Abstract

Background: Great quantity of star fruit (Averrhoa carambola) ingestion, or even smaller amounts in a patient with an empty stomach, may induce acute kidney injury (AKI). Case Presentation: We report a 65-year-old male patient with underlying multiple myeloma and normal kidney function, who developed alterations of consciousness and rapid increase in serum creatinine due to oxalate nephropathy after large ingestion of star fruit on an empty stomach. Kidney biopsy revealed the diagnosis of oxalate nephropathy. Conclusions: AKI due to oxalate nephropathy after star fruit ingestion is relatively uncommon (only eight other reported cases) but there is an increasing evidence of AKI associated with intoxication by star fruit. This case alerts health professionals, nephrologists in particular, to a new disease that is increasingly better known and diagnosed more frequently

Highlights

  • Great quantity of star fruit (Averrhoa carambola) ingestion, or even smaller amounts in a patient with an empty stomach, may induce acute kidney injury (AKI)

  • Case Presentation: We report a 65-year-old male patient with underlying multiple myeloma and normal kidney function, who developed alterations of consciousness and rapid increase in serum creatinine due to oxalate nephropathy after large ingestion of star fruit on an empty stomach

  • Kidneys are the primary organ for oxalate excretion, and AKI can occur due to acute oxalate nephropathy, with calcium oxalate crystals deposition within renal tubules

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Summary

Background

Plant toxins are an important cause of tropical acute kidney injury (AKI) [1]. Star fruit (Averrhoa carambola) is a plant with a high content of oxalic acid, which could contribute to acute nephrotoxicity [2]. Kidneys are the primary organ for oxalate excretion, and AKI can occur due to acute oxalate nephropathy, with calcium oxalate crystals deposition within renal tubules. We report the case of AKI related to oxalate nephropathy following star fruit ingestion. There was no history of oliguria, hematuria, or other urine abnormality He did not have fever, dysuria, and shortness of breath, dehydration or other neurologic symptoms. AKI due to oxalate nephropathy oriented, and blood pressure was 130/70 mm Hg. The patient had no edema, and his systems were normal. On day fourth postadmission, the serum creatinine level increased to 4.8 mg/dL, associated with a reduction in urine output. On further outpatient follow-up (75th day), the serum creatinine concentration was 1.2 mg/dL

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