Abstract
Background
Snakebite envenomation remains a health problem in tropical regions and is a recognized cause of acute kidney injury (AKI). Despite numerous regional studies, the global burden and predictors of snakebite-induced AKI have not been systematically quantified. This review aimed to estimate the pooled incidence of AKI following snake envenomation, identify key clinical and laboratory features, and determine the mortality rate and proportion of patients requiring renal replacement therapy (RRT).
Methods
A systematic search of PubMed, Embase, and Cochrane Library was conducted for studies published between 2015 and 2025 that reported AKI in snakebite patients. Eligible studies included observational and interventional designs with ≥ 10 participants. Data were extracted on study characteristics, incidence of AKI, need for RRT, mortality rate and associated clinical and laboratory features. Quality was assessed using the Joanna Briggs Institute checklist. Pooled incidence estimates were generated using a DerSimonian–Laird random-effects model, and heterogeneity was evaluated using the I² statistic.
Results
Thirty studies comprising 8,612 participants met the inclusion criteria. The pooled incidence of AKI following snake envenomation was 23% (95% CI: 17–33%; I² = 97.2%), and among these, 28% (95% CI: 17–43%; I² = 86.9%) required RRT and the pooled mortality rate was 10% (95% CI 4–21%), with substantial heterogeneity (I² = 83%). A high incidence was observed among Russell’s viper victims, 37% (95% CI: 21–57%), and 23% (95% CI: 15–34%) in non-Russell’s viper victims. Common clinical predictors of AKI included older age, male sex, comorbidities (hypertension, diabetes mellitus), local swelling, cellulitis, bleeding, hypotension, oliguria/anuria, and delayed presentation. Laboratory features included incoagulable 20-min whole blood clotting test (WBCT), prolonged prothrombin time/ international normalized ratio (PT/INR), elevated serum creatinine and blood urea and nitrogen (BUN), thrombocytopenia, and proteinuria. Biomarkers such as urinary neutrophil gelatinase–associated lipocalin (NGAL), cystatin C, and β-2 microglobulin were associated with early renal injury.
Conclusion
Approximately one-third of snakebite victims develop AKI, and nearly one in three affected patients requires dialysis. Clinical manifestations such as coagulopathy and local tissue injury are commonly observed. Early recognition, prompt antivenom therapy, and supportive renal management are critical to improving outcomes.
Clinical trial
Not applicable.
Keywords: Snake envenomation, Acute kidney injury, Renal replacement therapy, Coagulopathy
Background
As a tropical disease, snakebite envenoming contributes substantially to morbidity and mortality, especially in rural regions of the tropics and subtropics. An estimated 5.4 million people are bitten by snakes each year worldwide (World Health Organization, [47]). The burden is highest in low-income tropical countries where agricultural workers and children are most affected (World Health Organization, [47]). In recognition of its impact, the WHO has set a goal to halve snakebite deaths and disabilities by 2030 [34]. Envenomation by venomous snakes can trigger diverse systemic manifestations, including neurotoxicity, coagulopathy, and hemorrhage, and may culminate in severe end-organ injury, among these, AKI represents a serious and life-threatening complication [35].
AKI following envenomation is frequently associated with hemotoxic and myotoxic snakes, particularly viperids such as Russell’s viper, Bothrops, and Crotalus species [26, 31]. Venom-induced kidney injury occurs through multiple pathways, including direct nephrotoxicity, hemodynamic shock, microvascular thrombosis, and rhabdomyolysis [1, 35]. Some studies note that all kidney compartments can be affected by envenoming [35]. Early antivenom administration and supportive care are critical. Globally, about 8–43% of envenomated patients are reported to develop AKI [1]; Evidence from Sub-Saharan Africa is limited. In one Togolese cohort of 376 snakebite patients, 12.2% developed AKI (all Kidney Disease: Improving Global Outcomes (KDIGO) Stage 3) with a case-fatality of 58.7% [18]. Known predictors of death include markers of severe envenomation such as hypotension, disseminated intravascular coagulation, and respiratory failure [1, 32]. Among survivors, long-term renal sequelae are common: up to one-third or more of patients develop chronic kidney disease, persistent hypertension or reduced glomerular filtration on follow-up [32]. The absence of pooled evidence limits a clear understanding of the incidence, risk factors and clinical course of snakebite-associated AKI. Therefore in this systematic review and meta-analysis we set out to estimate the incidence of AKI after snake envenomation, identify clinical risk factors, determine the mortality rate and evaluate the need for renal replacement therapy.
Methods
Study design
This study protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO 2025 CRD420251162202), and the reporting of findings adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Figure 1 shows the PRISMA flow diagram for study selection and inclusion.
Fig. 1.
PRISMA diagram illustrating the study selection process for the systematic review and meta-analysis
Search strategy
We conducted a comprehensive search of PubMed, Cochrane Library, Embase, and other bibliographic databases from January 2015 to 2025. The search strategy was developed using a combination of Medical Subject Headings (MeSH) terms and free-text keywords to identify studies related to snake bites and AKI. Additionally, the reference lists of selected articles were screened to capture further eligible studies. For PubMed, (“snakebite“[MeSH] OR “snakebite” OR “snake envenomation” OR “snake envenoming” OR “venomous snake” OR “venomous snakebite”) AND (“acute kidney injury“[MeSH] OR “acute renal failure” OR “acute kidney injury” OR AKI OR ARF OR “renal failure” OR “renal impairment” OR dialysis)
Eligibility criteria
We included English-language studies (2015–2025) involving humans of any age with clinically or laboratory-confirmed snake envenomation. Eligible designs were observational studies (cohort, case–control, cross-sectional), randomized controlled trials (RCTs), and case series with ≥ 10 envenomed patients. The primary outcome was acute kidney injury (AKI), with secondary outcomes including AKI severity, mortality and need for renal replacement therapy (RRT/dialysis). Comparators were envenomed patients without AKI or groups with reported effect estimates. Case reports and series with < 10 patients were excluded. All geographic settings were considered.
Diagnostic criteria
For each included study we extracted the diagnostic criteria used to define AKI and recorded whether studies used KDIGO, Acute Kidney Injury Network (AKIN), serum creatinine-based definitions, hospital clinical diagnosis, or other (e.g., need for dialysis as surrogate). Severe AKI was defined as KDIGO or AKIN Stage 3 AKI, representing the most severe stage of kidney injury. These study-level definitions are summarized in (Table 2).
Table 2.
Diagnostic criteria, incidence of AKI and requirement for RRT among snakebite patients across included studies
| Study (Author, Year) | Diagnosis Criteria | Incidence | Need for RRT | AKI Severity (KDIGO/AKIN stage, among AKI cases) | AKI Mortality (among AKI cases) |
|---|---|---|---|---|---|
| [13] | NR | 24% (24/100 cases) | 25% | NR | 8% |
| [38] | KDIGO | 31% (16/51cases) | 6.3% | 6.3% (1/16) | 57% |
| [17] | NR | 0.5% (4/861 cases) | 50% | NR | NR |
| [36] | KDIGO | 44.92% (62/138cases) | NR | NR | NR |
| [21] | KDIGO | 20.7% (159/769 cases) | 71.7% | 76.7% (122) | 9.4% |
| [26] | KDIGO | 14.1% (10/71cases) | 10% | 10% (1/10) | No mortality |
| [32] | KDIGO | 43.8% (184 /420 cases) | 61.9% | 75.0% (138/184) | 24% |
| [33] | NR | 29.1% (20 /68 cases) | 29.4% | NR | 13.2 |
| [3] | KDIGO | 34.9% (22/63 cases) | 4.5% | 27.3% (6/22) | NR |
| [9] | NR | 54.3% (140/258 cases) | 49.3% | 78.6% (110/140) | 19.3% |
| [12] | KDIGO | 21.2% (184/866 cases) | 38% | NR | 7.6% |
| [19] | AKIN | 45.9% (28/61 cases). | 35.7% | 50.0% (14/28) | 14% |
| [22] | KDIGO | 13.4% (16/119 cases) | NR | NR | NR |
| [2] | AKIN | 6.6% (14/212 cases) | NR | NR | No mortality |
| [25] | NR | 37.9% (22/58 cases) | NR | NR | No mortality |
| [30] | KDIGO | 7.0% (6/86 cases) | 0.2% | NR | 1.1% |
| [20] | KDIGO | 18.73% (281/1500 cases) | 0.3% | NR | NR |
| [4] | NR | 6% (4/69 cases) | 50% | NR | Not classified |
| [27] | NR | 26.3% (20/76) | 40% | NR | NR |
| [39] | NR | 22.2% (12/54 cases) | 25% | NR | NR |
| [16] | KDIGO | 38.2% (139/364 cases) | Dialysis used when indicated, but exact proportion not specified | 25.9% (36/139) | 4.4% |
| [5] | AKIN | 12.8% (24/187 cases) | 16.7% | 16.7% (4/24) | NR |
| [8] | NR | 16.2% (6/37 cases) | NR | NR | |
| [28] | NR | 50% (15/30 cases) | 40% | NR | NR |
| [44] | RRT requirement or elevated peak creatinine (> 120 µmol/L males; >100 µmol/L females) with acute rise–fall | 59.8% (557/948 cases) | 40.8% | NR | NR |
| [40] | NR | 100% (30/30 cases) | NR | NR | NR |
| [29] | AKIN | 50% (17/34 cases) | NR | NR | NR |
| [45] | KDIGO | 23% (12/52 cases) | NR | 33.3% (4/12) | NR |
| [43] | KDIGO | 14% (33/237 cases) | 0.1% | NR | NR |
| [10] | KDIGO | 2.5% (21/838 cases) | NR | NR | NR |
KDIGO: Kidney Disease: Improving Global Outcomes; AKIN: Acute Kidney Injury Network; NR: Not Reported
Study selection and data extraction
Studies initially identified were screened by title and abstract to assess eligibility, after which full-text articles were retrieved for further evaluation. Data extracted included author information, year of publication, country and continent, study design and setting, participant characteristics (such as gender), snake species, diagnostic criteria, time of antivenom administration, specimen identification method, incidence of AKI, need for renal replacement therapy/dialysis, stage of AKI, mortality rate, clinical and laboratory features. Clinical predictors were extracted as reported in the primary studies. Predictors were recorded only if explicitly defined or described in the original study. Because studies varied in how clinical features were assessed, all predictors were extracted verbatim without attempting to standardize definitions across studies. The overall incidence of AKI from snakebites was estimated. Study selection and data extraction were conducted independently by two reviewers, with disagreements resolved through discussion and consultation with additional team members.
Quality assessment
The methodological quality of the included studies was evaluated using the JBI Critical Appraisal Checklist for Studies Reporting Prevalence Data. Two independent reviewers performed the quality assessment, and any disagreements were resolved through discussion or consultation with a third reviewer. A traffic light summary was generated to illustrate the reviewers’ judgments, where green indicates low risk of bias (“Yes”), yellow indicates unclear risk, red indicates high risk (“No”), and black denotes items not applicable to the study.
Statistical analysis
Meta-analyses were performed using the random-effects inverse-variance model with the DerSimonian–Laird estimator of τ² to account for between-study variability. Pooled incidence estimates were calculated for AKI following snake envenomation, as well as for the requirement of RRT and mortality rate among patients diagnosed with AKI. In addition, species-specific analyses were conducted, including subgroup analyses for commonly reported snakes such as Russell’s viper and non-Russell’s viper. Heterogeneity across studies was assessed using the I² statistic and corresponding p-values, with I² values > 50% indicating substantial heterogeneity. All analyses were conducted using R software.
Species identification and reliability coding
We extracted the snake species reported in each study and recorded the method of identification, which included: (i) presentation of the live/dead snake or photographs; (ii) patient or witness descriptions matched with reference images; (iii) clinician recognition based on characteristic envenoming features; or (iv) expert confirmation or venom-specific enzyme immunoassay (EIA).
Each study was assigned a species identification reliability code: C1 = Confirmed (expert-verified specimen/photo or EIA); C2 = Probable (specimen/photo available or reliable description matched with images); and C3 = Possible/Unconfirmed (verbal report only, clinical syndrome, or not reported). Species identification methods and codes are summarised in Table 3.
Table 3.
Snake Species, snake identification Method, Time-to-Antivenom reporting and associated clinical and laboratory features of AKI
| Author (year) | Snake species | Snake Identification Method (Species Id Code) | Clinical predictors or profile | Time-to-Antivenom Reporting | Laboratory features |
|---|---|---|---|---|---|
| [13] | Krait (Bungarus caeruleus), Russell’s viper (Daboia russelii), cobra (Naja naja), some unidentified. | NR (C3) | NR | NR | Incoagulable 20-min WBCT, PT > 15s and INR > 1.2 |
| [38] | Vipers such as Echis ocellatus | NR (C3) | Male sex predominance; oliguria | Median: 2 h | Increase serum creatinine; Increase BUN at admission |
| [17] | Russel’s viper, cobra, common krait, hump-nosed viper, nonvenomous snakes, some unidentified species. | NR (C3) | NR | NR | NR |
| [36] | Unidentified species of venomous snakes | NR (C3) | Older age; abdominal pain/tenderness; vomiting; cellulitis; bleeding diathesis; myalgia; dark (black/brown) urine | NR | NR |
| [21] | N. Naja (common cobra), B. Caeruleus (common krait), E. Carinatus (saw-scaled viper) and D. Russelii (russell’s viper) | NR (C3) | NR | 1–7 h | Acute tubular injury with pigment cast. |
| [26] | Gloydius species, unknown species | NR (C3) | Older age; hypertension | 1–3.5 h | Elevated white blood cell count, Abnormal creatine kinase levels (peaks at presentation and reaches the lowest concentration within 48 h) |
| [32] | Daboia russelii (russels viper), E. carinata (king ratsnake), unknown species | Patient description or expert confirmation (if snake specimen brought) (C1) | NR | 1.5–4 h | NR |
| [33] | Vipers, common cobra, krait, | NR (C3) | Local swelling and tenderness; bleeding manifestations; hypotension; oliguria/anuria | NR | Prolonged BT/PT/aPTT (coagulopathy); thrombocytopenia |
| [3] | Bothrops erythromelas | NR (C3) | NR | 4–157 min | lower levels of averaged haemoglobin and averaged hematocrit, lower nadir of serum sodium. Higher levels of averaged serum urea and creatinine on admission, lower eGFR, Proteinuria, higher Fractional excretion of potassium, higher aPTT, abnormal and incoagulable blood tests, higher urinary MCP-1, urinary NGAL |
| [9] | Russell’s viper, cobra, green pit viper, sea snake | NR (C3) | Shock, ARDS or respiratory failure, Hypotension, Local swelling | 0–2 h | WBC > 10 × 10³/µL, overt DIC; CK > 500 IU/L; Na⁺ <135 mmol/L; microscopic hematuria |
| [12] | Unidentified venomous snake species | NR (C3) | NR | NR | NR |
| [19] | Russell’s viper | (i) Snake brought dead/alive; or (ii) victim/witness matched description with images/photos (Russell’s viper) (C2) | Bleeding manifestations, shock. | NR | Proteinuria, high blood urea and serum creatinine values |
| [22] | Unidentified venomous snake species | NR (C3) | Advanced age; longer time to antivenin; regional lymphadenopathy; incision/drainage at bite site | NR | Higher creatine kinase and blood myoglobin, lower haemoglobin concentration |
| [2] | Possibly saw-scaled viper (Echis carinatus), and possibly burton’s carpet viper (Echis coloratus) | NR (C3) | Early bleeding from the site of the bite. | Median: 133 min | NR |
| [25] | Predominantly vipers | NR (C3) | Cellulitis | NR |
Deranged INR, prolonged WBCT on admission, delayed thrombocytopenia |
| [30] | Protobothrops flavoviridis | NR (C3) | Lower on-admission systolic BP, higher on-admission diastolic BP, | NR | Increased serum creatinine |
| [20] | Russell’s viper, common krait, hump-nosed pit viper, common cobra, saw-scaled viper, malabar pit viper, bamboo pit viper, banded krait, unidentified species. | NR (C3) | NR | Mean: 3 h | NR |
| [4] | Arabian cobra, unidentified species | NR (C3) | NR | NR | NR |
| [27] | Russell’s viper | Snake specimen/photo, patient/bystander description matched with local photos, confirmed by expert toxicologist (C1) | NR | NR | NR |
| [39] | Bothrops spp., crotalus spp. | Based on patient signs/symptoms and laboratory findings (C3) | NR | 6 h | NR |
| [16] | Unidentified snake species | Victim/relative/witness identification and clinical features of intoxication (C2) | NR | 1 h | NR |
| [5] | Bothrops genus | Clinical signs of envenomation by Bothrops genus (C2) | Comorbities, such as hypertension and diabetes, Local bleeding | NR | Thrombocytopenia, leukocytosis, increase in creatine kinase, as well as increase in lactate dehydrogenase. Clotting time was uncoagulable in 97.3%. |
| [8] | Rattlesnakes including Crotalus durissus ruruima | Animal presentation, neurotoxic signs, lab abnormalities, or victim report (e.g., tail rattle) (C1) | NR | NR | NR |
| [28] | Hump-nosed vipers including H. hypnale and H. zara | Proven (specimen available) and Probable (no specimen available) bites (C1) | NR | NR | NR |
| [44] | Russell’s viper (Daboia siamensis), cobra (Naja spp.), krait (Bungarus spp.), green pit viper (Trimeresurus spp.), unidentified species. | Combination of: dead snakes brought by patients, doctor’s clinical opinion, and patient identification (C1) | NR | NR | NR |
| [40] | Krait, cobra, viper, unidentified | NR (C3) | NR | NR | NR |
| [29] | Bothrops genus | NR (C3) | Bleeding at the bite site | At 24 h and 48 h | Lactate dehydrogenase (LDH) and creatinine high, fibrinogen values were decreased, proteinuria, higher values of leukocytes in the urine. Higher levels of CXCL-8, CCL-2, IL-10 and IL-6 molecules |
| [45] | Hump-nosed pit viper (hnv; Hypnale spp.) | Snake specimen, visual description, and/or clinical features (C2) | Pain and swelling at the bite site, haematemesis, bleeding | NR | Prolonged WBCT20, increased serum creatinine, serum cystatin c, urinary neutrophil gelatinase associated lipocalin, urinary cystatin c, urinary clusterin and urinary beta-2 microglobulin. |
| [43] | Russell’s viper, hump-nosed viper, nonvenomous snakes, unidentified species | Expert identification or venom-specific EIA (C1) | NR | NR | NR |
| [10] | Malayan pit viper | (1) Snake carcass brought to hospital; (2) patient could clearly describe/identify snake (C2) | NR | Median: 5 h 40 min | NR |
*NR = Not Reported; C1 = Confirmed; C2 – Probable; C3 – Possible / Unconfirmed
Results
Study selection
The search initially identified 620 articles from PubMed (291), Embase (290), Cochrane Library (9), and other sources (30). After removing duplicates, 300 articles remained for screening. Based on title and abstract review, 46 articles were selected for full-text assessment. 14 full-texts could not be retrieved, and 2 studies did not report the outcomes of interest. In the end, 30 articles were included in the systematic review and meta-analysis.
Characteristics of included studies
A total of 30 studies conducted between 2015 and 2025 were included in this review. Sample sizes ranged from 30 to 1,500 participants, with most studies involving patients admitted to hospitals with confirmed or suspected snake envenomation. The majority of studies employed prospective designs (n = 16), followed by retrospective (n = 8), combined retrospective/prospective (n = 2), and cross-sectional designs (n = 2). Most studies were conducted in Asia, particularly India (9 studies), Sri Lanka (4), and Myanmar (2). Other studies originated from Brazil (4), Benin (1), China (1), Oman (1), Japan (1), South Korea (1), Saudi Arabia (1), and Thailand (1). Across these studies, populations included both adult and pediatric patients with confirmed snake envenomation, focusing specifically AKI as a complication. Studies that focused on pediatric populations, includes Krishnamurthy et al., [19] and Islam et al., [16], while others enrolled mixed adult and pediatric cohorts [4]. Table 1 presents the characteristics of the included studies.
Table 1.
Characteristics of included studies on snakebite envenomation and AKI
| Study (Author, Year) | Country | Study design | Sample size | Population |
|---|---|---|---|---|
| [13] | India | Prospective | 100 | Adults admitted with proven or suspected snake envenomation. |
| [38] | Benin | Prospective | 51 | Patients suffering severe snakebite envenomation |
| [17] | Sri Lanka | Cross-sectional | 816 | Residents in a rural district |
| [36] | India | Retrospective | 138 | Snake bite patients |
| [21] | India | Retrospective/prospective | 769 | Admitted patients with snake bite envenomation-induced AKI. |
| [26] | South Korea | Retrospective | 71 | Patients with a history of venomous snakebite |
| [32] | India | Prospective | 420 | Adult patients admitted with AKI following haemotoxic envenomation |
| [33] | India | Prospective | 68 | Snake bite patients |
| [3] | Brazil | Prospective | 63 | Patients admitted due to snakebite caused by the Bothrops genus |
| [9] | Myanmar | Prospective | 258 | Snake bite patients |
| [12] | India | Retrospective/prospective | 866 | Admitted patients with snake envenomation |
| [19] | India | Prospective | 61 | Children with systemic features of Russell’s viper envenomation |
| [22] | China | Retrospective | 119 | Snake bite patients |
| [2] | Oman | Retrospective | 212 | Snake bite patients |
| [25] | India | Prospective | 58 | Snake bite patients |
| [30] | Japan | Retrospective | 86 | Victims of P. flavoviridis |
| [20] | India | Prospective | 1,500 | Patients with snakebite envenomation |
| [4] | Saudi Arabia | Retrospective | 69 | Pediatric and adult snake bite patients |
| [27] | India | Prospective | 76 | Patients who had suffered from vasculotoxic snake envenomation |
| [39] | Brazil | Prospective | 54 | Patients admitted with snakebites envenomation |
| [16] | India | Prospective | 364 | Children admitted with hematotoxic snakebite |
| [5] | Brazil | Prospective | 187 | Patients hospitalized due to the snakebite. |
| [8] | Brazil | Prospective | 37 | Patients who claimed to have been bitten by a rattlesnake. |
| [28] | Sri Lanka | Prospective | 30 |
Hump-nosed viper bite patients |
| [44] | Myanmar | Retrospective | 948 | Snake bite patients |
| [40] | India | Cross-sectional | 30 | Patients admitted with snakebite envenomation |
| [29] | Brazil | Prospective | 34 | Snake bite patients |
| [45] | Sri Lanka | Prospective | 52 |
Hump-nosed viper envenoming patients |
| [43] | Sri Lanka | Prospective | 237 | Snake bite patients |
| [10] | Thailand | Retrospective | 838 | Malayan Pit Viper bitten patients |
Incidence of AKI following snake envenomation, mortality rate and need for RRT
The pooled incidence of AKI among patients envenomed by snakebite estimated from 30 studies using a DerSimonian–Laird random-effects model was 23% (95% CI: 16–33%; I² = 97.2%, p < 0.001) (Fig. 2). 20 of the 30 studies reported on the need for RRT; the pooled proportion of AKI patients who received RRT was 28% (95% CI: 17–43%; I² = 86.9%, p < 0.001) (Fig. 3). Nine studies including 894 patients with AKI reported mortality. The pooled AKI-associated mortality was 10% (95% CI 4–21%), with substantial heterogeneity (I² = 83%) (Fig. 4). Among studies reporting AKI severity, the proportion of patients with stage 3 disease ranged from 6.3% to 78.6%, with several three studies reporting severe AKI in more than 70% of cases. When examined by offending species, envenomation by Russell’s viper was associated with a higher pooled incidence of AKI of 37% (95% CI:21–57%), with low heterogeneity (I² = 52.6%, p = 0.097) (Fig. 5). Envenomation by non-Russell’s viper was associated with a pooled incidence of AKI of 23% (95% CI: 15–34%), with high heterogeneity (I2 =94.9%, p < 0.001) (Fig. 6).
Fig. 2.
Incidence of AKI following snake bite
Fig. 3.
Analysis on the need for RRTr among AKI patients following snakebite
Fig. 4.
Pooled estimate of mortality among AKI patients across included studies
Fig. 5.
Subgroup analysis of AKI incidence following Russell’s viper envenomation
Fig. 6.
Subgroup analysis of AKI incidence following non-russell’s viper envenomation
Table 2 summarizes the diagnostic criteria, incidence of AKI, the requirement for RRT, and the proportion of patients who underwent dialysis.
Clinical predictors of AKI following snake envenomation
Across the reviewed studies, the main clinical predictors of AKI following snakebite included older age, male predominance, and comorbidities such as hypertension and diabetes. Frequent.
local manifestations were pain, swelling, cellulitis, and bleeding at the bite site, while systemic features such as hypotension, shock, oliguria/anuria, abdominal pain, vomiting, and myalgia were commonly associated with viper and cobra envenomation. Delayed presentation and longer time to antivenom administration were also linked with worse outcomes.
Laboratory features of AKI following snake envenomation
The key laboratory features were coagulopathy and renal dysfunction, reflected by incoagulable 20-min WBCT, prolonged PT/INR, and elevated serum creatinine and BUN. Proteinuria, microscopic hematuria, and increased urinary biomarkers (NGAL, cystatin C, clusterin, β-2 microglobulin) were noted in severe cases. Thrombocytopenia, leukocytosis, elevated CK and LDH levels, and electrolyte disturbances such as hyponatremia further indicated systemic envenomation. Table 3 shows the clinical and laboratory predictors of included studies.
Quality assessment
Thirty (30) studies were assessed. The majority of studies demonstrated a low risk of bias across all assessed domains. Only two studies Asato et al., [8] and Vijay Kumar [40] were rated as having a moderate risk of bias. All remaining studies were judged to have a low risk of bias (Fig. 7).
Fig. 7.
Risk of bias assessment of included studies
Discussion
Our study primarily focused on determining the incidence of AKI following snakebite and identifying its key clinical predictors and laboratory features. We also examined the need for RRT or dialysis and mortality rate among affected patients. Given the lack of a previously established pooled estimate, this study sought to quantify the overall incidence of snakebite-induced AKI and summarize the most frequently reported clinical and laboratory predictors associated with its occurrence.
According to established knowledge, the renal complications of snakebite have been attributed primarily to viper envenomation; however, increasing evidence suggests that AKI can result from a variety of venomous species, including elapids and even unidentified snakes. Although elapid envenomation has traditionally been associated with neurotoxicity rather than renal injury, accumulating evidence indicates that acute kidney injury can also occur following elapid bites, particularly from cobras (Naja spp.) and kraits (Bungarus spp.) ([35]; World Health Organization, [46]). The pathophysiology of AKI in elapid envenomation appears to be multifactorial, involving a combination of direct venom-mediated nephrotoxicity, systemic hypotension, hemolysis, rhabdomyolysis, and secondary inflammatory responses [9]. Experimental and clinical studies suggest that elapid venoms contain cytotoxins and phospholipases that can disrupt tubular epithelial cell membranes, leading to acute tubular necrosis [35]. In addition, severe neurotoxicity may result in respiratory failure and prolonged hypoxia, further exacerbating renal ischemic injury [15]. Although coagulopathy is less prominent than in viper envenomation, cases of pigment nephropathy secondary to rhabdomyolysis and hemoglobinuria have been described following elapid bites, underscoring the need to recognize AKI as a clinically relevant complication beyond hemotoxic snake species [9]. This overlap in pathophysiology reflects the multifactorial mechanisms of venom toxicity such as direct nephrotoxicity, hemolysis, rhabdomyolysis, hypotension, and disseminated intravascular coagulation [32].
The present meta-analysis synthesized data from 30 studies comprising 8,612 participants and revealed a pooled incidence of AKI of 23% following snakebite. This finding emphasizes that renal complications are relatively common, corroborating previous regional estimates ranging between 20% and 40% in hospitalized victims ([9]; [21, 32]). Higher incidences, such as 54.3% in Myanmar [9] and 43.8% in India [32], contrast with lower rates like 6.6% in Oman [2] and 7% in Japan [30], likely due to differences in snake species, promptness of antivenom administration, and diagnostic definitions.
The pooled incidence of patients requiring RRT was 28%, which is consistent with tertiary-care reports from India and Brazil [12, 27] and slightly higher than that reported by Daher et al., (2015) in Brazil (29%). The higher proportion observed in our analysis could be attributed to inclusion of studies involving severe envenomation or limited access to early dialysis in rural settings. This finding underscores the significant renal burden of snakebite, particularly in regions where access to RRT is limited, leading to worse outcomes among severely envenomed patients. The pooled mortality for snakebite-induced AKI was 10%, which aligns with prior reports ranging from 9% to 21% in hospital-based studies [21, 36]. A broader review reported mortality between 9% and 52%, largely depending on AKI severity and access to care [6]. Using KDIGO or AKIN stage 3 as a marker of severe AKI [11], available data suggest that snakebite -associated AKI is frequently severe. Several studies reported that more than 70% of affected patients presented with stage 3 disease, reflecting advanced renal injury at presentation. This may be attributed to delayed hospital presentation, limited access to early antivenom therapy, and restricted critical care resources in many endemic regions.
Common clinical predictors identified across studies included older age, male predominance, comorbidities such as hypertension and diabetes, and delayed presentation to the hospital. Children may differ from adults in susceptibility and outcomes following snakebite-associated AKI. Previous pediatric studies have shown that AKI is a frequent and serious complication in children with venomous snakebites, particularly following hematotoxic envenomation. A large prospective study reported AKI in approximately 38% of affected children, with delayed antivenom administration being a major predictor of adverse outcomes [16]. Other studies, especially involving Russell’s viper envenomation, have demonstrated high rates of severe AKI and dialysis requirement, whereas cohorts from Latin America have reported lower incidence and milder disease, suggesting that species variation and access to care influence outcomes [19, 24]. These findings indicate that children may have distinct risk profiles related to lower body mass and physiological vulnerability. However, age-stratified outcome data remain limited, and few studies directly compare pediatric and adult populations. Local features such as swelling, tenderness, and cellulitis were frequent, particularly following viper bites, while systemic manifestations including oliguria/anuria, hypotension, shock, and bleeding diathesis were strongly associated with AKI [33, 38]. Gastrointestinal symptoms such as abdominal pain, vomiting, and myalgia were also characteristic of severe envenomation [36]. Delayed administration of antivenom, observed by Li et al., [22], emerged as a major determinant of renal injury, emphasizing the importance of early intervention to prevent toxin-mediated tubular necrosis and circulatory compromise.
The most consistent laboratory features of AKI were coagulopathy (incoagulable 20-min WBCT, prolonged PT/INR, thrombocytopenia) and elevated renal indices (serum creatinine and BUN) [13, 33]. These derangements reflect venom-induced consumption coagulopathy and microvascular thrombosis, both of which contribute to renal ischemia. Proteinuria, microscopic hematuria, and early biomarkers such as NGAL, cystatin C, and β-2 microglobulin [3, 45] indicate early tubular damage and offer potential for early detection. Elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels [5, 26] suggest concurrent rhabdomyolysis and hemolysis, further potentiating renal tubular toxicity.
Inflammatory cytokines such as IL-6, CXCL-8, and IL-10, observed in Bothrops envenomation [29], illustrate the role of systemic inflammation and endothelial activation in venom-induced AKI. These findings underscore the multifactorial nature of snakebite nephropathy, involving hemodynamic, immune, and cytotoxic pathways.
Mechanistic comparison with other Toxin-Induced AKI
Envenomation and toxin-induced AKI share overlapping injury pathways, but each agent also has unique features. Like snake venom, other animal venoms often produce AKI through multifactorial mechanisms. Snake venoms especially hemotoxic viperid venoms combine direct nephrotoxicity with systemic effects: they induce hypotension, coagulopathy, microvascular thrombosis, hemolysis, and rhabdomyolysis, all of which converge to cause acute tubular necrosis (ATN). Russell’s viper venom contains metalloproteases and other enzymes that damage all renal compartments, trigger disseminated intravascular coagulation (DIC), and cause red cell fragmentation and pigment nephropathy [37]. Bothrops (pit viper) and Crotalus (rattlesnake) venoms likewise combine myotoxic and hemotoxic factors that injure tubules directly and indirectly [50].
Wasp (Hymenoptera) venom also causes AKI by direct tubular injury and by triggering massive rhabdomyolysis and hemolysis [49]. The venom contains phospholipase A and mastoparan, which destabilize muscle and tubular cell membranes [48]. Multiple wasp stings can release so much myoglobin and haemoglobin that the kidney is overwhelmed. Clinically, AKI occurs in roughly 30–50% of hospitalized wasp-stung patients. In these cases, acute tubular necrosis is the predominant lesion; a minority of patients develop acute interstitial nephritis from anaphylactic inflammation [49]. Wasp venom also induces a profound systemic inflammatory response through the cGAS-STING–IL-6 axis, exacerbating endothelial injury and tubular damage [23].
Scorpion venoms on the other hand are primarily neurotoxic, but a few species like Hemiscorpius lepturus in the Middle East and related “yellow” scorpions cause hemolysis and renal injury. As one review notes, scorpion envenomation are common worldwide but nephropathy is rare, reported mainly in Middle Eastern and North African cases. When scorpion AKI occurs, experimental and clinical data implicate venom enzymes, cytokine release, and renal vasoconstriction [7]. Animal studies show rapid venom redistribution leads to afferent arteriolar constriction and inflammatory cytokine release. Reported human cases describe haemoglobinuria and ATN, and occasionally interstitial nephritis or hemolytic-uremic syndrome, following stings [41]. Scorpion-induced AKI likely reflects pigment nephropathy combined with toxin-triggered vasoconstriction and inflammation.
Role and timing of antivenom or antidote administration
Effective treatment of toxin-induced AKI depends on both antitoxin therapy and supportive care. In snake envenomation, early antivenom is critical. Neutralization of circulating venom before it binds tissues can prevent downstream renal injury. Our review found that delayed antivenom was a major determinant of AKI – victims who received therapy later were far more likely to develop tubular necrosis and renal failure. This aligns with global guidelines: timely antivenom administration reduces coagulopathy and systemic toxicity in viper bites. In practice, antivenom should be administered as soon as possible after envenomation, ideally within hours of the bite [15]. Once AKI is established, antivenom cannot reverse tubular damage, so prevention via prompt treatment is paramount.
Clinically, this underscores the importance of rapid referral and antivenom administration in envenomation cases, particularly for viper bites. For future research, we recommend standardised recording of bite-to-antivenom intervals, antivenom brand/dose, supportive interventions (fluids, transfusions), and monitoring of renal function over time, to allow more robust analysis of timing effects.
Long-Term renal outcomes
Evidence on chronic sequelae varies by toxin. In snakebite-induced AKI, long-term kidney damage is well documented [14, 21, 42]. Studies following survivors report that up to one-third develop chronic kidney disease (CKD) [42], persistent hypertension, or reduced glomerular filtration on follow-up. These outcomes likely reflect unresolved acute injury, fibrosis from ATN, or immune-mediated glomerular injury after severe envenomation. Priyamvada et al., [32] found that many snakebite-AKI survivors had new-onset CKD within a year of the event [32].
Comparison with previous reviews
Prior literature has largely been descriptive, with narrative or single-center analyses failing to produce pooled estimates of AKI incidence. Reviews by Kumar et al., [21] and Priyamvada et al., (2019) highlighted regional burdens but lacked meta-analytic synthesis. Hence, our work represents one of the first quantitative attempts to summarize global incidence and predictors of snakebite-induced AKI.
Heterogeneity and interpretation of findings
The substantial heterogeneity observed across studies limits the generalizability of the pooled incidence estimates. This variability reflects the differences across studies in clinical setting, study design, and definitions used for AKI. AKI was diagnosed using heterogeneous criteria (KDIGO, AKIN, or creatinine-based clinical judgement), and several studies relied on peak creatinine without baseline values, which may inflate incidence. Also, snake species differed widely between cohorts and many studies involved unidentified species with low reliability of classification, adding to between-study variability. Antivenom type, dosing, and timing were inconsistently reported, limiting our ability to examine these factors as contributors to heterogeneity. Given these factors, the pooled estimate should be interpreted as an overview of global burden rather than a uniform risk applicable to all contexts.
Limitations
This review has limitations beyond statistical heterogeneity. Some included studies were retrospective and varied in methodological rigor, resulting in inconsistent reporting of essential clinical variables. Species identification was frequently incomplete or based solely on patient or witness description, reducing confidence in species-specific analyses. Information on key modifiers—such as baseline kidney function, precise timing of antivenom administration, and long-term renal outcomes—was often missing. Most studies originated from hospital-based populations, which may overrepresent severe cases. Finally, restricting inclusion to English-language full texts may have introduced publication bias.
Conclusion
AKI is a relatively frequent and clinically important complication of snake envenomation. Predictors such as hypotension, oliguria, coagulopathy, elevated renal biomarkers, and delayed treatment should alert clinicians to high-risk cases. Early detection, timely antivenom administration, and supportive renal care are critical for reducing morbidity and mortality.
Author contributions
RKDE and JA conceptualized the idea, IAG, ST and KA wrote the manuscript text and NLA and MOG prepared the figures. IAG, JA and NLA conducted the analysis. All authors reviewed the manuscript.
Funding
None.
Data availability
The datasets analyzed during the current study are derived from previously published articles that are publicly available and have been appropriately cited in this manuscript. The compiled dataset used for the meta-analysis is available from the corresponding author on reasonable request.
Declarations
Ethical approval
Not applicable.
Consent to participate
Not applicable
Consent to publish
Not applicable
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets analyzed during the current study are derived from previously published articles that are publicly available and have been appropriately cited in this manuscript. The compiled dataset used for the meta-analysis is available from the corresponding author on reasonable request.