Cirrhosis is defined by the liver developing fibrosis and nodules as a result of a persistent damage that changes the liver's typical lobular arrangement1. The global and regional burden of decompensated liver disease is a significant public health priority, with India bearing a disproportionate share of the mortality. Acute tubular necrosis (ATN), hepatorenal syndrome (HRS), and prerenal AKI (PRA) are the most prevalent AKI phenotypes in cirrhosis patients.2,3 The prognosis for cirrhosis patients with AKI is significantly influenced by these characteristics and the stage of AKI. Patients with cirrhosis who had PRA, HRS, or ATN have 3-month survival rates of 89%, 39%, and 38%, respectively. The epidemiological landscape of cirrhosis shifted significantly between 1990 and 2017, with total global cases exceeding 160 million as of recent data. There are many difficulties in evaluating renal function in people with cirrhosis4. Serum creatinine is an unreliable marker in cirrhosis as it frequently overestimates renal function. Factors like sarcopenia (muscle wasting) and increased tubular secretion falsely lower creatinine levels, while hyperbilirubinemia can interfere with laboratory assays. Consequently, standard GFR estimation formulas—including Cockcroft-Gault, MDRD, and CKD-EPI—consistently provide an inaccurately optimistic assessment of actual kidney health5. Alternative techniques for evaluating renal function present difficulties with regard to cost, accessibility, complexity, and radiation exposure risk. The renal resistive index (RRI) is the most common Doppler ultrasound variable to estimate intrarenal vascular resistance. It is also the most widely applicable and accepted tool due to the easy availability and non-invasive nature of ultrasonography6,7. Assessing the prognostic validity of the renal resistance index in adult patients with advanced liver disease, both with and without ascites, was the aim of this study. RRI essentially measures the resistance blood encounters when entering the kidneys. Integrating RRI into clinical research refines prognostic accuracy, as a high-resistance phenotype (RRI > 0.75$) identifies patients at a four-fold higher mortality risk. This allows for preventative strategies, including aggressive infection management and avoiding nephrotoxins or excessive diuretics. Furthermore, systemic inflammation acts as a "second hit," where cytokines exacerbate microcirculatory dysfunction, impairing renal perfusion regardless of systemic blood pressure8.This study seeks to bridge the gap between bedside ultrasound and long-term survival data. By evaluating the RRI in a diverse cohort—ranging from those with stable, compensated disease to those with refractory ascites—we aim to validate RRI not just as a diagnostic tool, but as a robust prognostic marker. AIM To evaluate the renal artery Doppler findings and renal resistive index (RRI) in patients with decompensated liver disease.

This cross-sectional observational study was conducted on 50 patients with decompensated liver disease with ascites and 50 cirrhotic patients without ascites admitted in JLN Medical College and hospital, Ajmer. The study was carried out between June 2024 to May 2026. Patients with age ≥18 years and with ascites secondary to chronic liver disease were included in the study. Patients with cardiovascular instability, diabetes mellitus, hypertension, malignancy, previous renovascular diseases, vascular disease affecting kidneys, congenital or acquired renal abnormalities, who underwent kidney transplant, on nephrotoxic agents, nephropathies, with pathomorphological findings in ultrasound like- decreased kidney size, reduction of renal parenchymal width, and significant renal parenchymal hyper echogenicity and Hypotension (systolic BP <90mm Hg) were excluded from the study.

Table No- 1 Distribution of patients according to Age Age Distribution (In Years) Group I (Decompensated Liver disease with ascites) Group II (Cirrhosis without ascites) No. of Patients Percentage No. of Patients Percentage 18-30 3 6% 4 8% 31-40 11 22% 12 24% 41-50 29 58% 26 52% ≥51 7 14% 8 16% Total 50 100% 50 100% Mean ± SD 43.24 ± 6.78 42.96 ± 7.66 p-value 0.847 A total of 100 patients were included in the final analysis. The age distribution peaked in the 41–50-year category for both Group I (58%) and Group II (52%). The mean age for patients in Group I was 43.24 ± 6.78 years, while for Group II it was 42.96 ± 7.66 years. The calculated p-value is 0.8470, which is greater than 0.05, indicating that there is no statistically significant difference in the age distribution between the two groups. This confirms that the groups are age-matched and comparable for further analysis. Table No-2 Distribution of patients according to Serum Bilirubin and INR and serum albumin Group I Group II No. of Patients Percentage No. of Patients Percentage Serum Bilirubin (mg/dl) <1.2 0 0 45 90% <0.0001 1.2 - 4 50 100% 5 10% ≥4.1 0 0 0 0 INR <1.5 0 0 50 100% <0.0001 1.5 – 2.2 45 90% 0 0 >2.2 5 10% 0 0 Serum Albumin (g/dl) <2.8 40 80% 0 0 <0.0001 2.8 – 3.5 10 20% 0 0 >3.5 0 0 50 100% Patients with decompensated liver disease and ascites had significantly higher serum bilirubin and INR levels, along with markedly lower serum albumin levels, compared with patients without ascites (p < 0.0001). Table No- 3 Distribution of patients according to Hepatic Encephalopathy Hepatic Encephalopathy Group I Group II No. of Patients Percentage No. of Patients Percentage Grade 1 0 0% 0 0 Grade 2 11 22% 0 0 Grade 3 7 14% 0 0 Grade 4 0 0% 0 0 Absent 32 64% 50 100% Total 50 100% 50 100% p-value <0.0001 (0.000017) In Group I, hepatic encephalopathy was absent in 64% of patients (n = 32), while 22% (n = 11) presented with Grade 2 and 14% (n = 7) presented with Grade 3 hepatic encephalopathy. No patients in either group presented with Grade 1 or Grade 4 hepatic encephalopathy. Table No- 4 Distribution of patients according to Child Pugh Score Child Pugh Score Group I Group II No. of Patients Percentage No. of Patients Percentage 5-6 (Class A) 0 0 50 100% 7-9 (Class B) 19 38% 0 0 10-15 (Class C) 31 62% 0 0 Total 50 100% 50 100% Mean ± SD 9.94 ± 1.99 5.00 ± 0.00 p-value <0.0001 In Group II, 100% of the patients (n = 50) were categorized into Child-Pugh Class A with a mean score of 5.00± 0.00, indicating well-preserved liver function and absence of major clinical decompensation.In contrast, patients in Group I exhibited advanced hepatic dysfunction. The majority of the patients in this group (62%, n = 31) were classified as Child-Pugh Class C, while the remaining 38% (n = 19) fell into Class B. No patients in Group I belonged to Class A. Table No- 5 Distribution of patients according to Serum Sodium Serum Sodium (meq/L) Group I Group II No. of Patients Percentage No. of Patients Percentage <130 36 72% 0 0 130-135 14 28% 0 0 >135 0 0 50 100% Total 50 100% 50 100% Mean ± SD 127.68 ± 2.82 139.64 ± 1.48 p-value <0.0001 In this study, a highly significant statistical difference was found in serum sodium levels between the two cohorts (p < 0.0001). In Group II (Cirrhosis without Ascites), all patients (100%, n = 50) maintained normal serum sodium levels (> 135 mEq), with a mean concentration of 139.64 ±1.48mEq/L, indicating stable electrolyte homeostasis. Table No- 6 Distribution of patients according to MELD Na Score MELD Score Group I Group II No. of Patients Percentage No. of Patients Percentage <11 0 0 50 100% 11-20 10 20% 0 0 >20 40 80% 0 0 Total 50 100% 50 100% Mean ± SD 25.50 ± 4.67 6.84 ± 1.06 p-value <0.0001 In Group II (Cirrhosis without Ascites), all patients (100%) had a MELD score of 10 or less, with a mean score of 6.84 ± 1.06. This indicates a stable clinical status and a relatively low risk of immediate mortality. Conversely, in Group I (Decompensated with Ascites), most patients (80%) had a MELD score greater than 20, reflecting severe liver dysfunction and an increased likelihood of complications. Table No- 7 Distribution of patients according to Renal Resistive index RI Group I Group II No. of Patients Percentage No. of Patients Percentage <0.5 0 0 0 0 0.5-0.7 0 0 50 100% >0.7 50 100% 0 0 Total 50 100% 50 100% Mean ± SD 0.80 ± 0.03 0.59 ± 0.03 p-value <0.0001 In Group II (Cirrhosis without Ascites), all patients (100%) had an RRI value below 0.70, with a mean of 0.59 ± 0.03, indicating normal renal perfusion. In contrast, patients in Group I (Decompensated Liver Disease with Ascites) exhibited significantly higher resistance, with all patients (100%) having an RRI >0.70. Figure 1:Distribution of patients according to Serum Creatinine level The mean value rose from 1.44 ± 0.23 mg/dl on Day 1 to 2.49 ± 0.65 mg/dl by Day 7. This steady increase reflects a rapid decline in the glomerular filtration rate (GFR) and underscores the high risk and incidence of acute kidney injury (AKI). Table No- 8 Distribution of patients according to Hepatorenal Syndrome Day HRS Group I Group II p-value No. of Patients Percentage No. of Patients Percentage Day 1 Present 20 40% 0 0 <0.0001 Absent 30 60% 50 100% Day 7 Present 40 80% 0 0 <0.0001 Absent 10 20% 50 100% The incidence of Hepatorenal Syndrome (HRS) was significantly higher in patients with decompensated liver disease and ascites, increasing from 40% on Day 1 to 80% on Day 7, whereas no patient in the compensated cirrhosis group developed HRS (p < 0.0001). These findings demonstrate the rapid progression of renal dysfunction in decompensated liver disease and emphasize ascites as a major risk factor for HRS.

The age distribution within both cohorts peaked in the 41–50-year category (58% in Group I vs. 52% in Group II). The mean age of Group I was 43.24 ±6.78 years, while that of Group II was 42.96 ± 7.66 years. This demographic balance is consistent with the comparative study by Mukherjee et al.9, who evaluated renal blood flow alterations in Indian cirrhotic patients and established an age baseline (45.10 ± 8.20 years) that matched our cohorts. In our study Serum total bilirubin levels were significantly higher in the ascitic cohort (p < 0.0001). In Group II, 90% of patients maintained normal bilirubin levels (< 1.2 mg/dL), with a group mean of 0.98± 0.12 mg/dL. In contrast, 100% of Group I patients showed pathological elevations, resulting in a mean of 2.10 ± 0.53 mg/dL, with all patients clustering in the 1.2 - 4.0 mg/dL range. A parallel trend was observed in the liver's prohemostatic synthetic capacity, measured via the INR (p < 0.0001). Group II patients maintained excellent coagulation control, with 100% keeping an INR below 1.5 (mean: 1.03 ± 0.09). Conversely, Group I patients displayed significant prothrombin time prolongation: 90% fell between 1.5 - 2.2 and 10% exceeded 2.2, leading to a group mean of 1.90 ±0.26. The most pathophysiologically definitive biomarker evaluated was serum albumin, which showed a stark contrast between the cohorts (p < 0.0001). All patients in Group II maintained normal serum albumin concentrations (> 3.5 g/dL), with a mean of 4.32 ± 0.19 g/dL. In Group I, severe hypoalbuminemia was universally present; 80% of patients had levels below 2.8 g/dL and the remaining 20% fell between 2.8 - 3.5 g/dL, resulting in a depressed group mean of 2.59 ± 0.23 g/dL. In our study HE was entirely absent in Group II (100% absent), confirming their status as compensated patients with preserved metabolic clearance. Within Group I, however, 36% of the cohort presented with clinically manifest HE (22% with Grade 2, 14% with Grade 3), while 64% (n = 32) remained mentally intact at baseline. The difference between the groups was highly significant (p < 0.0001, 0.000017). This connection between neuro-metabolic failure and circulatory issues is supported by Romero-Gómez et al. (69), who showed that patients with both ascites and HE face a significantly higher risk of rapid renal failure compared to patients with ascites alone. The Child-Pugh score in Group II, 100% of patients were classified as Child-Pugh Class A, presenting a minimal mean score of 5.00 ± 0.00. Group I patients, by contrast, showed advanced liver disease: 62% (n = 31) were classified as Class C and 38% (n = 19) as Class B, with a significantly higher mean score of 9.94 ± 1.99 (p < 0.0001). In Group II demonstrated complete stability, with 100% of patients scoring ≤ 10 (mean: 6.84 ± 1.06). In Group I, 80% of patients presented with MELD-Na scores exceeding 20, resulting in a markedly elevated mean score of 25.50 ± 4.67. Our findings closely match the validation data published by Kamath et al.10, who established that a MELD score threshold > 20 indicates severe systemic decompensation and is strongly predictive of acute kidney injury. Group II patients maintained stable electrolyte balance, with 100% showing normal sodium levels above 135 mEq/L (mean: 139.64 ± 1.48 mEq/L). In contrast, Group I patients uniformly demonstrated hyponatremia. Severe to moderate hyponatremia (< 130 mEq/L) was present in 72 (n = 36) of the group, while the remaining 28% (n = 14) had mild hyponatremia (130 - 135 mEq/L), leading to a significantly lower mean sodium level of 127.68 ± 2.82 mEq/L.This electrolyte trend matches the findings of Angeli et al.11 and Sigal et al.12 who conducted large surveys of cirrhotic patients with ascites. Our results showed a significant difference in the Renal Resistive Index (RRI) between the two groups (p < 0.0001). In Group II, 100% of patients maintained normal RRI values below 0.70, with a mean of 0.59 ± 0.03, indicating healthy renal perfusion. In stark contrast, every patient (100%) in Group I demonstrated an abnormal RRI exceeding 0.70, resulting in an elevated mean value of 0.80 ± 0.03.This diagnostic insight aligns with studies by Radhakrishnan et al.13 and Sanyal et al.14, which evaluated the role of non-invasive vascular imaging in cirrhosis. In our study In Group II, renal function remained remarkably stable. Serum creatinine values were normal on Day 1 (0.86 ± 0.11 mg/dL) and showed no significant change by Day 7 (0.87 ± 0.12 mg/dL), resulting in a 0% incidence of HRS. Conversely, Group I patients experienced a rapid, progressive decline in renal filtration (p < 0.0001). Mean serum creatinine in Group I started at an elevated baseline of 1.44 ± 0.23 mg/dL on Day 1 and rose sharply to 2.49 ± 0.65 mg/dL by Day 7. On Day 1, HRS was already present in 40% (n = 20) of Group I patients, driven by their high baseline vascular resistance. By Day 7, the proportion of active HRS cases doubled to 80% (n = 40), leaving only 20% (n = 10) free from this severe complication.

In this study we performed renal artery duplex Doppler imaging to evaluate the Renal Resistive Index (RRI) in patients with decompensated liver disease. We demonstrated that 100% of Group I (ascitic) patients exhibited an elevated RRI (>0.70), with a mean value of 0.80 ± 0.03 that directly correlated with a rapid decline in glomerular filtration rate and a surge in Hepatorenal Syndrome (HRS) from 40% on Day 1 to 80% by Day 7. Clinically, these findings establish RRI as a highly sensitive, non-invasive early warning metric. Routine bedside Doppler screening allows clinicians to initiate aggressive, pre-emptive renal protection therapies long before standard serum creatinine elevations manifest.

1. Naveau S, Perlemuter G, Balian A. Epidemiology and natural history of cirrhosis. Rev Prat. 2005 Sep 30;55(14):1527-32. 2. 2. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371(9615):838-51. doi: 10.1016/S0140-6736(08)60383-9. 3. 3.Sandeep M, Hemant K, Rowen K. Hepatorenal syndrome. eMedicine; 2008. 4. 4.Yeung E, Yong E, Wong F. Renal dysfunction in cirrhosis: Diagnosis, treatment, and prevention. MedGenMed. 2004;6:9. 5. 5. Hecker R, Sherlock S. Electrolyte and circulatory changes in terminal liver failure. Lancet. 1956;2:1221-5. 6. 6.Rockey DC, Caldwell SH, Goodman ZD, Nelson RC, Smith AD. Liver biopsy. Hepatology. 2009;49:1017-44. 7. 7. Scheuer PJ, Lefkowitch JH. Liver Biopsy Interpretation. 7th ed. Philadelphia: Elsevier Saunders; 2006. p. 171. 8. 8.McCormick PA, Nolan N. Palpable epigastric liver as a sign of cirrhosis: A prospective study. Eur J Gastroenterol Hepatol. 2004;16:1331-4. 9. 9.Mukherjee S, Santhosh R, Govil S. Intrarenal arterial doppler sonography in patients with chronic liver disease: Correlation with clinical stage and renal function. Indian J Radiol Imaging. 2018;28(3):295-301. 10. 10.Kamath PS, Wiesner RH, Malinchoc M, Kremers W, Therneau TM, Kosberg CL, et al. A model to predict survival in patients with end-stage liver disease. Hepatology. 2001;33(2):464-470. 11. 11.Angeli P, Wong F, Watson H, Ginès P. Hyponatremia in cirrhosis: Results of a patient population survey. Hepatology. 2006;44(6):1535-1542. 12. 12. Sigal SH, Stanca CM, Fernandez J. Dilutional hyponatremia as a marker of cardiovascular underfilling in decompensated cirrhosis. Am J Gastroenterol. 2012;107(4):540-547. 13. 13.Radhakrishnan R, Natarajan S, Ramachandran A. Renal resistive index as an early predictor of functional renal impairment in decompensated chronic liver disease. Indian J Gastroenterol. 2019;38(4):312-319. 14. 14. Sanyal AJ, Bosch J, Blei A, Arroyo V. Renal dysfunction in cirrhosis: Pathophysiology, clinical features, and management. Hepatology. 2010;51(1):345-356..