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biopsy revealed hemoglobinuric nephropathy, tubular necrosis, and marked intersti-
tial edema. The patient's complicated course required extended inpatient manage-
ment; he was discharged 48 days after admission. Notably, this patient also had a
markedly elevated bilirubin (with a high ratio of unconjugated bilirubin) during the
course of the venom disease. Although likely due to intravascular hemolysis related
to the venom-induced erythrocyte membrane fragility, the authors considered fibrin
thrombi and/or direct hepatotoxicity as additional factors contributing to the hyper-
bilirubinemia (Lakier et al., 1969).
In a fatal case of T. kirtlandii envenoming, daily hemodialysis had an insignificant
effect on the clinical course (Mebs et al., 1978). Similarly, R. tigrinus envenoming can
feature ARF and anuria that are unresponsive to dialysis (Mittleman and Goris, 1978).
A patient with R. tigrinus venom-induced consumptive coagulopathy/DIC developed
anuria and also showed evidence of digital ischemia 48 h postenvenoming (Nakayama
et al., 1973, reported by Mittleman and Goris, 1978). The patient remained in renal
failure and required almost daily dialysis. Ten days after admission, left renal biopsy
revealed “chestnut-sized” lumps, a softened cortex, and subcapsular “bloody swell-
ings” (Mittleman and Goris, 1978). Extensive, severe hemorrhage and necrosis were
noted in the glomeruli and tubules. Biopsy of the right kidney performed 1 month after
admission showed “almost complete destruction” of the majority of glomeruli, hyalin-
ization of remaining glomeruli, and extensive interstitial fibrosis (Mittleman and Goris,
1978). In their translation of this case, Mittleman and Goris (1978) interpreted the
impression of Nakayama et al. (1973) that the patient had “no possibility” of regain-
ing normal function of the left kidney, while the right kidney showed evidence of some
cortical tubular regeneration. At 62 days postenvenoming, the patient's urinary output
increased to 100-200 mL/day and dialysis was performed twice weekly. Unfortunately,
the patient expired shortly thereafter following two episodes of acute pulmonary
edema. Autopsy findings included renal atrophy (Mittleman and Goris, 1978).
These representative cases of AKI following life-threatening or fatal envenom-
ation by some hazard level 1 colubrids are very similar to those seen in coagulo-
pathic viperid or elapid envenoming. For example, Thein-Than et al. (1991) reported
renal effects in 15 out of 24 patients envenomed by D. siamensis (Eastern Russell's
viper) in Burma (Myanmar). Ten of these patients exhibited mild renal dysfunc-
tion, while five developed ARF. It is noteworthy that patients with ARF were oligu-
ric on admission, developed ARF despite treatment with appropriate antivenom, and
showed a positive clinical response to peritoneal dialysis (Thien-Than et al., 1991).
These authors identified albuminuria as a possible early marker of evolving venom-
induced nephropathy (Thien-Than et al., 1991). This is similar to the observation of
Kikuchi et al. (1987) regarding microhematuria as a potential early marker of sys-
temic envenoming by R. tigrinus . Therefore, after envenoming from some hazard
level 1 colubrid species, even a urine dipstick assay may facilitate early recognition
of systemic involvement with possible impending renal dysfunction.
Markers of renal function [e.g., blood urea nitrogen (BUN) and/or creatinine]
have been used to assess the risk of complications after coagulopathic envenomation.
In a retrospective study of 68 cases of Echis coloratus (Middle Eastern saw-scaled
viper or Burton's carpet viper) envenoming in Israel, Porath et al. (1992) evaluated
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