lactic acidosis ( la ) is a high anion gap metabolic acidosis with serum lactate levels > 5 mm / l and acidemia ( ph < 7.35 ) caused by over - production or underutilization of lactic acid from the body . thiamine deficiency is one of the causes and cases of refractory la treated successfully with thiamine were reported in the literature . though chronic kidney disease ( ckd ) and hemodialysis are proven risk factors for occult thiamine deficiency , we are not aware of any case report describing reversal of acute refractory la with intravenous ( iv ) thiamine in this patient population . a 48-year - old female with end - stage renal disease , hypertensive since past 7 years was electively posted for robotic assisted laparoscopic renal transplantation from a living related donor . she was on maintenance hemodialysis twice a week since 6 months , and her hypertension was well controlled with one antihypertensive agent . her fasting , postprandial blood sugar and glycated hemoglobin levels were within normal limits in more than three examinations preoperatively . preoperative hemodialysis was done within 24 h of the scheduled surgery . on the day of surgery her baseline vitals were heart rate ( hr ) 94/min , mean arterial pressure ( map ) 103 mm of hg , spo2 100% , central venous pressure ( cvp ) 12 cm of h2o , and core temperature 98.6f . arterial blood gas ( abg ) analysis after induction of anesthesia ( 10 am ) was unremarkable with a lactate of 1.9 mm / l [ table 1 ] . volume controlled ventilation was adjusted to maintain etco2 between 35 mm and 40 mm of hg . three hours after induction of anesthesia hemodynamic parameters deteriorated with hr of 122/min , map of 72 mm of hg and cvp of 16 cm of h2o . abg analysis showed metabolic acidosis with elevated lactate levels , hyperglycemia , elevated anion gap and fall in hemoglobin [ table 1 ] . blood sample for ketone bodies tested negative and it was repeated every fourth hourly to rule out diabetic ketoacidosis as a cause of the acidosis . considering occult blood loss , iv fluids and two units of packed red blood cells were transfused . as vascular anastomosis of the graft kidney was being carried out , noradrenaline infusion [ figure 1 ] was started to maintain a map of 90 mm of hg . abg analysis of the patient since the initiation of surgery till the next 22 h trend of lactate / blood glucose levels / mean arterial pressure from the initiation of surgery till the next 22 h depicting various interventions the patient was shifted to intensive care unit ( icu ) 7 h after induction of anesthesia with noradrenaline infusion ( 0.12 g / kg / min ) for elective ventilation and possible need for continuous renal replacement therapy to correct acidosis . abg analysis in the icu revealed progressively increasing la with hyperglycemia refractory to bicarbonate and insulin infusion [ figure 1 ] . considering the possibility of sepsis , procalcitonin levels were obtained ( 14.6 ng / ml ) . suspecting thiamine deficiency , empirical thiamine 300 mg was administered intravenously 3 h after surgery . abg analysis 2 h after thiamine administration showed rapidly decreasing lactate and sugar levels with improvement in map . abg analysis , 8 h after the first dose of thiamine injection was within normal limits [ table 1 ] . lactic acidosis is classified into two types : type a is caused by tissue hypoperfusion , hypoxia , etc . , whereas type b is caused by hereditary metabolic diseases , drugs , systemic disorders ( thiamine deficiency , liver / kidney failure , malignancy etc . , ) and release of endogenous catecholamines from stress response . among all the above - mentioned causes , numerous case reports of unexplained la in patients who were on parenteral nutrition without thiamine supplementation have been published in the past . ckd , uremia and chronic hemodialysis have variable effects over thiamine activity and metabolism in the body : diminished intestinal and mitochondrial thiamine transporters in spite of normal serum thiamine levels , diminished transketolase ( one of the enzymes requiring thiamine as a co - factor ) activity , chronic hemodialysis itself can lead to accelerated removal of thiamine from the body . thiamine requirement increases during stressful periods such as critical illness and major surgery etc . , which can precipitate symptoms of thiamine deficiency in such individuals . thiamine pyrophosphate is the cofactor for three important enzymes including pyruvate dehydrogenase ( pdh ) . pdh catalyzes the oxidative decarboxylation of pyruvate to acetyl coenzyme a ( coa ) which enters the kreb 's cycle . in thiamine deficiency , when pyruvate can not undergo this conversion , it is then converted to lactate by the action of lactate dehydrogenase [ figure 2 ] . this conversion also results in the release of protons in equal number to the molecules of lactate produced leading to acidemia . hyperglycemia can be an associated sign as excess lactate is metabolized by the liver into glucose through gluconeogenesis and thiamine deficiency per se can cause defective insulin secretion . lactate production and metabolism our patient was suffering from ckd and was on maintenance hemodialysis for 6 months , history and physical examination did not reveal the poor nutritional status or obvious signs and symptoms of thiamine deficiency . septicemia was ruled out as a probable cause as the patient was afebrile , normal total leukocyte counts and she did not have significant hypotension when the la was discovered . although her postoperative pro - calcitonin level was high , it is not diagnostic as she received t - cell antibody anti - thymocyte globulin as induction therapy intraoperatively . hence , acute thiamine deficiency was suspected , which was supported by dramatic improvement in her clinical and biochemical parameters after iv thiamine supplementation . probably , surgical stress stimulated accelerated glycolysis and enhanced pyruvate production , which increased her thiamine requirement unmasking occult thiamine deficiency and/or defective thiamine activity leading to severe la with hyperglycemia . intramuscular / iv thiamine 100 mg once a day is the recommended dose in suspected thiamine deficiency . we administered 300 mg of iv thiamine as the excess dose has no proven adverse effects in humans . if thiamine deficiency is suspected , erythrocyte transketolase activity and thiamine pyrophosphate effect can be measured for an objective documentation of the deficiency . we were not able to perform these biochemical tests as they were not available in local laboratories . however , the definitive test for vitamin b1 deficiency is an improvement of symptoms with thiamine administration . thiamine deficiency should be considered in the differential diagnosis of unexplained severe la with hyperglycemia in patients with ckd . physicians caring for these patients should maintain a low threshold for infusing a therapeutic dose of thiamine as treatment is safe , inexpensive , readily available and potentially life - saving .