Saudi Journal of Kidney Diseases and Transplantation

: 2019  |  Volume : 30  |  Issue : 1  |  Page : 231--234

Snake bite-induced renal medullary angitiis in a child: A case report

Lesa Dawman1, Aravind Sekar2, Tandra Harish Varma1, Ritambhra Nada2, Karalanglin Tiewsoh1,  
1 Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Karalanglin Tiewsoh
Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh


Snake bite envenomation is common in tropical countries during the summer. Snake bite-induced acute kidney injury (AKI) has varied histopathological manifestations such as acute cortical necrosis, acute tubular necrosis (ATN), and acute interstitial nephritis. However, snake bite-induced renal medullary angiitis has rarely been reported. We describe a nine-year-old child with AKI following viperine snake bite and renal biopsy revealed pigment cast nephropathy, ATN and medullary angiitis.

How to cite this article:
Dawman L, Sekar A, Varma TH, Nada R, Tiewsoh K. Snake bite-induced renal medullary angitiis in a child: A case report.Saudi J Kidney Dis Transpl 2019;30:231-234

How to cite this URL:
Dawman L, Sekar A, Varma TH, Nada R, Tiewsoh K. Snake bite-induced renal medullary angitiis in a child: A case report. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2019 Jun 25 ];30:231-234
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Full Text


Snake bite-induced acute kidney injury (AKI) is a known entity and is responsible for significant morbidity and mortality in these patients.[1],[2] The prevalence of AKI following snake bite has been reported to be 1%–25% in India depending on the severity of envenomation and species of the snakes.[3],[4] Snake bite occurs among adults in the age-group of 30–50 years, more so during monsoon season in May to July. Most of the bites occur in evening hours. The important venomous snakes in India are saw-scaled and Russell's viper which are hemotoxic, cobra, and krait which are neurotoxic and, sea snakes which are myotoxic. Snakes which cause nephropathy are usually the ones with hemotoxic or myotoxic venoms. Russell's viper and saw-scaled viper are notorious for causing AKI in India.[5] The histological lesions commonly seen are acute tubular necrosis (ATN) followed by cortical necrosis, crescentic glomerulonephritis, mesangiolysis, acute interstitial nephritis, and toxic vasculitis.[6]

Renal medullary angiitis is a rare description in kidney biopsies which may be due to the fact that renal cortex is given more focus than medulla during reporting and interstitial nephritis should be ruled out. However, if it is present, it usually suggests systemic vasculitis.[7] It is seen with anti-neutrophil cytoplasmic antibody (ANCA) associated disease, IgA nephropathy or drug-induced renal injury like nonsteroidal anti-inflammatory drugs. To the best of our knowledge, no literature has been reported on snake bite-induced renal medullary angiitis. We describe a nine-year-old child with AKI following viperine snake bite and renal biopsy showed pigment cast nephropathy, ATN and medullary angiitis.

 Case Report

Informed consent was obtained from the patient/relatives before writing this report. A nine-year-old girl from Garhiman village, Hoshiarpur, Punjab was admitted with alleged viperine snake bite four days before admission in our hospital. There was no previous history of any relevant renal or systemic disease or any history of drug intake before presenting to us. She gave a history of provoked snake bite on the left leg while walking in the fields after which she developed local pain and swelling. She was taken to a regional hospital within 1 h of bite but did not receive anti-snake venom (ASV). She subsequently passed red colored urine on day 3 and was transferred to another hospital where she received ASV. She developed anasarca and reduced urine output on day 4 and presented to us. In the emergency room, she was hypertensive[8] [blood pressure (BP): 130/90 mm Hg] for which she required multiple antihypertensive drugs (amlodipine 0.4 mg/kg/day, atenolol 2 mg/kg/day and prazosin 0.08 mg/kg/day). Local examination revealed a bulla over the anterior aspect of the left ankle and left medial malleolus while the remaining examination was normal. Her laboratory parameters showed deranged renal function with anemia and thrombocytopenia [Table 1]. In view of AKI with oliguria, the child was initiated on hemodialysis (HD) and underwent six sessions of HD. She had persistent thrombocytopenia, increased lactate dehydrogenase with no coagulopathy; hence, a possibility of snake bite induced thrombotic microangiopathy was considered. The platelet count spontaneously improved and renal biopsy was performed due to persistent derangement of renal function. Renal biopsy showed pigment cast nephropathy with toxic acute tubular injury and medullary angitis [Figure 1].{Figure 1}{Table 1}

In view of the presence of renal medullary angitis, work-up for systemic vasculitis was sent. Her anti-nuclear antibody, dsDNA, p-ANCA, c-ANCA, C3 and C4 levels were normal; hence, systemic vasculitis was ruled out.[9] The clinical profile and the investigations did not suggest any infective etiology. At discharge, she had good urine output with BP in the 90th centile and remained on anti-hypertensives. At seven weeks follow-up, her renal function tests were in the improving trend and BP was controlled.


Various factors responsible for the pathogenesis of snake bite induced AKI are direct nephrotoxicity of snake venom causing direct endothelial damage, intravascular hemolysis, hypotension due to bleeding, rhabdomyolysis, and coagulation defects leading to disseminated intravascular coagulation (DIC) which exaggerates renal ischemia.[6]

Renal medullary angiitis was demonstrated in the setting of snake bite in our case. In a review of 38 patients with medullary angiitis, majority (67%) had ANCA associated systemic vasculitis (AAV), 20% had IgA nephropathy and 17% had various infective etiologies such as brucellosis, leptospirosis, and osteomyelitis.[7] However, underlying systemic vasculitis, history of any drug intake and infections were ruled out in our child.[10]

Various mechanisms have been proposed for the medullary changes, such as poor renal perfusion with medullary hypoxia for the involvement of medullary peritubular capillaries. The vasa recta of renal medulla are involved in renal medullary angiitis. There is interstitial hemorrhage in the medulla with polymorphonuclear leukocyte infiltration around peritubular capillaries.[11] The renal medulla is hypoxic under normal circumstances and thus, the concentration of snake venom in the medulla may cause the injury.

In AAV, endothelial cell dysregulation and destruction of vessels has been implicated to be regulated by endothelial-specific angiopoietins.[12]

Another interesting finding in our index case was the presence of thrombocytopenia at presentation, which spontaneously improved. Many mechanisms have been proposed for thrombocytopenia in snake bite, the most common being platelet consumption during DIC or venom-induced consumptive coagulopathy.[13] Other proposed mechanisms are the effects of venom-induced damage to platelets, sequestration of platelets or combination of these. Although ASV and platelet transfusion causes transient elevation of platelets, most of the thrombocytopenia in these patients resolves spontaneously.[14] Our patient had received ASV.

In our case, renal medullary angiitis would have been precipitated by the direct effect of snake toxins as evident by the presence of toxic acute tubular injury in the renal biopsy and renal hypoperfusion leading to medullary hypoxia.


Medullary angiitis is a rare renal pathological finding, and if present suggests specific differrential diagnosis such as ANCA associated vasculitis, IgA nephropathy, or drug-induced injury. Snake bite induced AKI mostly shows findings involving the renal cortex and involvement of renal medulla is rarely described. It would require high index of suspicion by the clinician as well as the pathologist to give a correct diagnosis.

Conflict of interest:

None declared.


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