we describe a 73-year - old man who was admitted to our hospital with renal failure but no evidence of proteinuria , haematuria or any other renal signs or symptoms . he presented a new myocardial infarction 2 years ago and , after an extensive coronary study , underwent a quadruple aortocoronary bypass . after that admission , in every single analysis , blood eosinophilia appeared , but no further studies were done for clarification . four years before , he had been diagnosed with colon cancer that was treated successfully . he had no other significant health problems until he presented fatigue and symptoms of malaise . he came to the emergency room after being diagnosed with acute renal failure and was admitted to our nephrology department in order to study its aetiology and to initiate adequate treatment . clinical history failed to reveal any nephrotoxic drugs or any intercurrent processes that could result in acute renal failure . physical examination on admission to the nephrology department revealed no abnormalities . haematologic and biochemical values were as follows : haemoglobin 9.7 mg / dl , leukocytes 10 320/l [ 21% polymorphonuclears , 28% lymphocytes and 48% eosinophils ( 4953 eosinophils / l ) ] and platelets 170000/l . glucose was 4.5 mmol / l , urea nitrogen 23 mmol / l , creatinine 659 mol / l , creatinine clearance 10 ml / min , potassium 5.3 mmol / l , sodium 134 mmol / l , proteins 95 g / l and albumin 28 we requested a complete microbiological blood study in order to discard hypereosinophilia secondary to infections . tests for parasitic diseases were negative and hbsag , hiv antibody , cryoglobulines , ana , anti - dna and rheumatoid factor . serum immunoglobulin g was high ( 5710 ui / ml ) as was immunoglobulin e ( 796 mg / dl ) . the right renal artery could not be observed and the left renal artery was totally normal without any stenosis . no other abnormalities were found . to rule out multiple myeloma or other lymphoproliferative processes , a bone - marrow aspiration was performed but it was non - productive . finally , a bone biopsy was performed that showed a moderate eosinophilia without any malignancy . meanwhile , the patient 's general condition began to worsen due to oliguria and dyspnoea so a femoral catheter was inserted and he underwent regular haemodialysis every other day . a percutaneous renal biopsy was indicated to identify the aetiology of renal failure . on the day previous to the procedure , the patient suffered from angina pectoris , so treatment with sodium heparin was initiated . after that , hepatic parameters began to be altered as such : amino - asparate 0.55 kat / l , alanine - transferase 0.76 kat / l , gamma - glutamine transferase 3.76 kat / l , alkaline phosphatases 3.2 kat / l and bilirubin 4 mol / l . due to the emergency renal biopsy , while on anticoagulant treatment , a transjugular renal and hepatic biopsy was performed at the department of angiovascular radiology . the hepatic biopsy ( figure 2 ) displayed mild acute hepatitis with some chronic lesions and a huge number of eosinophils . the renal biopsy ( figure 1 ) showed severe chronic tubulointerstitial nephritis with intense eosinophilia and no evidence of malignancy . based on the clinical course and histological findings , the diagnosis of idiopathic hypereosinophilic syndrome with renal involvement as the first manifestation was made ; steroid therapy was then initiated at a dose of 1 mg / kg / day of oral prednisone . after treatment with corticosteroids for 24 h , eosinophilia on peripheral blood dramatically reduced to 10% and there was a rapid improvement in his clinical condition . five days after prednisone initiation , urinary output reappeared , renal function ameliorated and haemodialysis was withdrawn . he was discharged a few days later , and the steroids were tapered gradually when he became asymptomatic . three months later , renal function remained stable with a serum creatinine of 262 mol / l , normalized hepatic parameters and normal blood eosinophil count . , there is no evidence of any other organ involvement . in the outpatient clinica , the dose of steroids was reducen to 5 mg / day due to the improvement of renal paramenters ( serum creatinine was 190 mol / l and urea was 9 the total count of eosinophils rose to 4660/l ( 38% ) and renal biochemical parameters had worsened as well , serum creatinine was 265 mol / l and urea 14 mmol / l . three weeks later , eosinophilia on peripheral blood reduced to 130 eosinophils / l ( 1.1% ) and creatinine had improved to 194 mol / l again . eosinophilia can cause many lesions in different organs and tissues as a result of eosinophil cytotoxic properties . the diagnosis of idiopathic he s is based on chusid 's criteria , which are as follows : marked eosinophilia [ absolute eosinophil count ( aec ) > 150010/l ] , chronic course ( > 6 months ) , exclusion of other evident aetiologies for eosinophilia and signs or symptoms of eosinophil - mediated tissue injury . the aetiology of the he s has yet to be clarified . in some instances , our patient had surgery for a carcinoma of colon , but there are no reports in the medical literature implicating this kind of tumour . otherwise , the absence of relapse of the tumour at the time of diagnosis makes it improbable . he s has to be distinguished from reactive hypereosinophilia in parasitic infections , allergic diseases and haematological diseases . he s occurs at any age , though most cases occur between 20 and 50 years of age and it affects men more frequently than women ( 9:1 ) . our case reflects this ; he therefore had had blood eosinophilia for two years prior to admission to our nephrology department with renal insufficiency and blood eosinophilia . in previous reported cases of idiopathic hypereosinophilic syndrome , most patients present late during the course of idiopathic hypereosinophilic syndrome with ischaemic renal changes secondary to thromboembolism from endomyocardial disease . another cause of renal disease associated with increased blood eosinophils is cholesterol atheroembolism , but this complication has been reported in elderly patients with advanced atherosclerosis and is frequently associated with thrombocytopenia and low serum complement . there are some cases in the literature that presented as a mpo - anca - positive crescent and immunotactoid glomerulonephritis with immunoglobulin g , m and a and complement deposits in glomeruli . the mechanisms implicated in renal involvement are similar to those implicated in damaged tissue in other organs , such as eosinophil cytotoxicity , mass effect due to eosinophilic infiltrates and thromboembolic events secondary to cardiac damage . another described affectation is nephrotic syndrome due to membranous glomerulopathies complicated with renal vein thrombosis and thrombotic microangiopathy [ 58 ] . to our knowledge , this is the first documented case of severe eosinophilic interstitial nephritis as the only structural renal damage associated with hypereosinophilic syndrome . there is an article describing the case of a patient affected by hypereosinophilic syndrome associated with kidney insufficiency , specifically eosinophilic interstitial nephritis . however , the eosinophilic interstitial nephritis was not so severe as in our case and it was associated with arteriolar glomerulitis with vasculitis . steroids are the treatment of choice for idiopathic hypereosinophilic syndrome with progressive organ damage , but the dose should be lowered as soon as there is any evidence of response . when there is no response , other possibilities of treatment are possible , according to new published articles . this additional therapy consists of oral hydroxyurea , vincristine , immunosuppressant agents such as cyclosporine a , antimetabolite drugs such as methotrexate and colchicine ; interferon - alpha at high doses ; tyrosine kinase inhibitors such as imatinib mesylate that selectively inhibits a series of protein tyrosine kinases , including bcr - abl , platelet - derived growth factor receptor alpha ( pdgf - ra ) and platelet - derived growth factor receptor beta ( pdgfrb ) or a drug similar to imatinib mesylate , nilotinib , which is a competitive inhibitor at the atp - binding site of bcr - abl , and it has been demonstrated that it is more potent than imatinib . allogeneic stem cell transplantation has also been used as one of the final options as well as monoclonal antibodies such as anti - il5 ( mepolizumab ) or anti - cd52 ( campath ) . [ despite renal pathology in idiopathic hypereosinophilic syndrome being extremely rare , in recent years some cases have appeared describing different types of renal involvement . the diagnosis must be made in time in order to initiate treatment promptly and obtain a complete recovery in renal function . our patient could serve as an example , having had a very good response to corticosteroid therapy such that he could be withdrawn from haemodialysis . kidney  tubular atrophy and the presence of eosinophils in the interstitium .
idiopathic hypereosinophilic syndrome is characterized by elevated and prolonged blood eosinophilia along with organ system involvement and malfunction . 
 the heart is the most frequently involved organ , and renal participation is extremely rare 
 . herein , we report on a case of idiopathic hypereosinophilic syndrome with renal involvement as the first manifestation .