Type IV renal tubular acidosis following resolution of acute kidney injury and disseminated intravascular coagulation due to hump-nosed viper bite
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 patient had severe pain and swelling in the hand. The next day his urine output was reduced and he was transferred to a tertiary care institute for hemodialysis. On admission, patient was conscious and rational, febrile, and he was in pain. He was pale and mildly icteric. He had marked swelling and redness in his right hand with blistering at the bite site.\nHis pulse rate was 92 beats per minute and blood pressure was 118/78 mmHg. On auscultation of the heart, S1 and S2 were heard in normal intensity with no murmurs. Respiratory system examination was normal except for few fine basal crepitations. Abdominal examination was normal with no organ enlargement or free fluid. Neurological examination was normal with no ophthalmoplegia or other cranial nerve paralysis.\nHis investigation results were as follows: white cell count, 12,700 (80% neutrophils); platelet count, 40,000/μl; hemoglobin, 9.9 g/dl; International normalized ratio, 1.46; activated partial thromboplastin time, 43 s; serum creatinine, 1,040 μmol/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 μmol/l; total protein, 52 g/l (albumin 33 g/l). 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. Protein was present in urine in trace amounts. Abdominal ultrasound scan revealed enlarged and globular kidneys suggestive of acute renal parenchymal disease. Venom-induced acute tubular necrosis was suspected.\nHe was commenced on hemodialysis. 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. Glomeruli were normal.\nTen 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.\nEighteen weeks after the initial viper bite, he was admitted with sudden onset bilateral lower limb weakness. There was no respiratory muscle paralysis. Both lower limbs had grade two muscle power and upper limbs grade four. Reflexes were diminished and Babinski sign was negative. There was no objective sensory loss.\nDuring this admission, he was found to have acidotic breathing. Arterial pH was 7.31 and PCO2 18 mmHg, PO2 121 mmHg, and HCO3\n− 10.3 mmol/l. His serum potassium level was 7.0 mmol/l with sodium 130 mmol/l and chloride 114 mmol/l. ECG showed tall tented T waves suggestive of hyperkalemia. Serum creatinine was 114 μmol/l with an estimated glomerular filtration rate of 76 ml/min. 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.\nBlood anion gap was normal at 5.7 mmol/l. Urine pH was 5.0. Urinary electrolytes were as follows: Na+ 77 mmol/l, K+ 16 mmol/l, Cl− 84 mmol/l, pH 5.0, serum osmolality 300 mosm/kg, urine osmolality 380 mosm/kg, and urinary anion gap was 9 mmol/l. Transtubular potassium gradient (TTKG) was 1.80.\nPresence 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.\nPatient had a good response to fludrocortisone 100 μg twice daily with the correction of hyperkalemia and the metabolic acidosis. He was discharged while on fludrocortisone with serum potassium of 4.3 mmol/l. Three weeks later, fludrocortisone was stopped as serum potassium was 3.5 mmol/l and he was closely observed for the development of hyperkalemia or acidosis. Eight weeks after discharge, he had potassium of 4.2 mmol/l without any potassium-lowering drug therapy.