hump - nosed viper may account for upto 27 - 70% of all snake bites in sri lanka .
although previously considered a moderately venomous , hump - nosed viper bites cause significant morbidity in the wet zone ( hot and humid south western part of the island with an annual rainfall of more than 2,500 mm ) of sri lanka .
acute kidney injury ( aki ) necessitating hemodialysis and disseminated intravascular coagulation are known complications of hump - nosed viper bite .
the lack of an effective antivenom has contributed to the difficulty experienced by the clinicians during management of hump - nosed viper bites .
we describe a patient who developed disseminated intravascular coagulation and prolonged aki following a hump - nosed viper bite .
he was successfully managed with hemodialysis and blood product support but he after developed severe hyperkalemia and acidosis due to type iv renal tubular acidosis after discharge from hospital .
type iv renal tubular acidosis has not been described previously in patients who had snake bites .
a 51-year - old male was admitted to the local hospital after a hump - nosed viper bite on his hand while weeding his garden .
since the viper was brought alive by the neighbors , primary care physician was able to make a positive identification of the snake as merrem 's hump - nosed viper ( hypnale hypnale ) .
the next day his urine output was reduced and he was transferred to a tertiary care institute for hemodialysis . on admission ,
he had marked swelling and redness in his right hand with blistering at the bite site .
on auscultation of the heart , s1 and s2 were heard in normal intensity with no murmurs .
his investigation results were as follows : white cell count , 12,700 ( 80% neutrophils ) ; platelet count , 40,000/l ; hemoglobin , 9.9 g / dl ; international normalized ratio , 1.46 ; activated partial thromboplastin time , 43 s ; serum creatinine , 1,040 mol / l ; na , + 130 mmol / l ; k+ , 5.4 mmol / l ; erythrocyte sedimentation rate , 10 mm / hr ; c - reactive protein , 1 mg / l ; aspartate transaminase , 54 u / l ; alanine transaminase , 42 u / l ; serum bilirubin , 22.7 mol / l ; total protein , 52 g / l ( albumin 33
peripheral blood smear revealed marked red cell fragmentation , polychromasia and reduced number of platelets indicating disseminated intravascular coagulation .
serum calcium , 7.7 mg / dl ; serum phosphate , 3.1 mg / dl ; creatine phosphokinase , 122 u / l ; urine microscopy showing 10 - 12 pus cells and 1 - 2 red cells per high power field with no casts .
after 12 sessions of hemodialysis , he was dialysis dependent and renal biopsy was performed 8 weeks after the viper bite .
the biopsy revealed patchy areas of tubular atrophy with interstitial edema and patchy interstitial chronic inflammation suggesting subacute interstitial nephritis .
there was no evidence of acute tubular necrosis possibly because biopsy was performed very late after the onset of aki .
ten weeks after the viper bite , the patient 's renal functions and urine output were improved .
he was discharged from the hospital to be reviewed in clinic as an outpatient . at the time of discharge , he had a serum creatinine of 1.9 mg / dl and serum potassium of 3.9 mmol / l .
eighteen weeks after the initial viper bite , he was admitted with sudden onset bilateral lower limb weakness .
arterial ph was 7.31 and pco2 18 mmhg , po2 121 mmhg , and hco3 
  10.3 mmol / l .
mmol / l with sodium 130 mmol / l and chloride 114 mmol / l .
he was given intravenous calcium gluconate , nebulized with salbutamol and started on insulin - dextrose infusion until an urgent hemodialysis was arranged .
there was no history of use of angiotensin - converting enzyme inhibitors ( acei ) , angiotensin receptor blockers ( arb ) , or diuretics like spironolactone .
mmol / l , ph 5.0 , serum osmolality 300 mosm / kg , urine osmolality 380 mosm / kg , and urinary anion gap was 9 mmol / l .
presence of hyperchloremic metabolic acidosis and hyperkalemia with normal serum creatinine level was suggestive of type iv renal tubular acidosis .
the ability to lower the urine ph to 5.0 , positive urinary anion gap , and the low ttkg ( less than five ) were all supportive evidence for type 4 renal tubular acidosis .
patient had a good response to fludrocortisone 100 g twice daily with the correction of hyperkalemia and the metabolic acidosis .
mmol / l and he was closely observed for the development of hyperkalemia or acidosis .
type 4 renal tubular acidosis is due to failure of the collecting duct to excrete both potassium and protons .
this is caused by absolute or functional deficiency of aldosterone or a molecular defect in the relevant transporters .
aldosterone is necessary for the maintenance of the lumen negative potential by the reabsorption of na by the epithelial sodium channel on the luminal membrane of the principal cells .
this lumen negative potential in turn drives the secretion of potassium and protons into the lumen .
this subtype of renal tubular acidosis is usually observed in patients with diabetes mellitus and various forms of tubulointerstitial disease including sickle cell disease , amyloid , monoclonal gammopathy , and nsaid - induced interstitial nephritis .
drugs that cause a similar picture include acei , arb spironolactone , heparin , and -blockers .
the possible pathogenesis of renal tubular acidosis in this patient could be due to snake venom - mediated tubular damage leading to aldosterone receptor dysfunction or aldosterone resistance .
although disseminated intravascular coagulation necessitating blood product support and aki are known complications of hump - nosed viper bite , the development of type 4 renal tubular acidosis was a new finding .
this case is clinically informative because it describes a previously unknown complication following viper bite and makes a clinician more vigilant regarding renal function and serum electrolyte levels even after patient has recovered from snake venom - induced aki .
 hump - nosed viper bite can cause acute kidney injury ( aki ) and disseminated intravascular coagulation . in some patients , it can cause chronic kidney disease necessitating life - long renal replacement therapy . 
 lack of effective antivenom makes the management of these patients difficult . 
 a 51-year - old sri lankan male was admitted with aki and disseminated intravascular coagulation following a hump - nosed viper bite . 
 he made a complete recovery with blood product support and hemodialysis . 
 renal biopsy was performed as his renal recovery was prolonged which revealed patchy tubular atrophy and interstitial inflammation suggestive of subacute interstitial nephritis . 
 later , he presented with hyperkalemic paralysis and acidosis . 
 a diagnosis of late onset type 4 renal tubular acidosis was made and he responded well to a course of fludrocortisone . 
Introduction
Case Report
Discussion
Conclusions