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 Table of Contents  
REVIEW ARTICLE
Year : 2022  |  Volume : 17  |  Issue : 3  |  Page : 751-756

Doppler profiles of renal and hepatic hemodynamics in patients with cirrhosis of the liver


Department of Radio-Diagnosis, Jawaharlal Nehru Medical College, DattaMeghe Institute of Medical Sciences, Wardha, Maharashtra, India

Date of Submission15-Sep-2022
Date of Decision18-Sep-2022
Date of Acceptance20-Sep-2022
Date of Web Publication2-Nov-2022

Correspondence Address:
Dr. Shivesh Pandey
Department of Radio-diagnosis, Jawaharlal Nehru Medical College, DattaMeghe Institute of Medical Sciences, Wardha, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_411_22

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  Abstract 


One in five individuals with cirrhosis of the liver may experience renal impairment, a frequent consequence that is linked to increased mortality and morbidity. Even before changes in serum creatinine concentration can be detected, renal hemodynamic alterations start to occur early in the course of functional kidney failure caused by liver disease. Studying the Doppler profiles of renal and hepatic hemodynamics in people with liver cirrhosis is the goal of this review article. People with liver cirrhosis, even before clinical signs of renal impairment appear. Doppler is a quick, reliable, and noninvasive technique that makes it possible to identify renal hemodynamic changes in individuals with liver cirrhosis even before they become clinically obvious.

Keywords: Chronic liver disease, hepatic hemodynamics, hepatorenal syndrome, liver cirrhosis, renal dysfunction, renal hemodynamic


How to cite this article:
Pandey S, Dhande RP, Mishra GV. Doppler profiles of renal and hepatic hemodynamics in patients with cirrhosis of the liver. J Datta Meghe Inst Med Sci Univ 2022;17:751-6

How to cite this URL:
Pandey S, Dhande RP, Mishra GV. Doppler profiles of renal and hepatic hemodynamics in patients with cirrhosis of the liver. J Datta Meghe Inst Med Sci Univ [serial online] 2022 [cited 2023 Feb 1];17:751-6. Available from: http://www.journaldmims.com/text.asp?2022/17/3/751/360219




  Introduction Top


Renal dysfunction is a prevalent consequence linked with high mortality and morbidity in patients of cirrhosis, occurring in one out of every five individuals. Renal impairment is reported by 20%–50% of individuals brought to the hospital with hepatic dysfunction.

The most serious side effect of renal impairment in those with chronic liver illness is hepatorenal syndrome (HRS), that has been associated with very short survival duration.

Before increases in serum creatinine concentration, renal hemodynamic abnormalities begin early in the course of kidney damage caused by liver parenchymal disease. A feature of HRS change is severe intrarenal vasoconstriction. This vasoconstriction may start weeks or months before clinically obvious kidney illness and is associated with a decrease in renal plasma flow and an increase in the vascular resistance of the renal arteries.

Several nonazotemic patients with cirrhosis have significant renal vascular resistance, even though the significant reason of renal vasoconstriction is unexplained and most probably multifactorial. The likelihood of these patients eventually having overt HRS may be increased. Continuous monitoring of hemodynamic changes in the kidney is crucial for estimating renal blood flow and detecting the onset of HRS in patients with liver cirrhosis and portal hypertension.

The objective of this review article was to study Doppler parameters of renal and hepatic hemodynamics in liver cirrhosis patients.[1],[2],[3],[4],[5],[6],[7],[8],[9],[10]


  Literature Search Top


In March 2022, a literature search was conducted in several electronic databases, to find the articles needed for this narrative review. In addition to a manual search using cross-references and books, electronic databases such as PubMed, SCOPUS, Science Direct, Cochrane Library, and EMBASE were searched using the keywords renal hemodynamic, hepatic hemodynamics, liver cirrhosis, renal dysfunction, and chronic liver disease.

Inclusion criteria

Articles published in the English language between August 1994 and December 2020 that met the study's criteria were included in the study.

  • English research articles on Doppler of liver cirrhosis.


Exclusion criteria

  • Case reports and case series
  • Studies on endoscopic band ligation or past history of sclerotherapy treatment gastrointestinal bleed
  • Studies on hepatic tumors
  • Studies on HRS
  • Studies on significant concomitant disease and co-therapy, which may affect renal function and Doppler ultrasonography parameters.


Hepatic artery analysis

A pulsatile waveform describes the typical hepatic arterial waveform. Throughout the whole cardiac cycle, the blood flow in the hepatic arteries antegrade and is visible above the baseline. The hepatic artery shows low resistance with an approximated resistive index (RI) value from 0.55 to 0.7 because the liver needs constant blood flow. Hepatic artery unusually increased (RI >0.7) or decreased (RI <0.55) resistance may be a sign of liver illness.

Portal vein analysis

The direction of physiological flow is always antegrade, or toward the transducer, which results in a waveform that is higher than the baseline. Low-to-high phasicity is considered to be normal. A nonphasic waveform is produced by abnormally low phasicity, whereas a pulsatile waveform is produced by abnormally high phasicity. Pulsatility is measured using the pulsatility index (PI). A PI greater than 0.5 is the outcome of typical phasicity.

Intrarenal arteries analysis

The typical main renal artery shows a low-resistance waveform with a sharp systolic upstroke. In the typical intrarenal arterial waveform, the early systolic peak appears as a little notch in the systole. The acceleration time for the systolic upstroke is short, at or below 0.07 s.

After the evaluation of many research articles and applying the inclusion and exclusion conditions, 17 publications that met the study's goals were chosen for the review [Table 1] and [Figure 1].
Table 1: Features of the included research

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Figure 1: Flowchart of participants' recruitment

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  Discussion Top


Despite having many etiologies, liver parenchymal disease is a common clinical disease with a widespread distribution and no discernible gender or racial differences. It may also have the same long-term effects and complications, such as portal hypertension and hepatic decompensation.

Before HRS manifests in cirrhotic individuals, renal RI assessment using Doppler ultrasound (US) is a valuable index to measure renovascular resistance. Vasoconstrictor systems result in HRS.

The RI serves as, both prognostic indication and a simple noninvasive method to identify decline in renal function. Three values from one kidney must be averaged to provide a single representative value for the variability in RI measurement.[11],[12],[13],[14],[15],[16],[17],[18],[19],[20]

To assess the RI in a patient, one value averaged from three values in one region seems to be enough. According to earlier research, an intrarenal RI value of 0.70 was thought to be a threshold value that indicates enhanced renal vasoconstriction.

According to the research, cirrhotic patients had higher RI levels than normal individuals. In addition, the RI was more in ascitic patients than nonascitic patients and in nonascitic patients with liver cirrhosis than normal individuals (16% vs. 4%).

Study groups and RI are significantly correlated with one another. The RI value similarly rises with increasing liver disease severity, P < 0.001.

Intrarenal arterial RI values were even greater than those of the nonascitic liver cirrhotic patients, and even more in patients who had ascites than normal healthy persons. As a result, renal vasoconstriction appears to be detected by RI measurement earlier than by higher serum creatinine readings.

The RI value in patients with HRS was much more (≥0.70) compared to the normal individuals in Bardi et al.'s study in 2002. Patients who later developed the HRS had a mean initial RI of 0.77 ± 0.05. As part of their investigation into RI, Kastelan et al. classified 46 cirrhotic patients into three groups: those with cirrhosis and normal kidney function, those with cirrhosis and kidney failure without HRS, and those with cirrhosis and HRS. When compared to the other two groups, they discovered that the RI (≥0.70) was considerably higher in the cirrhotic patients with HRS.

In a follow-up study of 180 individuals with cirrhosis without azotemia, Platt et al. found that despite identical Child–Pugh ratings, those with initially elevated RI values had significantly worse outcomes for HRS and renal failure. Only 6% (6/104) of the people with normal RI <0.01, developed renal impairment, whereas, among the 76 patients with RI ≥0.70, 55% developed renal dysfunction and 26% of patients developed HRS.

Intrarenal RI appears to be a reliable predictor and may be used to identify a subgroup of patients at increased risk of kidney failure or HRS. The predictive value of high RI needs to be quantified by follow-up investigations.

In 2020, Baz et al. discovered a relationship between the MELD score and the hepatic artery velocity (HAV) which was statistically significant), with 70% of their individuals exhibiting elevated HAV. In 59% of their patients, the portal flow velocity was significantly reduced (20 cm/s) (mean ± standard deviation, 19.68 ± 6.49).

Renal artery Doppler US characteristics may be useful for the early identification of patients who are at a high risk for developing reduced renal function [Table 2].[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34]
Table 2: Radiological findings in included studies

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  Conclusion Top


The hepatic artery and renal artery Doppler US values show progressively increased levels with the deterioration of the liver function. Simultaneous evaluation of the liver and renal blood flow in patients with liver cirrhosis, using Doppler methods causes early identification of patients who are at particular risk for HRS development. This also underlines the importance of close cooperation with clinicians in diagnosis and management.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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2.
Huelin P, Piano S, Solà E, Stanco M, Solé C, Moreira R, et al. Validation of a Staging system for acute kidney injury in patients with cirrhosis and association with acute-on-chronic liver failure. Clin Gastroenterol Hepatol 2017;15:438-45.e5.  Back to cited text no. 2
    
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Epstein M, Berk DP, Hollenberg NK, Adams DF, Chalmers TC, Abrams HL, et al. Renal failure in the patient with cirrhosis. The role of active vasoconstriction. Am J Med 1970;49:175-85.  Back to cited text no. 7
    
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Neumyer MM, Blebea J. Duplex evaluation of the renal arteries. In: Noninvasive Vascular Diagnosis. London: Springer; 2013. p. 589-616.  Back to cited text no. 12
    
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Platt JF, Ellis JH, Rubin JM, Merion RM, Lucey MR. Renal duplex Doppler ultrasonography: A noninvasive predictor of kidney dysfunction and hepatorenal failure in liver disease. Hepatology 1994;20:362-9.  Back to cited text no. 15
    
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Iwao T, Toyonaga A, Oho K, Tayama C, Masumoto H, Sakai T, et al. Value of Doppler ultrasound parameters of portal vein and hepatic artery in the diagnosis of cirrhosis and portal hypertension. Am J Gastroenterol 1997;92:1012-7.  Back to cited text no. 16
    
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Celebi H, Dönder E, Celiker H. Renal blood flow detection with Doppler ultrasonography in patients with hepatic cirrhosis. Arch Intern Med 1997;157:564-6.  Back to cited text no. 17
    
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Rendón Unceta P, Macías Rodríguez MA, Guillén Mariscal P, Tejada Cabrera M, Martínez Sierra MC, Martín Herrera L. Renal Doppler ultrasonography and its relationship with the renal function in patients with liver cirrhosis. Med Clin (Barc) 2001;116:561-4.  Back to cited text no. 20
    
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[PUBMED]    
22.
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23.
Kastelan S, Ljubicic N, Kastelan Z, Ostojic R, Uravic M. The role of duplex-Doppler ultrasonography in the diagnosis of renal dysfunction and hepatorenal syndrome in patients with liver cirrhosis. Hepatogastroenterology 2004;51:1408-12.  Back to cited text no. 23
    
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31.
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    Figures

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    Tables

  [Table 1], [Table 2]



 

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