SNAKEBITE INDUCED ACUTE INTERSTITIAL NEPHRITIS: REPORT OF A RARE ENTITY

Abstract

Snakebite induced acute renal failure continues to occur in many tropical areas of the world. Renal histological lesions other than acute tubular necrosis and acute cortical necrosis as the cause of acute renal failure are rare. Only 3 cases of acute interstitial nephritis in patients with snakebite induced acute renal failure have been previously reported. We report a patient with acute renal failure following viperine snakebite due to acute interstitial nephritis. After a prolonged oliguric phase, there was complete recovery of renal function without institution of steroids. Interstitial nephritis may result from a hypersensitivity reaction to some component of the snake venom.

• Acute renal failure
• Hypersensitivity
• Renal biopsy
• Viperine snakebite

INTRODUCTION

Acute renal failure (ARF) after snakebite continues to be a major cause of morbidity and mortality in many parts of the world. It accounts for 3% of all cases of ARF seen at this Institute and is associated with a mortality rate of 28%.[[1]] In patients with snakebite induced ARF the renal pathology is characterized by either acute tubular necrosis (ATN) or acute cortical necrosis. Rarely other histological lesions like glomerulonephritis, vasculitis and acute interstitial nephritis (AIN) have been reported.[[2]] We report a patient with AIN as the cause of ARF occurring after a snake bite.

CASE REPORT

A 40-year-old female was bitten by a viperine snake on the right thumb. This was followed by oozing of blood from the bitten site for a few minutes along with swelling of the thumb. A day later she became anuric. She was managed in a district hospital with intravenous fluids and frusemide. As the patient continued to be anuric with progressive worsening of azotemia she was referred to this Institute after four days. Physical examination revealed moderate pallor and a swollen right thumb. Her pulse rate was 76 beats/min and blood pressure 130/80 mm Hg. Systemic examination was unremarkable.

Laboratory investigations revealed hemoglobin of 6.3 gm/dL with reticulocyte count of 2%, platelet count of 2.3 × 10⁵/mm³, total leukocyte count of 9300/mm³ with normal differential counts. The blood film showed a dimorphic picture with hypochromia, microcytes and macrocytes. Urine examination revealed albumin of 2 + on dipstick, with a field full of RBCs on microscopic examination. Blood urea on admission was 170 mg/dL and serum creatinine was 5.0 mg/dL. Coagulation studies revealed clotting time of 5 min, prothrombin time of 14 s (control 13 s), partial thromboplastin time of 35 s (control 35 s), serum fibrinogen of 300 mg/dL and no detectable fibrin degradation products. Hemolytic work up was negative. Ultrasound revealed normal sized kidneys on both the sides and no abnormality was detected in other intra-abdominal organs. Since her coagulation profile was normal, anti-snake venom was not given. Renal failure was managed with intermittent hemodialyses. Since she continued to remain anuric for three weeks and because of the presence of proteinuria with active urinary sediment, a kidney biopsy was done. The biopsy revealed normal glomeruli with severe interstitial edema with dense lymphomononuclear cellular infiltrate also containing a few eosinophils (Figure 1). A diagnosis of AIN was made. Over the next four days, patient's urine output improved spontaneously with improvement in azotemia and the renal functions normalized over the next 2 weeks.

Figure 1. Interstitial inflammation of the kidney comprising lymphomononuclear cell infiltrate (H&E, × 540).

DISCUSSION

In India, the incidence of ARF varies from 5 to 30% following viperine snakebites.[[1]] Factors implicated in the pathogenesis of snakebite induced ARF include volume loss secondary to vomiting and blood loss, disseminated intravascular coagulation, intravascular hemolysis and direct nephrotoxicity of the snake venom. ATN is the commonest renal lesion noted in these patients followed by cortical necrosis, which may be patchy or diffuse. Other histological lesions include mesangiolysis, mesangial proliferation, crescentic glomerulonephritis, vasculitis and AIN.[[1]], [[2]]

Although a mild lymphomononuclear interstitial infiltrate is commonly seen in patients with ATN, presence of severe interstitial inflammation is a hallmark of AIN. Although AIN accounts for 5–15% of all cases of ARF,[[3]] only three cases of AIN following snakebite have been reported earlier. In an autopsy study on snakebite patients, Sant and Purandare reported one patient with hemorrhagic interstitial nephritis.[[4]] Subsequently two more cases of AIN following Russell viper bite were described from Thailand.[[5]], [[6]] Clinically both these patients were oliguric and renal failure was unusually prolonged, prompting consideration of causes other than ATN as the cause of ARF. The clinical course of our patient was also similar to these two cases. Histopathology of these cases revealed severe interstitial inflammation comprising of lymphomononuclear cells, but presence of eosinophils in the interstitial infiltrate was not mentioned. In the index patient however, the interstitial infiltrate also comprised of a few eosinophils, suggesting the possibility of AIN secondary to drugs. Although our patient received frusemide, which can rarely cause AIN, she was already in established ARF prior to receiving this drug. Also presence of eosinophils as a part of interstitial inflammation along with lymphocytes and plasma cells in snakebite ARF patients has been described by Date and Shastry.[[7]] Further there was no evidence of dehydration, blood loss, disseminated intravascular coagulation or hemolysis, the common factors known to predispose to ATN. The sequence of events suggests that AIN in this patient is a result of snakebite. The rare occurrence of AIN in contrast to frequent occurrence of ARF in snakebite victims cast doubts about causative role of snakebite in its pathogenesis. However, even in drug induced AIN, in spite of widespread usage of the drugs only a minority develops this pathology. Similar analogy may be responsible for the occasional occurrence of AIN following snakebite and it may represent a hypersensitivity reaction to some component of snake venom.[[1]]