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Clinical Research

Severe acute kidney injury following Sri Lankan Hypnale spp. envenoming is associated with thrombotic microangiopathy

ORCID Icon, ORCID Icon, , ORCID Icon, & ORCID Icon
Pages 296-302 | Received 15 Jun 2020, Accepted 11 Aug 2020, Published online: 01 Sep 2020
 

Abstract

Context

Acute kidney injury (AKI) is the most serious clinical manifestation of the Sri Lankan hump-nosed pit viper (Hypnale spp.) bites. Thrombotic microangiopathy (TMA) is increasingly recognized in association with AKI in cases of Hypnale spp envenomation. We investigated AKI in a cohort of cases of Hypnale envenomation, its association with TMA and the early diagnostic value of common biomarkers for AKI occurring.

Materials and methods

We conducted a prospective observational study of suspected viper bites and included 103 confirmed cases of Hypnale envenomation, based on venom specific enzyme immunoassay of blood. AKI was defined using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Thrombotic microangiopathy was diagnosed based on thrombocytopenia (platelet count < 150,000 × 103/μL) and microangiopathic haemolytic anaemia (MAHA). We investigated the diagnostic performance of creatinine, platelet count and INR for AKI within 4 h and 8 h post-bite by area under the receiver operator characteristic curve (AUC–ROC).

Results

Ten patients developed AKI: seven AKI stage 1 and three AKI stage 3. Ten patients (10%) developed thrombocytopaenia while 11 (11%) had MAHA. All three AKI stage 3 had thrombocytopaenia and MAHA fulfilling the criteria for TMA. Two of them presented with oliguria/anuria and all three required haemodialysis. Serum creatinine within 4 h post-bite was the best predictor of AKI with AUC-ROC of 0.83 (95% CI: 0.67–0.99) and was no better within 8 h of the bite.

Conclusions

We found that AKI is uncommon in Hypnale spp. envenomation, but an important serious complication. Severe AKI was associated with TMA. A creatinine within 4 h post-bite was the best predictor of AKI.

Acknowledgements

We thank all the research assistants who were involved with the data collection, the staff of the medical wards, preliminary care unit and laboratory of Base Hospital Horana and staff of haematology laboratory of Faculty of Medicine, University of Colombo for their support. We also thank the staff of South Asian Clinical Toxicology Research Collaboration (SACTRC) for their support.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The study was partly funded by an Australian National Health and Medical Research Council (NHMRC) Centre for Research Excellence [ID1110343] and Geoffrey Isbister is funded by an NHMRC Senior Research Fellowship [ID1061041].

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