DONT EAT FISH GALLBLADDER IT IS POISON ask the doctor

Fish gall bladder consumption presenting as acute renal failure

It is a common practice in South East Asia to consume alternative medicine which may include toxic metals or animal products for various health reasons. These have been implicated in various side effects including renal failure. Herein we report a case of anuric acute renal failure with dyspnea and hemoptysis following volitional consumption of rohu fish (Labeo rohita) gallbladder.

 A Gupta, ND Karnik, VA Gupta, and NK Hase1

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Abstract

A forty-two-year-old male was admitted with a history of anuria and breathlessness following consumption of raw rohu fish gallbladder. He had azotemia and required hemodialysis. His renal failure improved over a period of about four weeks. Incidences have been reported from South East Asian countries associating consumption of raw rohu fish gallbladder with acute renal failure.

KEYWORDS: Acute renal failure, anuria, fish gall bladder, pulmonary renal syndrome

 

Introduction

It is a common practice in South East Asia to consume alternative medicine which may include toxic metals or animal products for various health reasons. These have been implicated in various side effects including renal failure. Herein we report a case of anuric acute renal failure with dyspnea and hemoptysis following volitional consumption of rohu fish (Labeo rohita) gallbladder.

Case Report

Forty-two year old male chronic alcoholic, smoker and marijuana addict presented with a history of diffuse abdominal pain with profuse vomiting followed by oliguria. He was treated with intravenous fluids and diuretics in a primary health center near Nagpur. As he developed edema feet, puffiness of the face, breathlessness and hemoptysis he was transferred to our tertiary care hospital. There was no history of fever, joint pains, rash, jaundice or bleeding from other sites. He did not give a history of diabetes, hypertension or analgesic intake. The patient under observation then developed complete anuria.

On admission, examination revealed medium frame, poorly nourished patient with pallor and no icterus. Pulse rate 100/min, regular, blood pressure 110/90 mmHg, respiratory rate 24/min. Jugular pulse not raised, mild edema feet. Respiratory system examination revealed bilateral basal crepitations. Rest of the systemic examination was unremarkable. Investigations revealed hemoglobin-11.4 gm/dl with total white blood cell count-9600/cumm and platelet count-80000/cumm. Urine routine showed protein 2+ with 20-25 red blood cells and 70-80 white blood cells per high power field. Renal chemistry revealed blood urea nitrogen-160 mg/dl, serum creatinine-16.8 mg/dl, serum sodium-113 mEq/L, serum Potassium-3.3 mEq/L, total proteins-6.6 g/dl with albumin 3.4 g/dl, AST/ALT-56/42 IU/L, serum bilirubin-1.1 mg/dl, serum uric acid-11.6 mg, serum calcium-8 mg/dl and serum phosphate-5.5 mg/dl. A 24 hours urine protein quantification was 300 mg. His Antinuclear antibody was negative and C3, C4 levels were normal. Ultrasonography of the abdomen showed a normal size kidney with no dilatation of the pelvicalyceal system. As the patient had hemoptysis and acute kidney injury there was a strong suspicion of a pulmonary-renal syndrome. However, his IgG anti-glomerular basement membrane (GBM) antibody was 1.8 U/ml (Negative <12 U/ml). A plain computerized tomography (CT) of the chest showed patchy perihilar ground glass opacities with peribronchial cuffing, segmental atelectasis of bilateral lower lobes with bilateral pleural effusion. Persistent inquiry as regards a possible toxic etiology for his acute onset complete anuria revealed he had consumed the entire bile from a raw fish gallbladder (rohu or Labeo rohita) a day prior to the onset of symptoms as a cure for his general debility.

In view of his pulmonary edema and deteriorating renal function, he was dialyzed once on admission after which there was a gradual increase in urine output over 6 days. He improved symptomatically with a decrease in serum creatinine from 16.8 mg/dl to 10 mg/dl on day 5 to 4.8 mg/dl on day 15. He was eventually discharged after 18 days of in-hospital treatment with a serum creatinine of 2.5 mg/dl. Subsequent follow-up after 15 days showed serum creatinine was 1.08 mg/dl. The patient had a complete recovery.

 

Discussion

The fish gallbladder is considered a traditional medicine to treat rheumatism, decreased visual acuity, and urticaria and to increase sexual vitality.[1] However it can lead to acute renal failure and acute liver injury as reported in cases of fish poisoning from India,[2] Japan[3] and Hong Kong.[4] The ichthyotoxic effects of the fish gallbladder is attributed to the presence of a toxin, sodium Cuprinol sulfate which is a C27 bile acid.[5] The toxin is heat stable and insoluble in alcohol as cases are reported even after consumption of cooked bile.[6]

Fish belonging to the family Cyprinidae are commonly reported for their toxicity. The family includes grass carp (C idellus), common carp (Cyprinuscarpio), silver carp (Hypophthalmichthysmolitrix), MylopharyngodonpiceusLabeorohita, and Aristichthys nobilis.[7] Amongst these, fish of the grass carp variety has been commonly reported for its toxicity but Xuan et al. also reported toxicity secondary to ingestion of shark (minnow) fish (M chrysophekadion) and the bony-lipped barb fish (O melanopi).[8]

Even though fish gallbladder can cause severe systemic complications, toxicity does not occur in all cases. In rural Vietnam, gallbladder from smaller fish is consumed regularly without evident toxicity. Thus it can be said that toxicity is directly proportional to the size and quantity of gallbladder or bile consumed.[8]

Following ingestion, almost all patients develop gastrointestinal symptoms within a few hours as reported by Xuan et al.[8] in his series of 17 cases from Vietnam. Deng et al.[9] has also reported extra-renal manifestations of the toxin with deleterious effects on the heart and liver with eventual multi-organ dysfunction syndrome.

However, patients usually seek therapy for renal failure which has an incidence of 55-100%. Renal failure is mostly secondary to acute tubular necrosis which may be a direct effect of the toxin. A kidney biopsy has shown the presence of proximal tubular cell damage with focal destruction of epithelial cells on light microscopy.[,9] The toxin is believed to damage lysosomes and inhibit cytochrome oxidase thus blocking cellular metabolism, leading to cell necrosis. This in addition to the loss of fluid can lead to decreased effective circulating blood volume and eventually renal failure. However the exact mechanism of systemic injury especially renal failure is not known and needs further study.

Our patient had reported hemoptysis prior to admission and had an abnormal CT scan of the chest. The cause for the same in such a setting could include fluid overload – pulmonary edema (anuria) or pulmonary-renal syndrome. Toxic bile is also reported to cause pulmonary-renal syndrome however the patient’s primary workup including ANA, C3, C4, and IgG anti-GBM was normal. Toxin-induced pulmonary-renal syndrome remains a possibility however a workup for the same including Kidney biopsy and bronchoalveolar lavave was not done in view of steady improvement in his condition.

Most of the reported cases till date have undergone hemodialysis in view of renal failure Pandey et al.[10] in their case have also given Niaoduqing, a traditional Chinese medicine, to protect renal function. Our patient had predominant gastrointestinal symptoms. He was transferred from primary care as anuric renal failure. He responded to good supportive and hemodialysis with complete recovery. This case exemplifies the practice of traditional folk medicine in rural India. Good awareness programs can aid diagnosis and prevent death from such a dangerous preventable cause of acute kidney injury which is the aim of International Society of Nephrology “0 by 25 Initiative”.

 

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

 

References

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