renal cortical necrosis ( rcn ) is a rare entity and is secondary to ischemic necrosis of renal cortex caused by vascular spasm , microvascular injury , or intravascular coagulation . rcn accounts for 3% of all cases of acute kidney injury ( aki ) in adults . obstetric and nonobstetrical causes account for 50 to 70% and 20 to 30% cases of rcn , respectively.[13 ] severe sepsis with shock is the most common ( 30 - 40% ) nonobstetrical cause of rcn . a 48-year - old normotensive , nondiabetic healthy female donor was admitted for left nephrectomy for kidney transplantation to her daughter . computed tomography ( ct ) renal angiography showed normal kidneys and urinary tracts as well as normal renal arteries originating from the aorta and branching well into the renal parenchyma [ figure 1a and b ] . diethylene - triamine - penta - acetic acid ( dtpa ) scan revealed total glomerular filtration rate ( gfr ) of 100.1 ml / min with differential function of 51.8% and 48.2% for the right and left kidneys , respectively . the medications used during the operation were glycopyrrolate , vecuronium , propofol , isoflurane , nitrous oxide , neostigmine , bupivacaine , fentanyl , furosemide 120 mg , and mannitol 70 g ( 350 ml of 20% solution ) . she received total of 5200 ml of fluid and urine output was 3400 ml during the time she was in operation theater for 2 hours . she did well with urine output of > 1.48 l / h for 2 hours and 1.25 l / h in subsequent 2 hours . in the fifth postoperative hour , her urine output decreased to 750 ml / h and subsequently to 50 - 60 ml / h in sixth and seventh hours after surgery and she became anuric at eighth postoperative hour . after ruling out catheter obstruction and dehydration , she was given furosemide infusion at 60 mg / h which resulted in only 110 ml of urine output in next 2 hours followed by no output . doppler study revealed patent renal vessels with good blood flow and absence of obstruction of urinary tract . on the first postoperative day ( pod ) , she was hemodialyzed for 3 hours because of fluid overload . laboratory investigations on pod1 revealed hemoglobin of 7.7 g/ dl , thrombocytopenia , leukocytosis , hyperbilirubinemia , elevated lactate dehydrogenase ( ldh ) ( 1222 peripheral smear revealed anisocytosis and few normoblasts with fragmented red blood cells ( rbcs ) . in view of low platelet count , raised ldh , drop in hemoglobin along with normal inr , a diagnosis of hemolytic uremic syndrome ( hus ) was made [ table 1 ] . she was transfused with two units of whole blood on pod3 due to drop in hemoglobin concentration to 5.3 g / dl . chest x - ray on pod3 showed right lower zone pneumonia and she was treated with cefpirome 2 g / day , ofloxacin 200 mg / day , and azithromycin 250 mg od . her chest infection improved ; thrombocytopenia , elevated ldh , and bilirubin became normal ; and leucocytosis showed a downward trend at pod11 . ( a ) volume - rendered ( vr ) image showing normal kidneys and urinary tracts bilaterally ; ( b ) maximum intensity of projection ( mip ) showing bilateral normal renal arteries originating from aorta and branching well into the renal parenchyma ; ( c ) right kidney shows uniform hypoattenuated subcapsular rim of cortex ( axial image ) ; ( d ) uniform hypoattenuated subcapsular rim of cortex ( coronal image ) . both c and d favor feature of renal cortical necrosis in kidney donor clinical characteristics of kidney donor following nephrectomy in view of persistent anuria , she was subjected to contrast - enhanced ct ( cect ) scan of abdomen on pod28 , which revealed features of acute rcn in right kidney [ figure 1c and d ] . she was discharged on pod30 with good bp control on amlodipine ( 15 mg / day ) and clonidine ( 0.3 mg / day ) and advised to continue maintenance hemodialysis . at two - month follow - up , her antihypertensive requirement reduced as well as her urine output increased to 125 ml / day and at the end of fourth month , her urine output was 400 ml/ day . three months after operation , she developed right lower lobe pneumonitis which improved with oral co - amoxiclav . four and half months after surgery , she developed cerebrovascular accident ( cva ) with complete left hemiplegia . plain ct scan of brain revealed acute right parietal lobe hemorrhage with chronic subdural hematoma over left frontoparietal region . unfortunately , almost 3 weeks after the cva , her sensorium deteriorated suddenly and she succumbed to aspiration pneumonitis . the recipient had brisk diuresis following release of clamp in the operation theatre as well as prompt recovery from anesthesia and was discharged on 12th pod with good graft function ( serum creatinine of 0.83 mg / dl ) . she was on triple immunosuppressive regimen consisting of cyclosporine 200 mg / day , azathioprine 100 mg / day , and prednisolone 20 mg / day . she developed evidence of acute graft rejection one year post - transplant which was treated successfully with intravenous pulse methyl prednisolone ( 500 mg / day for 3 days ) . she later developed heavy proteinuria ( 5.7 g / day ) at 15 months post - transplant . at this point , azathioprine was replaced by mycophenolate mofetil ( mmf ) ( 1 g / day ) . her current medications are cyclosporine 175 mg / day , mmf 1 g / day , and prednisolone 5 mg / day , along with amlodipine 10 mg / day and metoprolol 50 mg / day . at her last follow - up on february 11 , 2011 , bp was 120/70 mm hg . laboratory analysis revealed serum creatinine of 1.3 mg / dl , urea of 28 mg/ dl , hb of 12.6 g / dl , and 24 hours urinary protein of 4.9 g. most commonly , it is prerenal aki due to volume loss in the form of bleeding , vomiting , excess drainage , etc . , and is readily reversible . a more severe degree of hypovolemia leading to acute tubular necrosis ( atn ) also improves mostly with treatment . however , irreversible renal failure due to rcn related to massive volume loss associated with prolonged hypotension has been reported . aki can also occur due to thrombosis or thromboembolism of renal vessels in the postoperative period . atheroembolic renal artery obstruction has been described mostly after vascular surgery and occurs 1 to 2 weeks after the procedure . nephrotoxic drugs ( nsaids , aminoglycosides , beta - lactam antibiotics ) are known to cause aki in postoperative period , mostly by the end of the first week . osmotic nephrosis is a distinct pattern of acute tubular injury observed following parenteral infusion of hyperoncotic solutions like hexaethyl - starch , sucrose , mannitol , dextran , and contrast media . the mean dose of mannitol - producing osmotic nephrosis has been reported to be 626  270 g and 295  134 g over 2 to 5 days in those with previously normal and impaired kidney function , respectively . sepsis and disseminated intravascular coagulation ( dic ) can complicate postoperative course of surgical procedure and may cause aki by multiple mechanisms . the potential causes of aki in the patient described here consist of blood transfusion reaction , vascular and urologic obstruction , blood loss , hus , osmotic nephrosis , sepsis , dic , and nephrotoxic drugs . given the very sudden onset of anuria , thrombosis / obstruction of renal vessels or obstructed outflow were thought of initially but were ruled out by appropriate investigations . she did not have hypotensive episode during intraoperative and postoperative periods and there was no evidence of excessive blood loss . there was no evidence of hematuria , hemoglobinuria , or transfusion reaction in this patient . osmotic nephrosis due to mannitol used intraoperatively was considered an unlikely cause of aki because of low dose of mannitol ( 70 g ) given and early onset of aki . these agents lead to thrombotic microangiopathy ( tma ) by either an immune - mediated mechanism involving the adamts13 metalloprotease ( quinine / quindine , ticlopidine and clopidogrel ) or direct endothelial toxicity ( mitomycine c and calcineurin inhibitors ) . systemic infection was evident during postoperative course and sepsis is well known to cause aki by multiple mechanisms . an additional mechanism involves endotoxin - mediated endothelial damage that leads to vascular thrombosis and reduced renal perfusion . in our case , hus causing tma and subsequently rcn was a strong clinical possibility , because patient had definite clinical evidence of hus in postoperative period [ table 1 ] . rcn contributed to aki in 19.9% cases in an autopsy series of 131 patients with postsurgical aki . the finding on abdominal ct scan is often diagnostic of rcn , although renal biopsy is the diagnostic gold standard . on cect scan , nonopacification of the renal cortex sparing the subcapsular , juxtamedullary , and medullary areas is typical of rcn . renal biopsy was not done , as biopsy in a solitary kidney of a kidney donor was considered too risky and sensitive issue to settle the etiological dogma , while cect scan showed characteristic feature of rcn , and biopsy was thought to be noncontributory to her management . however , possibility of infection - associated hus can not be ruled out in the present case . to the best of our knowledge , the patient presented here is the first case of rcn in a live kidney donor in world literature . the aki developed abruptly within 5 hours of nephrectomy and was most likely related to hus causing rcn .
renal cortical necrosis ( rcn ) is a rare cause of acute renal failure ( arf ) . 
 there is no clinical case report of rcn in a live kidney donor . 
 a 48-year - old female kidney donor developed sudden anuria five hours postnephrectomy and remained anuric for more than three months on maintenance hemodialysis . 
 laboratory investigations revealed the features of hemolytic uremic syndrome . 
 contrast - enhanced computed tomography scan of abdomen showed hypoattenuated subcapsular rim of renal cortex favoring diagnosis of rcn . to the best of our knowledge , 
 this is the first clinical case report of rcn in a live kidney donor in world literature .