imatinib mesylate is an oral anticancer agent that selectively inhibits protein kinases involved in the pathophysiology of various human cancers . it is now the first - line therapy for patients with chronic myeloid leukaemia ( cml ) and has proven remarkably efficient in the treatment of patients with gastrointestinal stromal tumours and various myeloproliferative diseases , including idiopathic hypereosinophilic syndrome . here , we describe a case of a patient receiving imatinib for cml who developed severe hypophosphataemia accompanied by renal failure . a 60-year - old man with a history of hypertension , type ii diabetes and cml was admitted to the emergency room presenting diarrhoea , vomiting and malaise for 3 days . he was under regular treatment with enalapril , atenolol , aspirin , simvastatin , insulin and imatinib , the last having been initiated 4 years prior , upon diagnosis of the leukaemia . at that time , he was in haematologic , cytogenetic and molecular remission . on admission , his blood pressure was 130/ 70 mmhg , and his pulse was 80 bpm . he was confused and mildly dehydrated . although the laboratory tests revealed severe renal insufficiency and severe metabolic acidosis , the patient presented hypokalaemia and hypophosphataemia ( table 1 ) . the enalapril and imatinib were discontinued , and the patient received saline infusion . nevertheless , he required haemodialysis ( a single session ) . during the renal recovery phase , daily supplementation of magnesium and potassium , as well as , principally , phosphate , , there was complete recovery of renal function . however , the urinary fractional excretions of potassium and phosphate were elevated although that of sodium was normal . bone investigation showed a parathyroid hormone level of 107 pg / ml and normal serum bone alkaline phosphatase ( table 1 ) . a retrospective analysis of the outpatient records revealed evidence of episodes of hypophosphataemia and tubular renal dysfunction ( table 2 ) . recent laboratory test results pth , parathyroid hormone ; fena , fractional excretion of sodium ; fek , fractional excretion of potassium ; fepo4 , fractional excretion of phosphate ; feca , fractional of calcium ; ttkg , transtubular potassium concentration gradient ; hd , haemodialysis . to convert serum creatinine from mg / dl to mmol / l , multiply by 88.4 ; serum calcium from mg / dl to mmol / l , multiply by 0.2495 ; serum inorganic phosphorus from mg / dl to mmol / l , multiply by 0.3229 ; serum uric acid from mg / dl to mmol / l , multiply by 59.48 ; glucose from g to mmol , multiply by 0.05551 and urea from g to mmol , multiply by 357 . the options for treating patients with newly diagnosed cml have changed fundamentally since the introduction of imatinib , an orally administered inhibitor of the platelet - derived growth factor receptor ( pdgfr ) bcr - abl tyrosine kinase , the constitutive abnormal gene product of the philadelphia chromosome in cml . inhibition of this enzyme blocks proliferation and induces apoptosis in bcr - abl - positive cell lines as well as in fresh leukaemic cells in philadelphia chromosome - positive cml . in addition to tyrosine kinase , imatinib inhibits the stem cell factor ( scf ) c - kit and cellular events mediated by pdgf and scf . here , we have described the case of a patient who developed acute kidney injury ( aki ) while under treatment with imatinib . druker et al . reported renal failure during imatinib treatment in < 1% of patients with normal renal function at baseline . although such renal failure has not been thoroughly documented , several case reports have indicated that acute tubular necrosis ( atn ) is the cause . franois et al . demonstrated a case in which apical vacuoles were observed in some tubular cells under electron microscopy , suggesting proximal tubular injury . it has been shown that 81% of the dose of imatinib is eliminated within 7 days in faeces ( 68% of dose ) and urine ( 13% of dose ) . of the total dose , 25% ( 5% urine , 20% faeces ) was eliminated unchanged , the remainder being excreted as metabolites . therefore , imatinib blockade of the pdgf pathway might promote atn , especially in cases of preexisting renal failure . hypokalaemia is a known risk factor for the development of nephrotoxicity and ischaemic aki . in the present case , it is of note that , even in the presence of angiotensin - converting enzyme inhibitor treatment , diarrhea , metabolic acidosis and aki , the patient presented hypokalaemia . the hypokalaemia was accompanied by an increased transtubular potassium concentration gradient , demonstrating that the cause of the hypokalaemia was renal wasting . joensuu and reichardt reported that 80% of patients receiving imatinib presented hypophosphataemia on at least one occasion during the treatment . laboratory test results showed that our patient had previously suffered from hypophosphataemia . even during the acute phase , our patient presented hypophosphataemia , which was accompanied by a pronounced elevated urinary fractional excretion of phosphate . berman et al . hypothesized that hypophosphataemia induced by imatinib was related to changes in bone and mineral metabolism . in our case , the hypophosphataemia was attributed to tubular dysfunction , since the parathyroid hormone level was just slightly elevated , which can not explain the markedly low serum levels of phosphorus . the slightly elevated serum level of parathyroid hormone and the low serum levels of 25-hydroxyvitamin d can be explained by the episode of aki occurring a few days before and the limited exposure to sunlight in the preceding years , respectively . during the acute phase , our patient did not present hypomagnesaemia although it occurred later during the recovery phase . previous laboratory test results showed that our patient had suffered from hypomagnesaemia , which typically occurred during hypokalaemic episodes . hypokalaemia decreases reabsorption of sodium , potassium and chloride in the thick ascending limb of henle 's loop , as well as decreasing the lumen - positive potential difference at this site , reducing reabsorption of magnesium via the paracellular pathway , which can explain the hypomagnesaemia . however , we can not rule out the possibility that imatinib has a direct effect within the distal nephron . since imatinib is a potent inhibitor of tyrosine kinase and c - kit , which is also expressed in the distal tubule , we hypothesize that reduced expression of the encoding membrane renal transporter genes might form the molecular basis for the electrolyte disorder observed in imatinib - treated patients . in the case described here , the patient developed various hypoelectrolyte disorders ( hypokalaemia , hypophosphataemia and hypomagnesaemia ) . this occurred even in the presence of aki . early diagnosis and correction of imatinib - induced aki and electrolyte disorders
imatinib mesylate is an anticancer agent that selectively inhibits protein kinases involved in the pathophysiology of cancer . 
 it is now the first - line therapy for patients with chronic myeloid leukaemia ( cml ) and is generally well tolerated . here 
 , we describe a case of a patient receiving imatinib for cml . 
 the patient developed renal failure accompanied by severe hypophosphataemia , hypokalaemia and hypomagnesaemia . 
 we discuss the pathophysiological characteristics of imatinib - induced renal injury , and we demonstrate that these electrolyte disturbances were caused by increased urinary excretion of phosphate and potassium 
 . early diagnosis and correction of imatinib - induced renal injury and electrolyte disorders can improve clinical outcomes .