Summary at a Glance
Introduction
Methods
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Type of participants: studies which included humans bitten by a snake (any) in India.
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Concept: studies that report on histopathology (biopsy findings) of the kidney will be included. Studies done exclusively on autopsy findings were excluded.
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Study design - studies were included irrespective of study design, with the exception of in vitro studies, and case reports.
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Restrictions: no restrictions on language or date of publication.
Data search
Article selection
Data extraction
Results
Selection of sources of evidence
Characteristics of included studies
First Author | Year of publication | Population | Study design | State | Exclusively done on children | Snake species | Indication/ timing of biopsy | Total Number of Snakebite Patients | Total Number of snake bite induced AKI cases | Total Number of Renal Biopsies | |
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1 | Chugh et al., [8] | 1975 | AKI following snake-bite | Cohort with follow-up | Chandigarh | No |
Russell’s viper
| NR | 69 | 8 | 8 |
2 | Basu et al., [9] | 1977 | Patients with AKI following viperine bite | Cross-sectional | West Bengal | No |
Russell’s viper
| Early diuretic phase | NR | 45 | 37 |
3 | Shastry et al., [10] | 1977 | Patients with AKI following snake bite | Cohort with follow-up | Tamilnadu | No |
Russell’s viper
| Day 4 to 31 | NR | 19 | 19 |
4 | Sarangi et al., [11] | 1980 | AKI following viperine snake bite | Cross-sectional | Odisha | No |
Russell’s viper
| After oliguric phase of AKI | 48 | 23 | 22 |
5 | Date et al., [12] | 1982 | Patient with AKI following snake bite | Cross-sectional | Tamil nadu | No |
Russell’s viper
| Biopsy timing varied from 5–22 days. | NR | 9 | 9 |
6 | Chugh et al., [13] | 1984 | AKI following snake bite. Study was conducted to describe renal histopathological lesions in AKI following snakebite in humans and to know the effects of viperine venoms on the renal structure and function in subhuman primates. | Cross-sectional | Chandigarh | No | NR | During the polyuric phase. | 157 | 45 | 35 |
7 | Date et al., [14] | 1986 | Patient with AKI following snake bite | Cross-sectional | Tamilnadu | No |
Russell’s viper
| NR | NR | 24 | 15 |
8 | Acharya et al. [15], | 1989 | AKI following viper-ine snake bite | Prospective | Maharashtra | 4 patients were children below the age of 10years. |
Russell’s viper and Echis carinutus were the main snakes identified. One case of renal failure with sea snake bite was reported | 1.5 to 8 weeks | NR | 50 | 29 |
9 | Chugh et al., [16] | 1989 | All patients with snakebite with treated for viper bite [presumed] poisoning. | Cross-sectional | Chandigarh | No |
Russell’s viper and Echis carinatus
| NR | 246 | 70 | 44 |
10 | BV Mittal et al., [17] | 1994 | Patient with AKI following snake bite were included | Cross-sectional | Maharashtra | No |
Russell’s viper in 14 (34%), Echis carinatus or saw scaled viper in 20 (48%) and sea snake in one case. | Varied from 3–8 weeks | 253 | 41 | 41 |
11 | Chugh et al., [18] | 1994 | Patients dialysed for AKI and diagnosed to have ACN | Cohort with follow-up | Chandigarh | No | NR | NR | 16 | 16 | 16 |
12 | Vijeth et al., [19] | 1997 | Adult cases of viper bite with systemic envenomation | Observational | Pondicherry | No |
Russell’s viper
| Persistant renal dysfunction | 40 | 13 | 3 |
13 | Golay et al., [20] | 2012 | Patients with AKI after snake bite | Cohort with follow-up | West Bengal | No |
Russell’s viper
| In patients who remained oliguric or the serum creatinine did not decrease to less than 50% of the attained peak value at the end of 3 weeks | NR | 42 | 13 |
14 | Waikhom et al. [21], | 2012 | Post snake bite patients who developed dialysis-requiring AKI and had survived | Prospective observational | West bengal | No |
Russell’s viper
| NR | 499 | 410 | 10 |
15 | Waikhom et al., [22] | 2013 | All pediatric patients with AKI following Russell’s viper bite | Prospective study, supplemented by a retrospective chart review | West bengal | Children < 15 years were included |
Russell’s viper
| NR | NR | 61 | 5 |
16 | Golay et al. [23], | 2013 | Post snake bite patients with AKI who had survived | Prospective study, | West bengal | No |
Russell’s viper in 7 out of 9 cases (77%), 2 were unidentified | In whom AKI did not resolve by the end of 3 weeks | 126 | - | 4 |
17 | Mukhopadhyay et al., [24] | 2016 | All snakebite patient who received hemodialysis | Cross-sectional | West bengal | 29 patients were of age ≤ 18 years | NR | NR | 460 | 203 | 3 |
18 | Vikrant et al., [25] | 2017 | Patients with definitive history of snake bite; clinical picture consistent with snake bite, as presence of fang marks or cellulitis or coagulopathy or neuroparalysis; presence of AKI as defined using KDIGO criteria based on serum creatinine and presence of at least one or more indication of RRT | Retrospective | Himachal pradesh | No | NR | Patients who remain oligoanuric or whose serum creatinine did not decrease satisfactorily at the end of 3 weeks underwent kidney biopsy | 447 | 81 | 22 |
19 | Priyamvada et al., [26] | 2016 | Patients diagnosed with snake envenomation-induced AIN | Retrospective | Puducherry | No |
Daboia russelii 22.2% (n = 41) Echis carinatus, 14.1% (n = 26). The species of snake was not identified in 117 patients (63.6%). | Renal biopsies are performed if the serum creatinine remains greater than 2 mg/dL 4 weeks post-envenomation. | NR | 88 | 7 |
20 | Dinesh kumar et al., [27] | 2018 | Patients with AKI after snake bite and kidney biopsy showing AIN | Prospective observational | Tamil Nadu | No |
Russell’s viper 25% (n = 5), saw-scaled viper 20% (n = 4), and krait 5 % (n = 1) | Renal biopsy were performed if kidney dusfunction persisted for more than 3 weeks or earlier if persistant anuria for more than 2–3 weeks or pathology other than ATN was suspected for example fragmented RBCs in peripheral smear.10–40 days | 196 | 196 | Total 85 biopsies were done. Results for Twenty (23.5%) patients who underwent biopsy had AIN were presented in the study |
21 | Shaktirajan et al., [28] | 2018 | Cases of AKI with renal biopsy showing pigment nephropathy | Retrospective observational | Tamil Nadu | No | NR | Patients with persistent oliguria for > 7 days and renal failure for > 14 days despite supportive treatment. | 10 | 10 | 10 |
22 | Priyamvada et al., [29] | 2020 | All adult patients with AKI following haemotoxic snake envenomation were recruited | Prospective observational | Puducherry | No | Species identification was not done in 2 patients, and the rest were Daboia russelii (as reported by the patients) | Persistant renal dysfunction beyond 3 months | 420 | 184 | 3 |
23 | Rao et al., [30] | 2019 | Patients with age > 18 years with definitive history of snake bite( consistent clinical picture like the presence of fang marks, cellulitis, coagulopathy, neuroparalysis) and presence of AKI (as per KDIGO 2012 guidelines) | Case-record‐based retrospective analysis | Karnataka | No | NR | At day 18 in one patient and at day 31 in another patient | 103 | 103 | 2 |
24 | Islam et al. [31] | 2020 | Paients with hematotoxic snake envenomation characterized mainly by a positive 20 min whole blood clotting test (WBCT) admitted in pediatric emergency ward | Comparative | West Bengal | Yes ( Mean age 5.8 ± 1) years | NR | Children suffering who suffered from permanent renal damage and who died. | 371 | 139 | 64 |
25 | Kumar M et al., [32] | 2022 | Patients with AKI with (1) Definitive history of snake bite; (2) Clinical picture suggestive of snake bite with the presence of a fang mark. | Retrospective recruitment followed by a prospective follow | Chennai | No | Snake species was identified in 29 patients (18.2%)—Cobra in three, Russell’s viper in 14, Saw scaled viper in seven and Krait in five. | NR | 769 | 159 | 41 |
26 | Ariga et al. [33] | 2021 | All adult patients with AKI (as per KDIGO criterion) survived the episode and were discharged | Retrospective and prospective observational (Ambidirectional) | Puducherry | No | Unidentified 98 (50.7%) Russell’s viper 85 (445) Saw-scaled viper 10 (5.3%) | NR | NR | 193 | 6 |
27 | Acharaya et al., [34] | 2023 | All adult patients with AKI (as per KDIGO criterion) following haemotoxic snake envenomation were recruited | Prospective | Odisha | no |
Viperidae species | NR | NR | 202 | 30 |
28 | Prema et al., [35] | 2023 | Patients with hemoglobulin cast nephropathy | Retrospective analysis | NR | NR | NR | NR | NR | NR | 16 |
Timing and indication of renal biopsy
SL No | Primary Author | Light microscopy | IF | EM | ||
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Glomerular changes | Tubulointerstitial changes | Vascular changes | ||||
1 | Chugh et al. 1975, [8] | ACN in n = 3 (50%) of the cases. Surviving glomeruli in areas of necrosis showed fibrin thrombi and some proliferation of mesangial cells. | ATN in n = 3 (50%) of the cases | Not mentioned specifically | NR | NR |
2 | Basu et al., 1977, [9] | ACN in 2 (5.4%) of the cases. Glomerular tuft necrosis n = 5 (13.4%),Isolated Glomerular thrombosis n = 7 (19%) | ATN in 32 (86.4%) cases. Peritubular infiltration of inflammatory cells n = 6 (16.2%) Medullary haemorrhagen = 14 (27%) | Vessel wall necrosis n = 5 (13.4%) Fibrin thrombi in arteriole n = 2 (5.4%) | NR | NR |
3 | Shastry et al., 1977 [10] | ACN in 3 (15.7%) of the cases. Focal mesangial hypercellularity in n = 6 (32%). | ATN in 12 (63.2%) of cases, Interstitial haemorrhage n = 3 (15.7%). Presence of hyaline, granular and heme cast. Vacuolation and regeneration. Intertitial fibrosis in 1 case Interstitial oedema (10.5%) Interstitial inflammation n = 10 (52.6%) | Not mentioned specifically | NR | NR |
4 | Sarangi et al., 1980, [11] | ACN in one case. Aneurysmal capillary dilatation and inflammatory cell infiltration were seen in glomerulus | Acute tubular injury n = 3 (13.6%), Acute tubular necrosis n = 6 (27.2%), Presence of interstitial haemorrhage oedema (5 cases) and RBC tubular cast. | Not mentioned specifically | NR | NR |
5 | Date et al., 1982, [12] | Glomeruli was normal except for focal mesangial expansion and focal prominence of parietal epithelium. One case had necrosis of cortical tissue | ATN n = 9 ( 100%) .The interstitium was expanded and infiltrated by mononuclear cells and scattered eosinophils predominantly at the cortico-medullary junction. | No abnormality | NR | Glomeruli: Swollen bowman’s capsule epithelium containing numerous organelles. The visceral epithelium revealed microvilli, patchy foot process fusion and intracytoplasmic lipid vacuoles. Glomerular capillaries had irregular thickening and wrinkling of glomerular basement membrane. Mesangial expansion was present in all biospies. Subendothelial electron dense deposits were seen in one case and one case had features of ACN. Blood vessels: Swollen endothelial cells containing numerous vacuoles and a dilated smooth endoplasmic reticulum. Interstitium: Oedematus intertubular tissue and infiltration of inflammatory cells including eosinophils, 6mast cells, plasma cells and lymphocytes and some macrophages and basophils. |
6 | Chugh et al., 1984, [13] | ACN n = 10 (28.5%). Superficial cortical glomeruli were more severely congested compared to deep juxtamedullary glomeruli. Hilar glomerular capillaries were partly filled with recent thrombus. | ATN n = 23 (65.7%). PCT showed shrunken, pyknotic nuclei or no stainable nuclei with cytoplasmic cloudy swelling and considerable tubulorrhexis. Distal convolutions were collapsed. Collecting ducts contained brown heme casts or pigments. | The large intrarenal arteries were deeply congested. The intertubular capillaries were crowded with neutrophils. In some cases venules and veins were congested with inflammatory cells. | NR | NR |
7 | Date et al., 1986 [14] | ACN n = 3 ( 20%) | ATN n = 12 (80%) | NR | Not done | Done in 7 (46.6%) biopsies. Biopsies revealed platelet and fibrin clusters in glomeruli and small calibre vessels |
8 | Acharya et al., 1989 [15] | ACN in 7 (24.1) cases. Ballooning of glomerular capillaries (n = 10), swollen endothelial cells (n = 10), splitting of basement membrane (n = 19). Mesangial cell proliferation (n = 5). Proliferative glomerular changes in 5 cases. | ATN in 10 (40% ) cases with evidence of tubular degeneration in 17% cases (42.5%) | Vasculitis like changes in vesselsN = 3 (7%) cases. Fibrin thrombi in capillaries, n = 6(24.2% )cases. | Not done | Not done |
9 | Chugh et al., 1989 [16] | Patchy ACN in 4 cases (9%) and diffuse cortical necrosis in 8 patients (18%). | ATN was present in 32 (73%) of cases, AIN in 3 patients (6.8%). | Necrotizing arteritis of the interlobular arteries along with thrombophlebitis of the arcuate vein and its tributaries in 2 cases. | Dense deposits of C3 were seen in the walls of afferent and efferent arterioles in cases of necrotizing arteritis. | Not done |
10 | Mittal et al., 1994 [17] | ACN in 25 (60.9%) cases. Focal proliferation of mesangial cell n = 5 (12.1%). Mild mesangial proliferation n = 22 (53.6%). Mesangiolysis n = 7 (17.7%) Ballooning of glomerular capillaries n = 13 (31.7%), swollen endothelial cells n = 16 (39%), splitting of basement membrane n = 11 (26.8%). Capillary thrombi n = 5 (12.1%). | Tubular necrosis n = 5 (12.1%), Tubular regeneration n = 2 (4.8%). Pyelonephritis complicating tubular necrosis and one autopsied case revealed abscesses. Haemorrhagic interstitial nephritis with haemorrhage in subcapsular area in case. | Other than in cases of ACN. Not mentioned specifically | Done in 7 cases [17] IgG (weak +):2 cases IgM (weak +):1 case C3 (+):2 cases in mesangial area. Presence of fibrin in mesangial area: 1 case | Not done |
11 | Chugh et al., 1994 [18] | ACN in all 16 patients | NR | NR | NR | NR |
12 | Vijeth et al. [19] | NR | ATN in 3 (100%) cases | NR | NR | NR |
13 | Golay et al., 2012 [20] | Normal glomeruli | ATN in 8 (21.5% ) and AIN in 5 (11.9%) cases. Extensive interstitial inflammation was observed in all the AIN cases, with pre-dominantly lymphocytic infiltration, in one case where eosinophils were predominant. | Normal Blood vessels | No IF deposits | NR |
14 | Waikhom et al., 2012 [21] | ACN in 3 patients (30%) | ATN in 6 patients (60%). AIN in1 case | Not specifically mentioned | NR | NR |
15 | Waikhom et al., 2013 [22] | ACN in one case. | ATN in 3 patients.(60%).AIN in1 case | Not specifically mentioned | NR | NR |
16 | Golay et al., 2013 [23] | ACN in one (25% ) case | ATN in 3 (75% ) patients | Not specifically mentioned | NR | NR |
17 | Mukhopadhyay et al., 2016 [24] | ACN in one out of 3 patients | ATN in 2 out of 3 patients. (66.6%) | NR | NR | NR |
18 | Vikrant et al., 2017 [25] | Patchy ACN in one case. | ATN in 20 (91%) cases. In 9 (40.9%) ATN was associated with mild to moderate AIN. One (4.5%) patient only had moderate AIN | Not specifically mentioned | Findings not specifically mentioned | NR |
19 | Priyamvada et al., 2016 [26] | Diffuse mesangial proliferation; in 1(20% )out of 5 case. Rest were normal | ATN in 4 cases (57.1%). AIN in 5 out of 7 cases (71.4%). Lymphocyte-predominant infiltration in all patients. 4 patients (57.1%). had admixture of other cell types including eosinophils, neutrophils, and plasma cells. Neutrophil cast in was seen 1 patient. | Not specifically mentioned | Weak 1 + C1q deposits in mesangium of 1 patient | NR |
20 | Dinesh kumar et al., 2018 [27] | Not specifically mentioned | AIN was reported in 20 ( 23.5%) out of 85 biopsies. Marked infiltration of eosinophils and lymphocytes was seen along with tubular injury. | Not specifically mentioned | Negative in all patients | NR |
21 | Shaktirajan et al., 2018 [28] | None of the patients had significant glomerulosclerosis or any other specific glomerular abnormality | Snake bite envenomation was present in 10 out of 46 patient of pigment induced nephropathy. All renal biopsies revealed ATN with pigment casts in the tubules. No interstitial fibrosis or tubular atrophy were noted | Not specifically mentioned | NR | NR |
22 | Priyamvada et al. 2020 [29] | 1 out of 2 patients had features of chronic TMA | Not specifically mentioned | Not specifically mentioned | NR | NR |
23 | Rao et al., 2019 [30] | Biospsy of both patient was suggestive of ACN with fibrin thrombi in glomerular capillary lumen and arterioles. TMA was present in both cases. | One biopsy showed evidence of AIN along with TMA | Fibrin thrombi was present in in glomerular capillary lumen and arterioles. | NR | NR |
24 | Islam et al., 2020 [31] | ACN in n = 8 (12.5%) cases. | ATN in n = 25 (39.1) %. cases | NR | NR | NR |
25 | Kumar M et al., 2022 [32] | • 5 (12% ) out of 41 had ACN. • 4 (9.7 )out of 41 had TMA • One patient had TMA with renal cortical necrosis | • ATN in n = 18 (44%) cases. • N = 5 (12% ) biopsies showed pigmented casts • AIN was reported in 9 ( 22%). • N = 5 (12% )cases had ATN with AIN | NR | NR | NR |
26 | Ariga et al., 2021 [33] | NR | Out of 6, n = 2 (50%) were ATN and n = 4 (66.6% ) were AIN | NR | NR | NR |
27 | Acharya et al., 2023 [34] | • ACN in n = 7 (23%) | • AIN was reported in n = 6 ( 22%). • ATN in n = 18 (59.6)% cases. | NR | NR | NR |
28 | Prema et al. [35] | NR | • All 16 snake bite patients had ATN alongside hemoglobulin cast nephropathy. • Hemoglobin casts were seen present in the PCT. The casts were bright red to brown on hematoxylin and eosin stain weakly PAS positive, argyrophilic on Jones methenamine silver stain, and granular to globular in texture. Hemoglobin IHC was positive on the pigment casts. Two patients showed myoglobin immunostain positivity. | NR | NR | NR |