Acute kidney injury after TIPS in decompensated cirrhosis patients: a retrospective cohort study

Abstract

Background

Acute kidney injury (AKI) is a common postoperative complication associated with increased mortality. The transjugular intrahepatic portosystemic shunt (TIPS) is an effective intervention for portal hypertension in patients with decompensated cirrhosis; however, the incidence and risk factors for AKI following TIPS in patients with cirrhosis have not been fully elucidated. We aimed to investigate the clinical features of AKI after TIPS in patients with cirrhosis.

Method

Data from 384 patients with decompensated cirrhosis who underwent TIPS treatment were retrospectively collected. AKI was defined using the criteria recommended by 2012 the clinical practice guideline of Kidney Disease Improving Global Outcomes (KDIGO). We conducted univariate and multivariate logistic regression analyses to evaluate the risk factors for AKI and the association between AKI and all-cause mortality.

Results

Of these 384 cirrhosis patients, 8.3% developed AKI after TIPS treatment. Multivariate logistic regression analysis indicated that independent risk factors associated with AKI were diabetes (OR = 3.632, 95% CI 1.358–9.711, P = 0.010), baseline estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m² (OR = 4.312, 95% CI 1.884–9.868, P = 0.001), serum albumin level (OR = 0.862, 95% CI 0.768–0.968, P = 0.012), postoperative portal venous pressure gradient (PPG) (OR = 1.094, 95% CI 1.010–1.185, P = 0.028), and intraoperative hypotension (OR = 4.669, 95% CI 1.653–13.183, P < 0.004); and AKI was independently associated with an increased risk of all-cause mortality within 3 months after TIPS treatment (OR 3.141, 95% CI 1.091–9.038, P = 0.034) .

Conclusion

AKI in patients undergoing TIPS treatment is not uncommon; Diabetes, baseline kidney dysfunction, factors affecting effective circulatory volume, and higher postoperative PPG are closely associated with the occurrence of AKI. AKI is associated with an increased risk of all-cause mortality and medical expenses of those patients.

Introduction

Portal hypertension is one of the serious complications with higher mortality in patients with decompensated cirrhosis [1–4]. Currently, transjugular intrahepatic portosystemic shunt (TIPS) has become an effective treatment for portal hypertension in patients with decompensated cirrhosis [5–8]. Due to the process of TIPS includes some potential risk factors like the application of contrast regimen, bleeding, and infections, the risk of acute kidney injury (AKI) among those patients has also caused great attention in recent years [9–11]. Previous studies showed that the incidence of AKI in patients undergoing TIPS varies widely from 10% to 30.62%, and the occurrence of AKI also affected the prognosis of patients who received TIPS treatment [12–14]. The high variability of AKI incidence was believed to be related to differences in the enrolled patients and contrast regimens applied, as well as different definitions of AKI applied in the studies [12, 13]. Although TIPS treatment has been applied in decompensated cirrhosis patients in China for more than 30 years, there is still no systematic analysis of the incidence of AKI and its related issues.

Therefore, we performed a retrospective study based on clinical data of 384 Chinese patients with portal hypertension who underwent TIPS treatment. We aimed to evaluate the incidence, risk factors, and the impact of AKI on the outcomes of those patients.

Methods

Study design and population

We conducted a retrospective observational study. The study population included all patients with TIPS treatment between October 2020 and March 2022 at Beijing Shijitan Hospital. The inclusion criteria were as follows: (1) Age 18 years or older. (2) Diagnosis of decompensated cirrhosis, evidenced by clinically apparent ascites, variceal hemorrhage, and/or overt hepatic encephalopathy, as defined by the Baveno VII consensus [15]. (3) Presence of portal hypertension, defined by a hepatic venous pressure gradient (HVPG) ≥ 10 mmHg [15]. Patients with baseline estimated glomerular filtration rate (eGFR) < 15 ml/min/1.73m², and those with incomplete serum creatinine (SCr) data within 7 days after TIPS for AKI determination were excluded from the study.

The ethical approval for this study was granted by the Institutional Ethical Review Board of Beijing Shijitan Hospital, Capital Medical University [sjtkyll-lx-2023-028]). Informed consent for inclusion in the present study was waived because of its retrospective features. This study was conducted in accordance with the Declaration of Helsinki.

Data collection

The data were retrieved from the patient’s electronic medical charts in the database of our hospital. Each patient’s medical information was reviewed and recorded, including demographic information, etiology of cirrhosis, comorbidities (hypertension and diabetes mellitus), concomitant medications 7 days before operation (angiotensin-converting enzyme inhibitors [ACEI] or angiotensin receptor blockers [ARB], diuretics, non-selective beta blockers [NSBBs] and proton pump inhibitor [PPI]), body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), laboratory data on preoperative serum concentrations of hemoglobin, albumin, total bilirubin (TBIL), ammonia, sodium, creatinine, and uric acid. We collected Child-Pugh scores reflecting baseline liver function and estimated glomerular filtration rate (eGFR, calculated using the CKD-EPI formula) [16] reflecting baseline renal function. Key intraoperative and postoperative variables were documented. These included the intraoperative contrast dose, the occurrence of intraoperative hypotension (defined as a > 20% reduction in systolic blood pressure from baseline or a sustained mean arterial pressure [MAP] < 65 mmHg) [17], the postoperative portal pressure gradient (PPG), and any postoperative infections occurring within 7 days. In this study, we retrieved SCr levels before surgery, 48 h, and 7 days after TIPS treatment from medical records, as well as changes in SCr in AKI patients until discharge.

Ascertainment of AKI

AKI was defined and staged according to the clinical practice guideline of Kidney Disease Improving Global Outcomes (KDIGO) criteria 2012 [18]. (AKI stage I: increase in Scr > 0.3 mg/dl within 48 h, or increase to at least 1.5 times baseline within the prior 7 days; stage II: increase in Scr 2-2.9 times baseline; stage III: increase in Scr > 4 mg/dl or greater than 3 times of the baseline or receiving renal replacement therapy) [18].

We defined renal recovery at discharge as full recovery with serum creatinine decreased to below the threshold or to the baseline. We defined partial recovery as serum creatinine decreased by 25% or more from peak concentration but remained higher than the threshold or baseline. We defined failure to recover as the patient still being dependent on dialysis or serum creatinine decreased by less than 25% from peak concentration [19].

Outcomes

The primary outcome was all-cause mortality, which was defined as all causes of death within 3 months. Secondary outcomes included length of hospital stay and hospitalization expenses.

Statistical analysis

Data were presented as absolute variables and percentages (%) for categorical variables and either median with interquartile range (IQR: 25th–75th percentile) or mean with standard deviation according to the distribution of the variables. The Student’s t-test or Mann–Whitney test was implemented to test for differences between various characteristics. Fisher’s exact or chi-square test was used for categorical variables, as appropriate. Using univariate and multivariate logistic regression models, we analyzed the risk factors for AKI, with AKI as the dependent variable, and all baseline variables as covariates, including age, sex, BMI and comorbidities (hypertension and diabetes mellitus), concomitant medications (ACEI or ARB, diuretics, PPI, NSBBs), SBP, DBP, serum concentration of hemoglobin, albumin, TBIL, ammonia, sodium, creatinine, and uric acid, the grading of encephalopathy, ascites, and prothrombin time prolongation (seconds) in the Child-Pugh Score, eGFR, as well as some operative parameters (such as intraoperative contrast dosage, intraoperative hypotension, PPG value, and postoperative infection). We also examined the association between AKI and all-cause mortality within 3 months after TIPS treatment. An odds ratio (OR) with a 95% confidence interval (95% CI) was reported for each covariate of interest. Key clinical factors such as age, sex, BMI and all covariates with a P value of less than 0.10 on univariable analysis were entered into the multivariable model. Statistical significance was set at a value of P < 0.05. Analyses were performed with SPSS version 21.0 statistical software (SPSS Inc., Chicago, IL, USA).

Results

Demographics and clinical characteristics

We first enrolled 399 patients from the database of our hospital, 15 patients were excluded according to the exclusion criteria, and we finally included 384 patients in our study. Post-TIPS AKI occurred in 8.3% of patients (n = 32), while 91.7% (n = 352) were non-AKI patients. (Fig. 1).

Fig. 1.

Flowchart of participant selection. Abbreviations: TIPS: transjugular intrahepatic portosystemic shunt, eGFR: estimated glomerular filtration rate, AKI: acute kidney injury

Patients in the AKI group were more likely to have comorbid diabetes mellitus, concomitant medications of diuretics, baseline eGFR < 60 ml/min/1.73 m², a higher Child-Pugh Score, higher level of serum creatinine and uric acid, and lower level of hemoglobin and serum albumin (P < 0.05 or P < 0.001). Regarding operative parameters, patients in the AKI group were more likely to have a higher level of postoperative PPG and a higher proportion of intraoperative hypotension (P < 0.05). There were no significant differences in age, sex, etiology, TIPS indications, BMI, blood pressure, baseline serum level of TBIL, ammonia, and sodium, contrast dosages, and postoperative infection between the two groups (P > 0.05). (Table 1).

Table 1.

Baseline characteristics according to the presence of post-TIPS AKI

Characteristic	All (n = 384)	Non-AKI (n = 352)	AKI (n = 32)	P-value
Age (year)	53.17 ± 13.35	52.85 ± 13.07	56.75 ± 13.62	0.108
Female, n (%)	122(31.8)	110(31.3)	12(37.5)	0.467
Etiology of cirrhosis, n (%)				0.368
Viral hepatitis	184(47.9)	172(48.9)	12(37.5)
Drug-induced liver injury	46(12.0)	42(11.9)	4(12.5)
Alcohol-associated	36(9.4)	32(9.1)	4(12.5)
Autoimmune hepatitis	30(7.8)	26(7.4)	4(12.5)
Cholestatic hepatitis	24(6.3)	20(5.7)	4(12.5)
Others	64(16.7)	60(17.0)	4(12.5)
TIPS Indications				0.186
Refractory ascites	162(42.2)	148(42.0)	14(43.8)
Variceal Bleed	192(50.0)	179(50.9)	13(40.6)
Multiple Indications	30(7.8)	25(7.1)	5(15.6)
Child-Pugh Score	8.11 ± 2.24	8.32 ± 1.70	9.13 ± 1.68	0.011
Encephalopathy	2(1,2)	2(1,2)	2(1,2)	0.154
Ascites	2(2,3)	2(2,3)	2.5(2,3)	0.050
Bilirubin	1(1,2)	1(1,2)	1(1,2)	0.661
Albumin	2(2,2)	2(2,2)	2(2,2.75)	0.001
Prothrombin Time (sec prolonged)	1(1,2)	1(1,2)	1(1,1.75)	0.544
Complications, n (%)
Diabetes	74(19.3)	62(17.6)	12(37.5)	0.006
Hypertension	32(8.3)	32(9.1)	0(0)	0.148
Concomitant medications, n (%)
ACEI or ARB	31(8.7)	27(7.7)	4(12.5)	0.534
Diuretics	283(79.1)	254(72.2)	29(90.6)	0.039
PPI	302(84.4)	275(78.1)	27(84.4)	0.548
NSBBs	258(67.2)	238(67.6)	20(62.5)	0.555
BMI (kg/m2)	22.94 ± 3.50	22.73 ± 3.80	23.39 ± 3.97	0.353
SBP (mmHg)	128.82 ± 17.11	128.94 ± 17.16	127.50 ± 16.76	0.646
DBP (mmHg)	72.86 ± 9.90	72.69 ± 9.36	74.69 ± 14.66	0.455
Hemoglobin (g/L)	90.65 ± 24.28	90.76 ± 24.07	89.44 ± 26.89	0.012
Albumin (g/L)	32.56 ± 3.79	32.76 ± 3.76	30.36 ± 3.42	0.001
TBIL (umol/L)	29.34 ± 18.07	29.39 ± 18.20	28.94 ± 16.85	0.895
Ammonia (mmol/L)	49.35(35.95, 54.98)	43.95(36.10, 53.93)	44.55(28.98, 64.95)	0.997
Sodium (mmol/L)	139.17 ± 4.32	139.23 ± 4.38	138.50 ± 3.52	0.358
SCr (umol/L)	65.50(54.25, 78.50)	65.00(52.00, 75.75)	90.50(70.00, 128.75)	< 0.001
Uric acid (umol/L)	318.50(239.25, 406.75)	306.00(226.75, 402.75)	392.00(275.25, 562.25)	0.004
eGFR < 60 ml/min/1.73 m²(%)	52(13.5)	38(10.8)	14(43.8)	< 0.001
Administered contrast (ml)	95.36 ± 46.83	94.65 ± 46.63	103.13 ± 49.08	0.328
Postoperative PPG (mmHg)	10.96 ± 5.41	10.60 ± 5.44	13.69 ± 4.34	0.003
Intraoperative hypotension (%)	26(6.8)	18(5.1)	8(25)	0.001
Postoperative infection (%)	206(53.6)	184(52.3)	22(68.8)	0.074

Note: Values for categorical variables are given as number (percentage); for continuous variables, as mean ± standard deviation or median [IQR]

Abbreviations: AKI, acute kidney injury. ACEI, angiotensin-converting enzyme inhibitors. ARB, angiotensin receptor blockers. PPI, proton pump inhibitor. NSBBs, non-selective beta blockers. BMI, body mass index. SBP, systolic blood pressure. DBP, diastolic blood pressure. TBIL, total bilirubin. SCr, serum creatinine. eGFR, estimated glomerular filtration rate. PPG, portal pressure gradient

AKI stages and renal recovery

Among the patients who developed AKI, the majority of them were in mild severity [stage 1: 18 (56.3% of AKI episodes) patients, stage 2: 8 (25%) patient, and stage 3: 6 (18.7%) patients], 2 (6.25%) patients received acute renal replacement therapy. The median time from surgery initiation to AKI was 3.5 (IQR 2.5 to 6.5) days. At the time of discharge, among 32 patients with AKI, 6 (18.8%) patients had full renal recovery, 22 (75.0%) patients had partial recovery, and 4 (6.3%) patients had no recovery. (Fig. 2).

Fig. 2.

ASKI stages and renal recovery. Abbreviations: AKI, acute kidney injury

Risk factors associated with AKI

Results of univariable and multivariable logistic regression analyses were summarized in Table 2. Unadjusted analysis revealed post-TIPS AKI was associated with comorbidities of diabetes, concomitant medications of diuretics, baseline eGFR < 60 ml/min/1.73 m², Child-Pugh Score-Ascites, baseline serum level of albumin and uric acid, postoperative PPG, and intraoperative hypotension(P < 0.10); Multivariate logistic regression analysis showed that the risk factors independently associated with post-TIPS AKI included combination of diabetes (OR = 3.632, 95% CI 1.358–9.711, P = 0.010), baseline eGFR < 60 ml/min/1.73m² (OR = 4.312, 95%CI 1.884–9.868, P = 0.001), decreased albumin level (OR = 0.862, 95%CI 0.768–0.968, P = 0.012), increased postoperative PPG (OR = 1.094, 95%CI 1.010–1.185, P = 0.028), and intraoperative hypotension (OR = 4.669, 95%CI 1.653–13.183, P = 0.004).

Table 2.

Risk factors associated with post-TIPS AKI

Variables	Unadjusted			Multivariate adjusted *
	OR	95% CI	P-value	OR	95% CI	P-value
Age (year)	1.025	0.995–1.056	0.109	-	-	-
Female, n (%)	1.320	0.623–2.795	0.468	-	-	-
BMI (kg/m2)	1.039	0.940–1.149	0.455	-	-	-
Diabetes	2.806	1.304–6.040	0.008	3.632	1.358–9.711	0.010
Diuretics	5.551	1.301–23.684	0.021	-	-	-
Child-Pugh Score-Ascites	1.659	0.991–2.779	0.054	-	-	-
Serum albumin (g/L)	0.840	0.795–0.929	0.001	0.862	0.768–0.968	0.012
Uric acid (umol/L)	1.003	1.001–1.006	0.005	-	-	-
eGFR < 60 ml/min/1.73 m²	6.386	2.941–13.867	< 0.001	4.312	1.884–9.868	0.001
Postoperative PPG (mmHg)	1.110	1.025–1.190	0.004	1.094	1.010–1.185	0.028
Intraoperative hypotension	6.185	2.440-15.679	< 0.001	4.669	1.653–13.183	0.004

Key clinical factors such as age, sex, BMI and all covariates with a P value of less than 0.10 on univariable analysis were entered into the multivariable model, including comorbidities of diabetes, combined diuretics, the grading of ascites in the Child-Pugh Score, the serum level of albumin and uric acid, baseline eGFR < 60 ml/min/1.73m², postoperative PPG, and intraoperative hypotension

Abbreviation: OR, odds ratio. CI, confidence interval. eGFR, estimated glomerular filtration rate. PPG, portal pressure gradient. The hyphen symbol (‘-‘) indicates that the variable was excluded from the final multivariate logistic regression model

The association between AKI and outcomes

During a median follow-up of 3.0 (interquartile range, 2.8–3.3) months, there were 7(21.9%) and 22(6.3%) deaths in the AKI group and non-AKI group, respectively. The all-cause mortality of AKI group is higher than that of non-AKI group (P = 0.004) (Table 3).

Table 3.

Comparison of outcomes between non-AKI group and AKI group patients

Characteristics	Non-AKI (n = 352)	AKI (n = 32)	P-value
3-month mortality, n (%)	22(6.3)	7(21.9)	0.004
Cause of death			0.494
Hepatic encephalopathy	6(27.3)	2(28.6)
Esophageal variceal bleed	7(31.8)	2(28.6)
AKI	0	1(14.3)
Severe infection	4(18.2)	1(14.3)
Other causes	5(22.7)	1(14.3)
Hospitalization time (days)	25.99 ± 5.35	29.63 ± 7.21	0.009
Hospitalization expenses (×10,000 CNY)	12.65 ± 4.11	15.17 ± 3.63	< 0.001

Abbreviations: CNY, Chinese Yuan. AKI, Acute Kidney Injury

The leading causes of mortality were hepatic encephalopathy, esophageal variceal bleed, AKI and severe infection. A comparison of the spectrum of causes of death between patients with and without AKI revealed no statistically significant differences (Table 3).

Compared with non-AKI patients, AKI patients had significantly longer hospital stays (P = 0.009) and higher hospitalization costs (P < 0.001).

The results of logistic regression analysis showed AKI was associated with higher odds ratios for 3-month all-cause mortality compared with that in non-AKI group in unadjusted analyses (OR = 4.200, 95% CI 1.636–6.560, P = 0.003). After adjusting (Model 1 was adjusted for demographics, comorbidities, and primary diseases, including age, sex, BMI and comorbidities of hypertension, diabetes and the grading of encephalopathy, ascites, and prothrombin time prolongation (seconds) in the Child-Pugh Score; Model 2 was adjusted for model 1 plus laboratory tests and operative related factors, including serum levels of albumin, total bilirubin, baseline eGFR and postoperative PPG, intraoperative hypotension, and postoperative infection), the association was slightly affected but observed consistent as before (Model 1: OR = 3.129, 95% CI 1.133–8.645, P = 0.028; Model 2: OR = 3.141, 95%CI 1.091–9.038, P = 0.034) (Table 4).

Table 4.

The association between post-TIPS AKI and 3-month all-cause mortality

Groups	Unadjusted Model		Multivariate Model 1		Multivariate Model 2
	OR (95% CI)	P-value	OR (95% CI)	P-value	OR (95% CI)	P-value
Non-AKI	1.000 (reference)		1.000 (reference)		1.000 (reference)
AKI	4.200(1.636–6.560)	0.003	3.129(1.133–8.645)	0.028	3.141(1.091–9.038)	0.034

Unadjusted and multivariable-adjusted ORs were analyzed by the binary logistic regression model with all-cause death. Multivariable model 1 was adjusted for age, sex, BMI and comorbidities of hypertension, diabetes and the grading of encephalopathy, ascites, and prothrombin time prolongation (seconds) in the Child-Pugh Score. Multivariable model 2 was adjusted for model 1 plus serum levels of albumin, total bilirubin, baseline eGFR and postoperative PPG, intraoperative hypotension and postoperative infection.

Discussion

In this retrospective analysis, we found that the incidence of postoperative AKI was 8.3% in a group of decompensated cirrhosis patients with portal hypertension and receiving TIPS treatment, the associated risk factors with the incidence of AKI among these patients were diabetes, baseline eGFR less than 60 ml/min/1.73 m², lower serum albumin level, intraoperative hypotension, and postoperative high PPG. Patients who developed AKI had significantly increased length of hospital stay, medical expenses, and risk of 3-month all-cause mortality compared to non-AKI patients.

The reported incidence of TIPS-related AKI varies considerably across existing studies [12–14]. The difference in AKI incidence in previous studies may be related to the following aspects. First, the TIPS-related treatment has been gradually improved and modified in recent years [20, 21], such as the appearance of newly designed TIPS surgical instruments [22, 23], application of low-osmotic or iso-osmotic contrast agents, and a more accurate and safer volume detection system [24, 25] have brought great improvement in the safety of the operation and reduced the occurrence of complications. Second, there were differences in the race and primary diseases of TIPS-treated patients in different studies. In the ALTA study, the leading cause of the disease was alcoholic cirrhosis [13], while in our study, the leading cause was hepatitis B. These differences in race and primary diseases might be involved in the occurrence of AKI in patients experiencing TIPS treatment. Third, the diagnostic criteria of AKI were inconsistent until the 2012 KDIGO AKI guideline was published; this inconsistency in AKI definition affected the assessment of AKI. Compared with previous studies, we used the AKI diagnostic criteria recommended by the 2012 KDIGO guidelines, ensuring the sensitivity and specificity of AKI diagnosis in the selected patients. Future studies about the incidence of AKI in patients of different races and regions are needed by using this criterion of AKI.

Another important issue concerning TIPS-related AKI is the associated risk factors for the incidence of AKI. Previous studies have found that diabetes, baseline kidney function abnormalities, and decreased serum albumin levels were independent risk factors for AKI after TIPS. Danziger et al. observed 163 TIPS-treated patients from 2001 to 2011 and found that for every 50 ml increase in contrast agent dose during TIPS treatment, the risk of AKI increased by 1.6-fold [12]. Besides, some studies also indicated that the concentration and dose of iodine-containing contrast agents are important determinants of renal toxicity [26–28]. In our study, the use of contrast regimens did not become an independent risk factor for the occurrence of AKI, possibly because the patients in this study generally received low-osmotic or iso-osmotic contrast agents with lower renal toxicity [29], and the contrast dose was significantly lower than those in the abovementioned studies (95.4 ± 46.8 ml vs. 165.2 ± 50.7 ml). At the same time, diabetes and baseline kidney dysfunction were also identified as independent risk factors of AKI [30–34] in our analysis among patients undergoing TIPS treatment. In our study, postoperative PPG in the AKI group was significantly higher than in the non-AKI group, and postoperative high PPG became an independent risk factor for the occurrence of AKI. Portal hypertension is associated with elevated levels of endogenous vasodilatory substances, including nitric oxide [35–38]. TIPS could reverse these changes by lowering PPG [39, 40]. A reduction in the PPG following TIPS placement is a critical step in achieving the therapeutic goals for portal hypertension, exerting a direct influence on renal hemodynamics and perfusion status [41]. An appropriate reduction in PPG contributes to a decrease in portosystemic vascular resistance, which can alleviate organ congestion secondary to portal hypertension and improve systemic and renal hemodynamics [42]. Consequently, this enhances renal arterial perfusion pressure, promotes the restoration of renal tissue blood flow, improves the glomerular filtration rate, and thereby ameliorates renal function. Hypoalbuminemia is a common complication in patients with decompensated liver cirrhosis. Albumin in the plasma plays a critical role in maintaining plasma colloid osmotic pressure, which is essential for stabilizing blood volume. This mechanism helps prevent fluid extravasation from the intravascular compartment into the interstitial space, thereby reducing the occurrence of edema. Additionally, albumin exhibits both antioxidant and anti-inflammatory properties. Its antioxidant activity is primarily manifested through the scavenging of free radicals and binding to harmful metal ions, which mitigates oxidative stress-induced tissue damage [43]. Furthermore, albumin modulates inflammatory responses by inhibiting the release of pro-inflammatory mediators, thereby exerting a protective effect in systemic inflammatory states [44], particularly in conditions such as liver disease and infections [45]. In addition, decreased serum albumin and the occurrence of intraoperative hypotension were related to the occurrence of AKI in end-stage liver disease patients by affecting effective circulating volume [46–48]. The changes in the associated risk factors of AKI in TIPS-treated patients also reflect that the TIPS treatment procedure continues to be upgraded.

Furthermore, there were significant differences in prognosis and medical expenses between AKI and non-AKI patients in this study. Due to the differences in the primary disease of cirrhosis with portal hypertension in previous studies, there are variations in the overall mortality rates of patients in different studies [49]. However, the comparison between the AKI and non-AKI groups both suggested that the former had a significantly higher mortality rate [50] and a significant increase in medical costs. This indicated that early prevention of AKI is important in improving the overall treatment outcomes for those patients.

Limitations

This study has several limitations. First, due to the retrospective nature of this study, specific time points of renal function data may be missing during the data collection process, resulting in patients being unable to be included in our study. Second, patients with portal hypertension who progress to TIPS treatment often have multiple complications, leading to neglecting the monitoring of changes in kidney function, ultimately resulting in their exclusion from this study. Future studies are needed to evaluate the clinical features of AKI among patients undergoing TIPS treatment.

Conclusions

In conclusion, AKI in decompensated cirrhosis patients undergoing TIPS treatment is not uncommon; Diabetes, baseline renal function abnormalities, factors affecting effective circulatory volume, and higher postoperative PPG are closely associated with the occurrence of AKI. AKI is associated with an increased risk of all-cause mortality and medical expenses of those patients. Early detection and proper intervention of AKI based on individual characteristics are necessary.

Abbreviations

AKI

Acute kidney injury

TIPS

Transjugular intrahepatic portosystemic shunt

eGFR

estimated glomerular filtration rate

PPG

Portal venous pressure gradient

HVPG

Hepatic venous pressure gradient

ESRD

End-stage renal disease

SCr

Serum creatinine

ACEI

Angiotensin-converting enzyme inhibitors

ARB

Angiotensin receptor blockers

PPI

Proton pump inhibitor

NSBBs

Non-selective beta blockers

BMI

Body mass index

SBP

Systolic blood pressure

DBP

Diastolic blood pressure

MAP

Mean arterial pressure

TBIL

Total bilirubin

PT

Prothrombin time

KDIGO

Kidney Disease Improving Global Outcomes

IQR

Interquartile range

OR

Odds ratio

CI

Confidence interval

CNY

Chinese Yuan

ALTA

Advancing Liver Therapeutic Approaches

RAAS

Renin-angiotensin-aldosterone system

Author contributions

MJ:​​ Data collection, analysis, manuscript writing. ​YDG, PPY:​​ Statistical data analysis.XLZ:​​ Data collection. ​YL:​​ Study design, manuscript revision.

Funding

This work was supported by the Science and Technology Research and Development Project of China Railway Co., Ltd. (J2022Z608), and Capital’s Funds for Health Improvement and Research (CFH 2022-2-2081).

Data availability

The datasets analyzed in the current study are not publicly available to ensure the privacy of research participants and comply with the regulations of the ethics approval. The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

The data analysis was performed according to the Declaration of Helsinki and was approved by the Medical Ethics Committee of Beijing Shijitan Hospital, Capital Medical University [Ethics Approval Number: sjtkyll-lx-2023(028)].

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.