinicians must be aware of management principles of hepatorenal syndrome to improve the quality of care for patients and optimize the clinical conditions.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Grazia Maria Virzì ◽  
Anna Clementi ◽  
Massimo de Cal ◽  
Alessandra Brocca ◽  
Sonya Day ◽  
...  

Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P<0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.


2018 ◽  
Vol 8 (3) ◽  
pp. 208-216 ◽  
Author(s):  
Andrea Breglia ◽  
Grazia Maria Virzì ◽  
Silvia Pastori ◽  
Alessandra Brocca ◽  
Massimo de Cal ◽  
...  

Background: Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Its pathophysiology is complex and not completely understood. In this study, we examined the role of apoptosis and the caspase pathways involved. Material and Methods: We enrolled 40 acute heart failure (AHF) patients, 11 of whom developed AKI characterizing CRS type 1. We exposed the human cell line U937 to plasma from the CRS type 1 and AHF groups and then we evaluated apoptotic activity by annexin-V evaluation, determination of caspase-3, -8 and -9 levels, and BAX, BAD, and FAS gene expression. Results: We observed significant upregulation of apoptosis in monocytes exposed to CRS type 1 plasma compared to AHF, with increased levels of caspase-3 (p < 0.01), caspase-9 (p < 0.01), and caspase-8 (p < 0.03) showing activation of both intrinsic and extrinsic pathways. Furthermore, monocytes exposed to CRS type 1 plasma had increased gene expression of BAX and BAD (intrinsic pathways) (p = 0.010 for both). Furthermore, strong significant correlations between the caspase-9 levels and BAD and BAX gene expression were observed (Spearman ρ = – 0.76, p = 0.011, and ρ = – 0.72, p = 0.011). Conclusion: CRS type 1 induces dual apoptotic pathway activation in monocytes; the two pathways converged on caspase-3. Many factors may induce activation of both intrinsic and extrinsic apoptotic pathways in CRS type 1 patients, such as upregulation of proinflammatory cytokines and hypoxia/ischemia. Further investigations are necessary to corroborate the present findings, and to better understand the pathophysiological mechanism and consequent therapeutic and prognostic implications for CRS type 1.


2018 ◽  
Vol 53 (12) ◽  
pp. 1590-1596 ◽  
Author(s):  
Jian Xiong ◽  
Lin Pu ◽  
Haofeng Xiong ◽  
Pan Xiang ◽  
Ming Zhang ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
pp. 5-22 ◽  
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin

The combination of heart failure and renal failure is called cardiorenal syndrome. It is a stage of the cardiorenal continuum and, possibly, a small link of the cardiorenal-cerebral-metabolic axis. Despite the fact that the phrase “cardiorenal syndrome” and its five types have become a part of the medical lexicon, many aspects of this problem are still not clear. Cardiorenal syndrome can be diagnosed in 32-90.3% of patients with heart failure. Cardiorenal syndrome type 1 or 2 develops in most cases of heart failure: cardiorenal syndrome presents with the development ofchronic kidney disease in patients with chronic heart failure and acute kidney injury in patients with acute heart failure. Impaired renal function has an unfavorable prognostic value. It leads to an increase in the mortality of patients with heart failure. It is necessary to timely diagnose the presence of cardiorenal syndrome and take into account its presence when managing patients with heart failure. Further researches are needed on ways toprevent the development and prevent the progression of kidney damage in patients with heart failure, to which the efforts of the multidisciplinary team should be directed. The first part of this review examines the currently definition, classification, pathogenesis, epidemiology and prognosis of cardiorenal syndrome in patients with heart failure.


2019 ◽  
Vol 9 (5) ◽  
pp. 308-315
Author(s):  
Grazia Maria Virzì ◽  
Andrea Breglia ◽  
Ghada Ankawi ◽  
Chiara Bolin ◽  
Massimo de Cal ◽  
...  

Background: Cardiorenal syndrome (CRS) type 1 is characterized by a rapid worsening of cardiac function that leads to acute kidney injury (AKI). This study evaluated the role of lipopolysaccharide (LPS) in the development of AKI in patients with acute heart failure (AHF) and its relationship with renal parameters, to enable a better comprehension of the pathophysiology of CRS type 1. Methods: We enrolled 32 AHF patients, 15 of whom were classified as having CRS type 1. Eight of these 15 exhibited AKI at the time of admission (caused by AHF) and the other 7 developed AKI during their stay in hospital (in the first 48 h). We evaluated the plasmatic LPS concentrations as well as conventional (serum creatinine [sCr] and urea) and unconventional (neutrophil gelatinase-associated lipocalin [NGAL] and cystatin C) renal markers. Results: LPS levels were significantly higher in the CRS type 1 patients. No significant difference in LPS level was found in patients who were admitted with AKI and those developed AKI in hospital, but there was a tendency towards a higher level of LPS in CRS type 1 patients admitted with AKI. The LPS concentrations at admission were similar in CRS type 1 survivors (n = 12) and nonsurvivors (n = 3) (p = 0.22). We observed a positive correlation between LPS level and NGAL, Scr at admission and peak Scr during hospitalization and urea at admission. Conclusion: CRS type 1 patients present with an increased level of LPS and there is a direct correlation between LPS and renal parameters. This pilot research is the first study to explore the premise of LPS as novel pathophysiological factor in CRS type 1.


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