2026 Volume 51 Issue 10 Pages 527-532
Fish gallbladder ingestion remains a traditional folk remedy in several Asian countries but may result in severe hepatorenal toxicity. We report three patients admitted to the Poison Control Center, Bach Mai Hospital, Hanoi, Vietnam, following ingestion of grass carp (Ctenopharyngodon idella) gallbladders. A 44-year-old man developed severe hepatocellular injury (peak AST 4442 U/L, ALT 5115 U/L), moderate acute kidney injury (AKI), and prolonged severe hypertension requiring intravenous nicardipine infusion for 88 hr. A 48-year-old man presented with severe AKI (peak creatinine 749 µmol/L) and toxic hepatitis and underwent intermittent hemodialysis because of rapidly progressive renal dysfunction despite preserved urine output. A 73-year-old woman developed severe acute hepatocellular injury with AST and ALT levels exceeding 7000 U/L and ferritin of 40,000 ng/mL but without clinically significant AKI. Peak total bilirubin concentrations were 83.6, 102, and 99 µmol/L in Cases 1, 2, and 3, respectively. Viral hepatitis investigations were negative in all patients. Despite variable clinical phenotypes, all patients recovered with supportive treatment. These cases further illustrate the variable patterns of hepatorenal involvement following grass carp gallbladder ingestion, ranging from dialysis-requiring acute kidney injury to predominant hepatocellular injury with preserved renal function. Because toxin exposure could not be quantified, the observed variability may reflect differences in ingested toxin dose, host susceptibility, or both. These findings highlight interindividual variability in patterns of hepatorenal involvement following grass carp gallbladder ingestion.
Ingestion of raw fish gallbladder is a traditional practice in several Asian countries, including Vietnam, China, India, and Japan, where it is believed to improve health, vision, rheumatism, and sexual performance (Chan et al., 1985; Xiaodan et al., 2012). However, ingestion of fish bile, particularly from cyprinid fish such as grass carp (Ctenopharyngodon idella), has been associated with severe toxicity, most commonly acute kidney injury (AKI) and acute hepatocellular injury (Chan et al., 1985; Lin and Huang,1991). Previous reports have described a wide spectrum of toxicity ranging from transient biochemical abnormalities to multiple-organ dysfunction requiring intensive care management (Xiaodan et al., 2012; Lim et al., 1993; Lin and Huang, 1991; Zhou et al., 2021).
The toxic effects are generally attributed to sodium cyprinol sulfate and related bile alcohol compounds that are resistant to heat and alcohol processing (Yip et al., 1981). Experimental studies suggest that these compounds induce direct cellular injury through mitochondrial dysfunction, oxidative stress, and tubular epithelial damage (Yip et al., 1981; Munilkumar et al., 2024).
Although fish gallbladder poisoning has been reported previously, previous reports have demonstrated variable degrees of hepatic and renal injury, ranging from isolated organ involvement to combined hepatorenal toxicity. However, direct comparison of different patterns of organ involvement within a single case series has rarely been described in detail. Here, we describe three patients with grass carp gallbladder poisoning who exhibited variable patterns of hepatic and renal involvement, including mixed hepatorenal injury with severe hypertension, dialysis-requiring acute kidney injury, and predominant hepatocellular injury with preserved renal function.
This retrospective case series included three consecutive patients admitted to the Poison Control Center, Bach Mai Hospital, Hanoi, Vietnam, after ingestion of raw grass carp (Ctenopharyngodon idella) gallbladders. The diagnosis of fish gallbladder poisoning was established based on a documented history of grass carp gallbladder ingestion, compatible clinical manifestations, exclusion of alternative causes, and temporal association between exposure and onset of symptoms. Clinical records were reviewed to collect demographic characteristics, exposure history, clinical manifestations, laboratory findings, imaging results, treatment interventions, and clinical outcomes.
All laboratory investigations were performed as part of routine clinical care. Serial biochemical measurements were reviewed to evaluate the temporal evolution of hepatic and renal injury. All patient data were anonymized before analysis. Because no validated clinical assay for sodium cyprinol sulfate or related bile alcohol toxins was available at our institution, toxin exposure could not be quantified. Consequently, differences in clinical manifestations could not be attributed to toxin dose, individual susceptibility, or both.
Ethics approval and consent to participateAccording to institutional policy at Bach Mai Hospital, anonymized retrospective case reports and small case series derived from routine clinical care are exempt from formal Institutional Review Board review. Written informed consent for publication was obtained from all patients.
A 44-year-old previously healthy man ingested two raw grass carp gallbladders derived from one 6-kg and one 3-kg fish. Approximately 20 min later, he developed bilateral eyelid edema, suprapubic abdominal pain, and diarrhea. He was admitted to the Poison Control Center 3 hr after ingestion.
On admission, blood pressure was markedly elevated at 190/120 mmHg. Laboratory evaluation demonstrated severe hepatocellular injury (AST 4442 U/L, ALT 5115 U/L) and moderate AKI (creatinine 161 µmol/L). Urinalysis showed proteinuria, low urine specific gravity, and microscopic hematuria. Total bilirubin progressively increased and reached a peak value of 83.6 µmol/L. Viral hepatitis investigations, including hepatitis A, B, and C, HIV, HSV, CMV, and EBV, were negative. Coagulation studies remained within the normal range throughout hospitalization (lowest PT: 73%; peak INR: 1.24), and no clinically significant coagulopathy developed.
The patient received intravenous fluids, furosemide, oral silymarin, and continuous intravenous nicardipine infusion. Severe hypertension persisted for approximately 88 hr before gradual normalization. Peak serum creatinine reached 252 µmol/L. The patient recovered without renal replacement therapy and was discharged on day 15 after ingestion. The temporal changes in AST, ALT, creatinine, and bilirubin are shown in Fig. 1
Temporal evolution of serum AST, ALT, and serum creatinine in Case 1 following ingestion of raw grass carp (Ctenopharyngodon idella) gallbladders.
A 48-year-old previously healthy man ingested one raw grass carp gallbladder obtained from a 3-kg fish. Nineteen hours later, he developed abdominal pain and diarrhea and presented to our center 33 hr after ingestion.
Physical examination revealed jaundice. Initial laboratory testing demonstrated severe AKI with serum creatinine of 447 µmol/L, which subsequently increased to a peak of 749 µmol/L. AST and ALT levels reached 1631 U/L and 3958 U/L, respectively. Peak total bilirubin concentration was 102 µmol/L. Urinalysis demonstrated proteinuria, low urine specific gravity, and trace hematuria. Renal ultrasonography revealed bilateral increased renal parenchymal echogenicity without hydronephrosis, supporting intrinsic toxic nephropathy.
Despite preserved urine output and the absence of conventional emergent indications for dialysis, serum creatinine continued to increase progressively from 447 to 749 µmol/L. The patient underwent a total of two intermittent hemodialysis sessions. The first session was initiated approximately 154 hr after ingestion because of rapidly progressive severe acute kidney injury despite preserved urine output. The second session was performed according to serial clinical and biochemical reassessment. Renal function subsequently improved, and the patient was discharged on day 14. The temporal changes in AST, ALT, creatinine, and bilirubin, including the timing of intermittent hemodialysis, are shown in Fig. 2.
Temporal evolution of serum AST, ALT, and serum creatinine in Case 2 following ingestion of a raw grass carp gallbladder. Vertical dashed lines indicate the timing of intermittent hemodialysis (IHD) sessions. AST, aspartate aminotransferase; ALT, alanine aminotransferase; IHD, intermittent hemodialysis.
A 73-year-old woman with a history of hypertension treated with candesartan ingested one raw grass carp gallbladder from a 3.5-kg fish. Four hours later, she developed vomiting, abdominal pain, and diarrhea and presented to our center 37 hr after ingestion.
Laboratory investigations demonstrated severe acute hepatocellular injury with AST and ALT levels exceeding 7000 U/L. Serum ferritin, measured only in this patient, reached 40,000 ng/mL during hospitalization. Peak total bilirubin concentration was 99 µmol/L. Mild coagulopathy was present (PT 62%; INR 1.36). In contrast to the marked hepatic injury, renal function remained preserved throughout hospitalization, with serum creatinine ranging from 65.9 to 83 µmol/L.
The patient received intravenous fluids, N-acetylcysteine infusion, and lactulose. Liver enzymes gradually improved, and no hepatic encephalopathy or renal failure developed. She was discharged on day 11. The temporal changes in these biochemical parameters are shown in Fig. 3. The main clinical and laboratory characteristics of the three patients are summarized in Table 1.
Temporal evolution of serum AST, ALT, and serum creatinine in Case 3 following ingestion of a raw grass carp gallbladder. AST, aspartate aminotransferase; ALT, alanine aminotransferase.
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Fish gallbladder poisoning remains an important toxicological problem in several Asian countries where ingestion of raw fish bile continues to be practiced as a traditional remedy. Previous reports have demonstrated that fish gallbladder poisoning most commonly results in varying degrees of acute hepatic and renal injury, although the severity and relative involvement of each organ differ considerably among patients (Xiaodan et al., 2012; Lim et al., 1993; Lin and Huang,1991; Wu and Deng, 2011; Zhou et al., 2021). Reports describing isolated predominant hepatocellular injury or severe acute kidney injury have also been published, indicating that the clinical spectrum is broader than concurrent hepatorenal injury alone. In the present series, all three patients developed hepatic and/or renal injury after confirmed grass carp gallbladder ingestion; however, the relative severity of hepatic and renal involvement differed substantially. One patient developed mixed hepatorenal injury accompanied by prolonged severe hypertension, another developed dialysis-requiring acute kidney injury with comparatively less severe hepatotoxicity, whereas the third exhibited predominant severe hepatocellular injury with preserved renal function. Rather than representing a unique pattern, these cases further illustrate variable patterns of hepatorenal involvement following grass carp gallbladder ingestion. Severe acute hepatocellular injury without clinically significant renal dysfunction appears to be less commonly reported but has been described previously (Wu and Deng, 2011). Unlike previously reported case series in which most patients developed concurrent hepatic and renal injury, our patients demonstrated distinct patterns of hepatorenal involvement, including dialysis-requiring AKI, prolonged severe hypertension, and severe acute hepatocellular injury without clinically significant renal dysfunction. Although similar manifestations have been reported individually in previous publications, relatively few reports have presented these different clinical phenotypes side by side within a single case series using detailed serial biochemical follow-up. Such direct comparison may facilitate recognition of the variable clinical course of fish bile poisoning in routine practice.
The mechanisms underlying this clinical variability remain uncertain. Experimental studies indicate that sodium cyprinol sulfate causes direct hepatocellular and renal tubular injury through mitochondrial dysfunction and oxidative stress (Yip et al., 1981; Munilkumar et al., 2024). However, because toxin concentrations were not measured in the present study, we could not determine whether the observed variability reflected differences in toxin dose, individual susceptibility, or a combination of both. Interindividual differences in toxin exposure, age, comorbidities, delayed presentation, and host susceptibility may contribute to the observed variability.
Another notable observation was the presence of objective findings supporting intrinsic nephrotoxicity in Case 2, including proteinuria, low urine specific gravity, and increased renal parenchymal echogenicity on ultrasonography. These findings are consistent with toxic tubular injury and support previous experimental observations regarding the nephrotoxic effects of fish bile toxins (Yip et al., 1981; Munilkumar et al., 2024).
Prolonged severe hypertension observed in Case 1 was an unusual finding. Because blood pressure before poisoning was unknown, a causal association with fish gallbladder ingestion cannot be confirmed. Pain, stress, sympathetic activation, or previously unrecognized hypertension remain plausible alternative explanations.
The markedly elevated ferritin concentration observed in Case 3 likely reflected extensive hepatocellular necrosis and systemic inflammatory activation. Although hyperferritinemia has been described in severe acute liver injury, its significance in fish gallbladder poisoning remains unclear (Douglas and Etheresia, 2014). Because ferritin was measured only in Case 3, the clinical significance of hyperferritinemia in fish gallbladder poisoning requires further investigation.
Importantly, all three patients survived with supportive treatment despite severe biochemical abnormalities. These observations reinforce the importance of early recognition, careful monitoring, and timely supportive management, including renal replacement therapy when clinically indicated (Xiaodan et al., 2012; Lin and Huang,1991; Zhou et al., 2021).
The present study has several limitations. First, this was a small retrospective case series from a single center, limiting the generalizability of the findings. Second, serum sodium cyprinol sulfate or related bile alcohol toxin concentrations were unavailable; therefore, the actual toxin exposure could not be quantified. Consequently, we could not determine whether the observed variability reflected differences in toxin dose, individual susceptibility, or both. Third, histopathological confirmation of organ injury was unavailable. Finally, the limited number of patients precluded exploration of factors associated with different clinical phenotypes.
Alternative causes of acute liver injury and AKI were carefully considered. None of the patients reported exposure to potentially hepatotoxic or nephrotoxic medications, herbal remedies, or traditional medicines. There was no evidence of shock or hypotension to suggest ischemic hepatitis, no clinical or laboratory evidence of sepsis, and no features suggestive of rhabdomyolysis. Viral hepatitis investigations were negative in all cases. The close temporal relationship between gallbladder ingestion and symptom onset supported fish bile poisoning as the most likely diagnosis (Xiaodan et al., 2012; Lim et al., 1993; Zhou et al., 2021). In conclusion, grass carp gallbladder poisoning may present with variable patterns of hepatorenal involvement, ranging from predominant hepatocellular injury with preserved renal function to dialysis-requiring acute kidney injury. Recognition of this variability is important for early diagnosis, close monitoring, and timely supportive management. Further studies involving larger patient cohorts are required to clarify the determinants of different clinical phenotypes.
The authors thank the physicians, nurses, and staff of the Poison Control Center, Bach Mai Hospital, Hanoi, Vietnam, for their contribution to patient care and clinical data collection.
FundingNo external funding was received for this study.
Conflict of interestThe authors declare that they have no competing interests.
Data availabilityThe data supporting the findings of this study are available from the corresponding author upon reasonable request.
Author contributionsNguyen Dang Duc: Conceptualization, Investigation, Data curation, Writing – original draft.
Nguyen Trung Nguyen: Investigation, Data curation.
Lam Nguyen Hong Khanh: Literature review, Writing – review and editing.
Le Thi Dieu Hien: Supervision, Writing – review and editing.
All authors read and approved the final manuscript.
Ethics approval and consent to participateAccording to institutional policy at Bach Mai Hospital, anonymized retrospective case reports and small case series derived from routine clinical care are exempt from formal Institutional Review Board review.
Patient consent for publicationWritten informed consent for publication was obtained from all patients.
