patients commonly present with acute cholinergic crisis , intermediate syndrome , or delayed polyneuropathy . they may also present with pancreatitis or hepatitis . here a 75-year - old homemaker presented to our emergency department following deliberate self - harm consuming around 100 ml chlorpyrifos along with small amount of kerosene . she was known to have systemic hypertension and was not on any treatment for the same . pulse rate was 120 beats / min and irregular . rest of the examination was normal . electrocardiogram showed rate 140/min , electrical alternans , multifocal ventricular ectopics , ventricular reentrant beats , ventricular couplets , and prolonged qt interval ( corrected qt = 512 ms ) . transtubular potassium gradient was 6.85 , and urine analysis revealed inappropriately raised urinary ph ( 7.5 ) with positive urine anion gap all suggestive of distal renal tubular acidosis . however , her cholinergic symptoms subsided , and potassium values started improving once atropinization was attained . blood gas analysis , urine potassium excretion , urine ph , and urine anion gap done were normal with serum potassium 4.5 meq / l . they inhibit acetylcholinesterase enzyme reversibly as well as irreversibly producing excess of acetylcholine in neuromuscular junction . hence , usually , clinical presentation of organophosphates includes excessive muscarinic symptoms such as increased salivation , lacrimation , urination , diarrhea , gastrointestinal cramps , emesis , and nicotinic symptoms such as tachycardia , hypertension , mydriasis , fasciculation , and weakness . rarely may they present with intermediate syndrome or delayed polyneuropathy . . it may be intense sympathetic activity due to nicotinic effect producing tachycardia and hypertension or muscarinic activity producing bradycardia and hypotension . third case , they may present with polymorphic ventricular tachycardia with prolonged qt in early phase of toxicity which is attributed to rise in free fatty acid levels by some authors . however , in all studies , echocardiogram was normal showing no permanent damage to heart . cardiac injury is a strong predictor of mortality in organophosphate poisoning , and direct myocardial injury is maximum in acute early phase of severe organophosphate poisoning . potassium value if <3 meq / l is known to present with multifocal ventricular ectopics , ventricular reentrant beats , ventricular couplets , and prolonged qt interval . in our patient , cardiac arrhythmias may be due to either organophosphate poisoning or hypokalemia or both combined . our patient had severe hypokalemia which was evaluated and detected to be due to distal renal tubular acidosis . transient distal tubular acidosis may be seen in paraproteinemia , medullary sponge kidney , nephrocalcinosis , obstructive uropathy , and autoimmune diseases . there was one reported case where distal tubular acidosis was detected with accidental kerosene ingestion . however , that patient also had concomitant ingestion of metformin in a high dose which produced lactic acidosis and acute renal failure . however , in our case , very minimal amount of kerosene has been ingested which can not explain her tubular acidosis . hence , the same may be attributed to organophosphates itself as it completely improved after atropinization . toluene poisoning presenting with transient distal renal tubular acidosis was reported , which has been attributed to impaired active hydrogen ion transport and hydrogen ion back diffusion . the same mechanism may be the cause of transient distal renal tubular acidosis due to organophosphate poisoning also though conclusive proof is yet to be availed . hence , it is better to know about all atypical presentations and expected complications of its toxicity . although neurological complications are quite well described , many others such as pancreatitis , hepatitis , and cardiac toxicities are seldom accounted . we are presenting this case just to open up possibility of a rare complication of organophosphate poisoning , distal renal tubular acidosis which should be thought of in the presence of persistent hypokalemia refractory to treatment .