|Year : 2012 | Volume
| Issue : 1 | Page : 48-51
Renal cortical necrosis in a live kidney donor
J Prakash1, A Srivastava2, S Singh1, B Ghosh1
1 Department of Nephrology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
2 Department of Radiodiagnosis, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
|Date of Web Publication||26-Dec-2011|
Department of Nephrology, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221 005, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
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.
Keywords: Acute renal failure, hemolytic uremic syndrome, live kidney donor, renal cortical necrosis
|How to cite this article:|
Prakash J, Srivastava A, Singh S, Ghosh B. Renal cortical necrosis in a live kidney donor. Indian J Nephrol 2012;22:48-51
| Introduction|| |
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. ,, Severe sepsis with shock is the most common (30-40%) nonobstetrical cause of RCN. , Drug-induced thrombotic microangiopathy is an important cause of RCN. , However, RCN has not been previously reported in a live kidney donor.
| Case Report|| |
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 1]a 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. Left nephrectomy was done and was transplanted successfully to the recipient. The donor was hemodynamically stable throughout the operation. 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. The surgery was uneventful as was the immediate postoperative recovery from anesthesia. 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 IU/l), and INR of 1.12. 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. She became afebrile on POD4. Her chest infection improved; thrombocytopenia, elevated LDH, and bilirubin became normal; and leucocytosis showed a downward trend at POD11.
|Figure 1: Kidney, ureter, and renal vessels of living donor (Mother). (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|
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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 1]c 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. Neurological deficit remained stable since its onset. However, her clinical course became complicated by urinary tract infection and sepsis. Unfortunately, almost 3 weeks after the CVA, her sensorium deteriorated suddenly and she succumbed to aspiration pneumonitis. Her salient laboratory investigations and clinical course are given in [Table 1].
The recipient was the 30-year-old daughter of the donor. 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. Prednisolone was gradually tapered over 3 months to 5 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. Allograft biopsy revealed features of chronic allograft nephropathy. However, graft function was stable with serum creatinine of 1.4 mg/dl. 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.
| Discussion|| |
Donor nephrectomy is a major surgery carried on a healthy individual. Postoperative AKI after major surgery is not uncommon and has multifactorial causes. 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.  High cumulative dose is required to produce this lesion. 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. Drug-induced RCN is an important cause 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). , The drugs known to cause HUS were not given to our patient. Systemic infection was evident during postoperative course and sepsis is well known to cause AKI by multiple mechanisms. ,
Intense and sustained vasospasm of small renal vessels can cause RCN. In HUS, 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. We believe that she developed anuric AKI on account of RCN related to HUS. But, the cause of HUS is not evident in this case. However, possibility of infection-associated HUS cannot 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. However, the cause of HUS remained unclear.
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