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      Thrombotic Microangiopathy: An Under-Recognised Cause of Snake-bite-related Acute Kidney Injury

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          Abstract

          Introduction:

          Thrombotic microangiopathy (TMA) as a cause of snake-bite-induced acute kidney injury (AKI) is rarely reported. Very little is known about the clinical course, optimal management, and prognosis of this entity. We describe a series of snake-bite-induced TMA and compare their outcomes with those without TMA.

          Methods:

          This was a single-center retrospective study of patients with AKI following snake envenomation admitted between January 2012 and December 2017. Demographic profile, clinical parameters, and outcomes were studied. TMA was diagnosed based on presence of triad of microangiopathic hemolytic anemia, thrombocytopenia, and AKI, and groups with and without TMA were compared.

          Results:

          Of 103 patients with AKI following snake bite, 19 (18.5%) had clinical evidence of TMA. All patients with TMA had advanced azotemia (mean peak serum creatinine 9.5 ± 3.0 mg/dL), with 18 (95%) requiring renal replacement therapy (RRT). Thirteen (68%) had either complete or partial recovery of renal functions, two (10%) progressed to end-stage renal disease, and one died (three patients were lost to follow-up). Age ≥50 years, presence of oliguria/anuria, anti-snake venom dose ≥10 vials, and urea ≥80 mg/dL at presentation were independently associated with TMA ( P < 0.05). RRT requirement (95% vs. 57%), mean number of RRT sessions (18 vs. 4.5 sessions), and hospital stay ≥7 days (84% vs. 58%) were higher in patients with TMA ( P < 0.05), but patient outcomes did not differ.

          Conclusions:

          In conclusion, TMA was seen in 18.5% of patients with snake-bite-related AKI in our study and was associated with almost universal need for RRT, longer duration on RRT, and hospital stay compared with patients without TMA.

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          Most cited references13

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          Snake-bite-induced acute renal failure in India.

          K.S. Chugh (1989)
          Acute renal failure complicates the course in 5% to 30% of victims of severe viper poisoning. No consensus exists on the single mechanism causing acute renal failure after viper bite. It is known, however, that viper venom induces several clinical abnormalities that favor the development of acute renal failure. These alterations include a varying degree of bleeding, hypotension, circulatory collapse, intravascular hemolysis, and disseminated intravascular coagulation with or without microangiopathy. A direct cytotoxic action of snake venom on the kidney is suspected, but convincing evidence is still lacking. Severe hypocomplementemia is consistently present, but I doubt its role in the causation of renal lesions. Hypersensitivity to venomous or antivenomous protein occasionally causes acute renal failure. In sea snake poisoning, myonecrosis and myoglobinuria appear to play the predominant pathogenetic role. The renal lesions of clinical significance in envenomed patients are acute tubular and patchy or diffuse cortical necrosis. Glomerulonephritis, interstitial nephritis, and papillary necrosis have been reported in rare patients. I trust that this overview of the clinical and basic-science aspects of snake-bite-induced acute renal failure will prompt investigators to further define the pathogenetic mechanisms involved. Lessons learned may aid patients with acute renal failure of diverse causes, both here in India and around the world.
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            Snakebite nephrotoxicity in Asia.

            Snakebites have the highest incidence in Asia and represent an important health problem. Clinical renal manifestations include proteinuria, hematuria, pigmenturia, and renal failure. Nephropathy usually is caused by bites by snakes with hemotoxic or myotoxic venoms. These snakes are Russell's viper, saw-scaled viper, hump-nosed pit viper, green pit viper, and sea-snake. Renal pathologic changes include tubular necrosis, cortical necrosis, interstitial nephritis, glomerulonephritis, and vasculitis. Hemodynamic alterations caused by vasoactive mediators and cytokines and direct nephrotoxicity account significantly for the development of nephropathy. Hemorrhage, hypotension, disseminated intravascular coagulation, intravascular hemolysis, and rhabdomyolysis enhance renal ischemia leading to renal failure. Enzymatic activities of snake venoms account for direct nephrotoxicity. Immunologic mechanism plays a minor role.
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              Thrombotic microangiopathy and acute kidney injury in hump-nosed viper (Hypnale species) envenoming: a descriptive study in Sri Lanka.

              Hump-nosed viper (Hypnale species) bites are common in Sri Lanka and a proportion of these bites lead to coagulation abnormalities and acute kidney injury (AKI). We observed thrombotic microangiopathy (TMA) among some of these patients, but its contribution to severity of AKI and other morbidities remains unknown. Thus, we report a case series of TMA following hump-nosed viper bite addressing the complications and renal out comes in Sri Lanka. This was a prospective observational study carried out at the nephrology unit, Kandy in Sri Lanka from October 2010 to October 2011 and included 11 patients with AKI following hump-nosed viper bites. All eleven cases needed renal replacement therapy (RRT) with intermittent haemodialysis for a period of 1-5 weeks. Of them, 7 patients developed TMA with evidence of microangiopathic haemolytic anaemia (MAHA), thrombocytopenia and severe anaemia needing multiple blood transfusions. They needed longer duration of RRT (range 2-5 weeks); 2 patients developed chronic kidney disease and two died during acute stage. Autopsy study found thrombosis of micro-vessels. Thrombotic microangiopathy could be a causative pathology of AKI in hump-nosed viper bite carrying poor outcome. Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Indian J Nephrol
                Indian J Nephrol
                IJN
                Indian Journal of Nephrology
                Wolters Kluwer - Medknow (India )
                0971-4065
                1998-3662
                Sep-Oct 2019
                : 29
                : 5
                : 324-328
                Affiliations
                [1] Department of Nephrology, Kasturba Medical College and Hospital, Manipal Academy of Higher Education, Manipal, Karnataka, India
                Author notes
                Address for correspondence: Dr. Indu Ramachandra Rao, Department of Nephrology, Kasturba Medical College and Hospital, Manipal Academy of Higher Education, Manipal - 576 104, Karnataka, India. E-mail: indu.rao@ 123456manipal.edu
                Article
                IJN-29-324
                10.4103/ijn.IJN_280_18
                6755934
                31571738
                6dad7b93-d452-4be4-956e-ba702284fdc3
                Copyright: © 2019 Indian Journal of Nephrology

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Categories
                Original Article

                Nephrology
                acute kidney injury,hemolytic uremic syndrome,snake envenomation,thrombotic microangiopathy

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