Saudi Journal of Kidney Diseases and Transplantation

: 1996  |  Volume : 7  |  Issue : 3  |  Page : 309--312

Acute Renal Failure Following Snake Bite: Case Report and Review

Mohammed Al-Homrany 
 College of Medicine, King Saud University, Abha, Saudi Arabia

Correspondence Address:
Mohammed Al-Homrany
College of Medicine, King Saud University, P.O. Box 641, Abha
Saudi Arabia


We present an adult male patient who presented with history of having been bitten by a snake. Despite administration of antivenom and adequate hydration, he developed acute renal failure secondary to disseminated intravas-cular coagulation and rhabdomyolysis. He improved with daily hemodialysis and at discharge had normal renal function. Although we did not perform a renal biopsy on him, the clinical course was highly suggestive of acute tubular necrosis. The pathogenesis, pathology, as well as therapy of renal involvement following venomous snake bite is discussed.

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Al-Homrany M. Acute Renal Failure Following Snake Bite: Case Report and Review.Saudi J Kidney Dis Transpl 1996;7:309-312

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Vipers belong to the genus Echis and are represented by the two main species, Echis coloratus and Echis carinatus. The latter is found world-wide, including Saudi Arabia, whereas the former, Echis coloratus gunther, is found only in the Arabian Peninsula, East Egypt, Sinai, Palestine and Jordan [1] . Echis coloratus is the commonest snake inflicting bites in the Asir region of Saudi Arabia [2] . Acute renal failure (ARF) associated with poisonous snake bite has been reported from various parts of the world [3],[4],[5] including Saudi Arabia [6],[7],[8] . This report describes a case of reversible ARF induced by poisonous snake bite. Also, a brief review of the pathogenesis, pathological features and management of this entity is presented.

 Case History

A 52-year old Saudi male from Tihama area was admitted to the Asir Central Hospital four hours after having been bitten over the. right foot by a snake; the snake was killed and brought to the hospital and identified as Echis coloratus. The patient denied any past history of diabetes, hypertension or any other medical diseases. Clinically, he was conscious, pale, and jaundiced, the pulse rate was 100 per minute and regular, blood pressure was 140/90 mm Hg with no postural fall and the jugular venous pressure was not elevated. There was a marked swelling of the right leg extending from the foot to mid thigh. The laboratory parameters at admission are given in [Table 1].

The patient was given repeated doses of polyvalent immune serum (anti-snake venom serum, Near and Middle East, Behring, Marburg, Germany). He was given intravenous (i.v.) normal saline according to the volume status and urine output, and alkalinization of the urine was performed using sodium bicarbonate. He was started on cloxacillin 500 mg i.v. administered every 6 hrs and a booster dose of tetanus toxioid was given Eighteen hours after admission, the patient developed spontaneous bleeding from nose and rectum and, oliguria. Laboratory parameters at this stage are given in [Table 1]. Thus, despite good hydration, the patients's renal function had deteriorated. The patient was started on hemodialysis and repeated doses of fresh frozen plasma, packed red cells and platelet transfusions were administered. Hemodialysis was needed daily for six days to control acidosis, hyperkalemia and fluid overload. The patient's general condition as well as renal function started to improve and by the end of the fourth week (time of discharge), his renal function had normalized and salient laboratory parameters were as follows: blood urea nitrogen, 8.6 mmol/L; serum creatinine, 96 /miol/L; hemoglobin, 125 gm/L; white blood cell count, 8.2xl0 9/ L; platelet count, 130 x 109/L; prothrombin time 14 seconds.; partial thromboplastin time, 41 seconds.; aspartate aminotransferase, 40 IU/L; alanine amino­transferase, 30 IU/L; lactate dehydrogenase, 300 IU/L; creatine phosphokinase, 190 IU/L and normal urine analysis.


Over 2000 species of snakes are known world-wide; however, only 400 of these are venomous [9] . These snakes belong to four families: elapidae, viperidae, hydrophidae, and colubridae [9] . Renal involvement has been reported following bites from members of the latter three families, including the Russell's viper, Echis carinatus [5],[10],[11] . The most important of all renal syndromes is ARF which has been reported with varying frequency in different studies [3],[4],[5],[12],[13],[14] . Although most of the venomous snakes are known to cause ARF, the vast majority of these cases are due to viper bites [3] . Data on the precise incidence in different geographical regions is lacking but obviously varies with the distribution of the snakes. In India, the incidence of ARF is reported to be 13-32% following Echis carinatus or Russell's viper bites [5],[15] . In Nigeria, the reported inci­dence rate for ARF after Echis carinatus bite is 1% and following puff adder bite is 10% [10] ; In Israel it is 6.2% following Palestinian viper bite [13] ; in Thailand it is 5% following Russell's viper and sea snake bite [11] and in ceylon the reported incidence of ARF following bite of unidentified vipers is 27% [4] . The incidence of ARF following snake bite in Saudi Arabia is not well documented.

 Renal Manifestations of Snake Bite

Hematuria and proteinuria are the commonest renal abnormalities found in 20­-70% of the reported cases [2],[16],[17] . Oliguria or anuria may develop from within a few hours, to as late as 96 hours, after the bite [5],[14],[18] .

Tubulointerstitial lesions, predominantly tubular necrosis, are observed in 60-80% of patients who develop ARF following snake bite [5],[11] . Renal biopsy, performed in the first week after the bite, has shown dilated tubules lined by flattened epithelium and, in severe cases, tubulorrhexis with cell necrosis and desquamation of the necrotic cells from the basement membrane has been reported [5],[14] . Interstitial edema, infiltration of inflammatory cells, and hemorrhage were also observed [5],[14] . Features unique to snake bite-induced ARF are the severe tubular and vascular lesions, increased apoptosis in the distal tubules, and the infiltration of eosinophils, mast cells, and hyperplastic fibroblasts in the interstitium [19] . Glomerular lesions are uncommon; however, there are documented cases of proliferative and crescentic glomerulonephritis [20],[21],[22],[23] . Renal papillary necrosis, necrotizing arteritis and cortical necrosis have also been reported in some patients [19],[24],[25] . We did not perform kidney biopsy on our patient but the clinical course was highly suggestive of acute tubular necrosis.

Ultrastructural and immunofluorescence data are scanty. Granular deposits of C3 without immunoglobulins in the glomerular mesangium and arterial wall have been described. Some authors have also described electrondense mesangial deposits [19],[26] .


Several mechanisms including hemorrhage, hypotension, hemolysis and hemoglobinuria, rhabdomyolysis, disseminated intravascular coagulation (DIC) as well as the direct effect of the venom have been incriminated in the pathogenesis of snake bite-related ARF. Among all these mechanisms, the cytotoxic effect of the venom on the kidney is considered to play a major role in the pathogenesis of ARF [27] . Raab and Kaiser observed a significant increase in urinary alkaline phosphatase and aminopeptidase activities following administration of Agkis­trodon piscivorus venom in rats and attributed this to the effect of the venom on the tubular epithelial cells [27] . Hypotension, due to bleeding or other factors such as a release of bradykinin or depression of the vasomotor center, can produce circulatory collapse and ischemic tubular, necrosis [28],[29],[30] . The presence of fibrin thrombi in the renal micro­vasculature and in the glomerular capillaries, together with the finding of microangiopathic hemolytic anemia and thrombocytopenia in patients with cortical necrosis strongly sug­gests that DIC plays an important role in the pathogenesis of snake bite-induced ARF [5] . In our patient, the likely pathogenic mechanisms include DIC and rhabdomyolysis.

Therapeutic Approach

The basic approach to treat patients with ARF following snake bite is similar to that for ARF due to other causes. However, complications other than ARF can cause major threat to an envenomated patient.

These complications include coagulation disturbances, bleeding, hypotension and shock, and electrolyte disturbances. Antivenom should be given to all patients who experience systemic manifestations of envenomation. Adequate dose of antivenom is known to correct the coagulopathy [1],[31] . In severe cases, or if no response to antivenom is forthcoming, fresh frozen plasma should be given. Adequate hydration and alkalinization of the urine is recommended in cases of intravascular hemolysis or rhabdomyolysis. Other measures include treatment of electrolyte disturbances, administration of tetanus toxoid and the treatment of pyogenic infection with appropriate antibiotics. Hemodialysis or peritoneal dialysis have both been used in cases where dialysis was indicated.

Although snake bite is not uncommon in Asir region, ARF is a complication that has been rarely reported [2],[6] . The possible explanation to this observation is that our patient presented with features suggestive of rhabdomyolysis and DIC which were not observed in other patients from the region [2],[6] . It is also possible that our patient was envenomated with a higher dose of snake venom and that some patients die in the community before reaching the hospital.


I would like to thank Mr. Rollie Go for his secretarial assistance.


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