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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2016  |  Volume : 27  |  Issue : 5  |  Page : 1018-1020
Transient distal renal tubular acidosis following hump nosed viper bite: Two cases from Sri Lanka


1 Renal Services, University Medical Unit, National Hospital of Sri Lanka, Colombo, Sri Lanka
2 Department of Anesthesiology, National Hospital of Sri Lanka, Colombo, Sri Lanka
3 Department of Internal Medicine, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka

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Date of Web Publication22-Sep-2016
 

   Abstract 

Hump-nosed viper (Hypnale hypnale; HNV) is one of the six major snake species in Sri Lanka that cause envenomation. Nephrotoxicity, coagulopathy, and neurotoxicity are wellrecognized features of its envenomation. Type 4 renal tubular acidosis (RTA4) has only once been described previously in this condition, and we report two further cases. Two patients aged 53 and 51 presented following HNV bites with acute kidney injury and microangiopathic hemolytic anemia. Both underwent multiple cycles of hemodialysis until the polyuric phase was reached. Despite polyuria, both patients developed resistant hyperkalemia that needed further hemodialysis. The urinary pH, arterial pH, delta ratio, and transtubular potassium gradient confirmed RTA4. HNV venom has been shown to damage the proximal convoluted tubules in animal studies, but not the distal convoluted tubule, and hence the mechanism of our observation in these two patients is unclear. Unexplained hyperkalemia in recovery phase of HNV bite should raise suspicions of RTA4.

How to cite this article:
Weerakkody RM, Lokuliyana PN, Lanerolle RD. Transient distal renal tubular acidosis following hump nosed viper bite: Two cases from Sri Lanka. Saudi J Kidney Dis Transpl 2016;27:1018-20

How to cite this URL:
Weerakkody RM, Lokuliyana PN, Lanerolle RD. Transient distal renal tubular acidosis following hump nosed viper bite: Two cases from Sri Lanka. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2019 Nov 22];27:1018-20. Available from: http://www.sjkdt.org/text.asp?2016/27/5/1018/190879

   Introduction Top


Hump-nosed viper (HNV) is one of the six major snake species in Sri Lanka that cause envenomation. In its natural habitat of the low land wet zone, it is the main snake species that is responsible for envenomating bites. Nephrotoxicity, coagulopathy, and neurotoxicity have been described with humped nose viper envenomation, and local tissue necrosis is not uncommon. Here, we report two cases of Type 4 renal tubular acidosis (RTA4), of transient nature, developing in humped nose viperbitten patients. It has only been once [1] described in literature, and to the best of our knowledge, these cases are second and third instances of such a complication.


   Case Report Top


Two Sri Lankan adult males, both from the Western province, aged 53 and 51, presented with confirmed HNV envenomation. Both were transferred in, due to dropping urine output and rising creatinine (254 and 388 μmol/L respectively on admission) and for the need of possible dialysis for the treatment of acute kidney injury. Both patients have developed fully blown coagulopathy with INR of 2.5 and 2.8, respectively, with background microangiopathic hemolytic anemia. The 53-yearold patient was transferred three days after being bitten, whereas the other was transferred after four days of the bite. Neither of them had a past history of diabetes or renal disease. They underwent hemodialysis (5 and 8 sessions, respectively) and entered polyuric phase on day 12 and 19, respectively. After the onset of polyuria, both had intractably high potassium levels which failed to normalize even in the face of massive urine output and with medical management. Both underwent two further dialysis cycles each for the management of hyperkalemia. They were commenced on oral NaHCO[3], which brought down the potassium level effectively. [Table 1] shows their investigations summary.
Table 1: Summary of the blood gas and electrolyte reports of the two cases.

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The second patient's urinary investigations are as follows: Na + 70 mmol/L, K + 18 mmol/L, Cl 80 mmol/L, serum osmolality 294 mosm/ kg, urine osmolality 377 mosm/kg, and urinary anion gap was 8 mmol/L. Transtubular potassium gradient (TTKG) was 2.30. Both patients were managed with blood products, furosemide, sodium bicarbonate, and omeprazole. Intravenous cefotaxime and co-amoxiclav were used as antibiotics, respectively. Their maximum capillary blood sugar levels were 10.1 and 11.4 mmol/L, respectively, and urine was negative for ketone bodies. However, their fasting and postprandial plasma glucose levels were normal during the convalescent period. We could neither estimate the aldosterone/ renin levels in both patients and urinary sodium excretion in the first due to economic and technical constraints. They recovered fully, with baseline creatinine levels of 136 and 218 μmol/L indicating some degree of preexisting chronic kidney disease, or permanent damage due to envenoming. Ultrasound scan in the convalescent period showed normal-sized kidneys with normal cortical echogenicity and corticomedullary demarcation. The first patient declined a biopsy and was lost to follow-up, but the second was biopsied after 12 weeks, and the biopsy showed tubular atrophy and focal segmental glomerulosclerosis pattern, but no tubular atrophy. After three months of discharge, the creatinine levels remain at 120 and 178 μmol/L, respectively.


   Discussion Top


Distal renal tubular acidosis (dRTA) is a metabolic disorder. These are further classified into hypokalemic (Type I) and hyperkalemic (Type IV) types. [2] The pathogenesis of RTA4 is either due to defect of a voltage-gated channel or aldosterone deficiency/resistance.

HNV is a common source of snake bite in Sri Lanka, [3] and it's venom has shown to possess strong procoagulant, hemorrhagic, and necrotic activities through the presence of phospholipase A2, hyaluronidase, L-amino acid oxidase, thrombin-like enzymes, arginine esterase, and various proteases. [4] The nephrotoxicity is brought about by the direct toxicity [5],[6] as well as through microangiopathic hemolytic anemia. [7] The direct nephrotoxicity of HNV venom mainly involves the proximal convoluted tubule and to a lesser degree in the glomerulus, as demonstrated in animal studies. [5] Hence, the exact pathophysiology of RTA4 occurring in HNV bite is unclear. Adrenal hemorrhage [8] following the use of heparin and resulting Addisonian crisis would have explained the symptoms but for transient nature of the disease as well as the negative imaging findings.

The diagnosis of RTA4 was not straight forward in both patients as they had acidosis which was due to RTA4 as well as acute renal insufficiency. In addition, they received large doses of NaHCO[3] via hemodialysis, and as a result, there are three acid-base disorders are at play. An acid loading test would have given better results, however, in the setting of a preexisting acidosis, administration of an acidifying agent is unnecessary and potentially harmful. [2] The delta ratios are 0.67 and 0.75, which is consistent with mixed type of metabolic acidosis, with normal and raised AGs. [9] The TTKG <6 is also supportive of RTA4. [1] The dramatic improvement showed with bicarbonates therapy helped to confirm the diagnosis. Fludrocortisone, has been used to treat dRTAs, could have been useful in this setting. [1]


   Conclusion Top


RTA4 should be suspected in hyperkalemic patients, who are resistant for medical management, with recovering acute kidney injury due to HNV envenomation. Early recognition will allow aggressive medical treatment and to save few hemodialysis which will have a significant impact on an already resource poor setting.

Conflict of interest: None declared.

 
   References Top

1.
Karunarathne S, Udayakumara Y, Govindapala D, Fernando H. Type IV renal tubular acidosis following resolution of acute kidney injury and disseminated intravascular coagulation due to hump-nosed viper bite. Indian J Nephrol 2013;23:294-6.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.
Yeung SC, Sarlis NJ, Agraharkar M, Baweja K, Fahlen MT. Hyperchloremic Acidosis; 4 July, 2012. Available from: http://www.emedicine.medscape.com/article/240809-overview. Last aceessed 01.08.2014  Back to cited text no. 2
    
3.
Ariaratnam CA, Thuraisingam V, Kularatne SA, et al. Frequent and potentially fatal envenoming by hump-nosed pit vipers (Hypnale hypnale and H. nepa) in Sri Lanka: Lack of effective antivenom. Trans R Soc Trop Med Hyg 2008; 102:1120-6.  Back to cited text no. 3
    
4.
Jeevagan V, Chang T, Gnanathasan CA. Acute ischemic stroke following hump-nosed viper envenoming; first authenticated case. Thromb J 2012;10:21.  Back to cited text no. 4
    
5.
Gunatilake M, Jayakody RL, Angunawela P, Tissera AD. Direct nephrotoxic effects produced by venoms of Sri Lankan cobra, Russell′s viper and hump nosed viper. Ceylon J Med Sci 2003;46:61-6.  Back to cited text no. 5
    
6.
Silva A, Gunawardena P, Weilgama D, Maduwage K, Gawarammana I. Comparative in-vivo toxicity of venoms from South Asian hump-nosed pit vipers (Viperidae: Crotalinae: Hypnale). BMC Res Notes 2012;5:471.  Back to cited text no. 6
[PUBMED]    
7.
Herath N, Wazil A, Kularatne S, et al. Thrombotic microangiopathy and acute kidney injury in hump-nosed viper (Hypnale species) envenoming: A descriptive study in Sri Lanka. Toxicon 2012;60:61-5.  Back to cited text no. 7
[PUBMED]    
8.
Ketha S, Smithedajkul P, Vella A, Pruthi R, Wysokinski W, McBane R. Adrenal haemorrhage due to heparin-induced thrombocytopenia. Thromb Haemost 2013;109:669-75.  Back to cited text no. 8
[PUBMED]    
9.
Wrenn K. The delta (delta) gap: An approach to mixed acid-base disorders. Ann Emerg Med 1990;19:1310-3.  Back to cited text no. 9
[PUBMED]    

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Correspondence Address:
Ranga M Weerakkody
University Medical Unit, National Hospital of Sri Lanka, Colombo
Sri Lanka
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DOI: 10.4103/1319-2442.190879

PMID: 27752013

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