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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2014  |  Volume : 25  |  Issue : 6  |  Page : 1259-1262
Snake bite complicated by acute kidney injury secondary to necrotizing glomerulonephritis


1 Department of Medicine, King Abdul Aziz Medical City, Riyadh, Saudi Arabia
2 Department of Laboratory and Histopathology, King Abdul Aziz Medical City, Riyadh, Saudi Arabia

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Date of Web Publication10-Nov-2014
 

   Abstract 

We present a 38-year-old man who presented to the emergency department with complaints of a snake bite. He developed acute kidney injury (AKI) and the kidney biopsy showed necrotizing glomerulonephritis, which is rarely reported in AKI after snake bite.

How to cite this article:
Al Qahtani MA, Altheaby A, Al Anazi T, Al Saad K, Binsalih S, Al Helail M. Snake bite complicated by acute kidney injury secondary to necrotizing glomerulonephritis. Saudi J Kidney Dis Transpl 2014;25:1259-62

How to cite this URL:
Al Qahtani MA, Altheaby A, Al Anazi T, Al Saad K, Binsalih S, Al Helail M. Snake bite complicated by acute kidney injury secondary to necrotizing glomerulonephritis. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2020 Jun 5];25:1259-62. Available from: http://www.sjkdt.org/text.asp?2014/25/6/1259/144263

   Introduction Top


Although the majority of snake species are non-venomous, the outcome of a snake bite depends on numerous factors, including the species of snake, the area of the body bitten, the amount of venom injected and the health condition of the victim. The morbidity and mortality associated with snake bite are serious public health problems in many regions of the world, particularly in the rural areas that have inadequate medical facilities. [1],[2],[3],[4] Acute kidney injury (AKI) complicates the course of the snake bite in 5-30% of the victims of severe viper poisoning. No consensus exists on a single mechanism causing the AKI after the snake bite. In most cases, the renal failure is attributed to tubular necrosis and cortical nec­rosis, although necrotizing arteritis and the nephrotic syndrome have also been reported. [1],[2],[9]

Proliferative glomerulonephritis due to a toxic action of the venom was reported by Seedat et al. [5] Furthermore, Sant and Purandare [5] have reported toxic proliferative glomerulonephritis in patients as well as experimental animals following viperine snake envenomation. However, most of the other reports do not mention the glomerular changes following snake bite.

We present this case because of its patho­logical findings, which have been rarely des­cribed with AKI post snake bite.


   Case Report Top


A 38-year-old man presented to the emer­gency room with a swelling in his right hand five hours after being bitten by a snake. He could not describe the snake because it ran away quickly. On clinical examination, he was conscious, anxious, pale and jaundiced with marked swelling in his right hand. His heart rate was 95 beats per minute and blood pressure was 135/90 mm Hg. The rest of the physical examination was unremarkable. His laboratory investigations were compatible with disseminated intravascular coagulation (DIC) and advanced renal failure [Table 1].
Table 1:

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The pathological examination of the kidney biopsy obtained on the patient included the preparation of 2-μm-thickness sections from the formalin-fixed, paraffin-embedded renal tissue, which were stained with hematoxylin and eosin, periodic acid Schiff, Masson's Trichrome and Methenamine silver special stains. For immunofluorescence, 3 μm cryostat sec­tions of the biopsy were stained with fluorescein isothiocyanate (FITC)-conjugated rabbit antihuman IgG, IgM, IgA, C3, C4, C1q and kappa and lambda light chains (Dako, Carpinteria, CA, USA). Ultrastructural examination was not performed as the submitted tissue to the electron microscopy contained no glomeruli.

Light microscopic examination of the kidney biopsy revealed renal cortical tissue, which contained 27 glomeruli; two glomeruli were globally sclerosed. The remaining glomeruli showed a mild to moderate increase in the mesangial matrix, but no increase in mesangial cellularity was observed. Glomerular con­gestion and ischemic changes were noted, and segmental glomerular scarring in the form of obliteration of the glomerular capillaries was identified in three glomeruli [Figure 1]A. The glomerular basement membranes (GBM) showed segmental corrugation, moderate increase in thickness and replication on periodic acid Schiff (PAS) and silver stains [Figure 1]B. The endothelial cells lining the glomerular capillaries appeared prominent, and segmental karyorrhexis debris was seen in two glomeruli. Three glomeruli appeared necrotic [Figure 1]C. No endocapillary hypercellularity, subendothelial deposits or crescent formation were detected. Hyperplasia of the glomerular epithelial cells was noted in some glomeruli. Meticulous examination failed to identify microthrombi in the glomerular capillaries or interstitial blood vessels. Mild to moderate acute tubular epithelial cell degenerative and regenerative changes/ AKI were noted. Mild interstitial edema and focal hemorrhage and mild interstitial inflammation were evident. The interstitial inflammatory infiltrate consisted pre­dominantly of lymphocytes and neutrophils [Figure 1]D. There was mild interstitial fibrosis and tubular atrophy. Mild arteriolar hyalinosis was noted, but there was no arterial sclerosis. No arterial mucoid degeneration or fibrinoid necrosis was identified. Immunofluorescence study showed no significant positivity to the immunoglobulins or complements. The pathological findings were compatible with acute thrombotic microangiopathy with segmental glomerular scarring and concurrent AKI.
Figure 1:

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The patient was managed by intravenous fluids, multiple doses of polyvalent antivenom, packed red blood cells and fresh frozen plasma. The DIC was corrected, but his renal function continued to deteriorate. Hemodialysis was started on the third day of admission and a percutaneous renal biopsy was performed. The patient was discharged three weeks after admission in good clinical condition, but re­quired hemodialysis three times per week. The hemodialysis was stopped after two months following improvement of the patient's renal function.


   Discussion Top


The published statistics on the incidence of morbidity and mortality from snake bite worldwide are grossly inadequate. More than 2700 species of snakes are recognized world­wide, but only about 450 of them have frontal fangs that make them capable of injecting venom during the bite. The venomous snakes belong to four families: Elapride, viperide, hydrophide and colubrid. In Saudi Arabia, there are at least five snakes that have fatal bite: (1) the Arabian cobra (Naja haje arabica),

which is neurotoxic; (2) black desert cobra (Walterinnesia aegeptia), which causes local swelling; (3) puff adder (Bitis arietans); (4) stiletto snakes (Atractaspis microlepidoka andersoni and A. engaddensis), which can produce anaphylactic shock; and (5) saw scaled viper (Echius carinatus and E. coloratus), which can cause severe hemostatic disturbances. [5],[6],[7]

Renal injury has been associated with bite by the members of the last three families of snakes. AKI has been reported with a varying frequency in the different studies, ranging from 13-32%. The incidence of AKI follo­wing snake bite in Saudi Arabia is not well documented; in one study by Al Durihim at el, [1] four (19%) in a cohort of 28 patients deve­loped renal impairment following a snake bite.

The most common clinical renal manifes­tations of a snake bite are hematuria and proteinuria, which present in 20-70% of the re­ported cases. In India, 94% of the patients in a cohort of 70 developed oliguric renal failure (RF) in the first few hours to as late as 96 h following snake bites; the remaining patients developed non-oliguric RF. Hemodialysis was required in 53 (72%) patients. The patholo­gical findings on renal biopsy from 56 patients reported as acute tubular necrosis (ATN)/AKI in 44 (73%), patchy cortical necrosis in four (9%) and diffuse cortical necrosis in eight (18%). The clinical outcome was complete recovery in 46 patients (66%), persistence of mild to moderate renal insufficiency in four patients (6%) and death in 20 patients (28%). [7]

The pathogenesis of AKI in envenomed pa­tient includes several causes such DIC, hypo­tension, hemolysis, hemoglobinuria, rhabdomyolysis as well as direct cytotoxic effect of the venom. The histopathological findings on kidney biopsy are variable; ATN is the most common and is observed in 70-80% of pa­tients. Myoglobin casts are observed in pa­tients bitten by see snake or the Australian small-eyed black snake. Acute interstitial nephritis alone has been observed following E. carnatus and Russells viper bites. A recent report from India described renal papillary necrosis. [7]

Solid data on the glomerular lesions in the envenomed patients are still not available. In 1960, Stem beck described a patient who deve­loped nephrotic syndrome following snake bite, but unfortunately no renal histology was performed. [8] In the 1970s, Sant and Purandare reported proliferative glomerulonephritis in a patient bitten by E. carnatus.[5] Recently, Sitprija and boom Puck rang have described another case of extracapillary glomerulonephritis asso­ciated with ATN after a Russells viper bite. [8]

We conclude that our case report revealed the development of glomerulonephritis after a snake bite. Because of its rarity, a large study, although required, is still difficult to perform in order to address the issues of morbidity and mortality and patterns of glomerulonephritis in patients after snake bites.

 
   References Top

1.
Al-Durihim H, Al-Hussaini M, Bin Salih S, Hassan I, Harakati M, Al Hajjaj A. Snake bite envenomation: Experience at King Abdulaziz Medical City, Riyadh. East Mediterr Health J. 2010;16:438-41.  Back to cited text no. 1
    
2.
Athappan G, Balaji MV, Navaneethan U, Thirumalikkolundusubramanian P. Acute renal failure in snake envenomation: A large prospec­tive study. Saudi J Kidney Dis Transpl 2008; 19:404-10.  Back to cited text no. 2
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3.
Al-Homrany M, Acute renal failure following snake bites: A case report and review of the literature. Saudi J Kidney Dis Transpl 1996;7: 309-12.  Back to cited text no. 3
    
4.
Malik GM. Snake bites in adults from the Asir region of southern Saudi Arabia. Am J Trop Med Hyg 1995;52:314-7.  Back to cited text no. 4
    
5.
Chugh KS, Sakhuja V. Renal disease caused by snake venom. In: Tu AT, ed. Handbook of Natural Toxins. New York: Marcel Dekker Inc; 1991. p. 471-93.  Back to cited text no. 5
    
6.
Kanjanabuch T, Sitprija V. Snakebite nephrotoxicity in Asia. Semin Nephrol 2008;28:363-72.  Back to cited text no. 6
    
7.
Chugh KS. Snake-bite-induced acute renal failure in India. Kidney Int 1989;35:891-907.  Back to cited text no. 7
    
8.
Kohli HS, Sakhuja V. Snake bites and acute renal failure. Saudi J Kidney Dis Transpl 2003;14:165-76.  Back to cited text no. 8
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9.
Harshavardhan L, Lokesh A J, Tejeshwari H L, Halesha B R, Siddharama S Metri.A study on the acute kidney injury in snake bite victims in a tertiary care centre. J Clin Diagn Res 2013;7:853-6.  Back to cited text no. 9
    

Top
Correspondence Address:
Dr. Mohammad A Al Qahtani
Department of Medicine, King Abdul Aziz Medical City (KAAMC), P. O. Box 22490, Riyadh 11426
Saudi Arabia
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DOI: 10.4103/1319-2442.144263

PMID: 25394446

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