|Year : 2015 | Volume
| Issue : 4 | Page : 540-542
A rare entity of acute bilateral cortical renal necrosis following acute pancreatitis
Kruti D Dave, Ruchit B Patel, Bhavin J Patel, Shwetang M Solanki, Bhavik K Shah
Deptartment of Radio Diagnosis, Jivraj Mehta Hospital, Ahmadabad, Gujarat, India
|Date of Web Publication||14-Jul-2015|
Shwetang M Solanki
Department of Radio Diagnosis, Jivraj Mehta Hospital, Ahmadabad - 380 007, Gujarat
Source of Support: None, Conflict of Interest: None
Acute bilateral renal cortical necrosis following acute pancreatitis is extremely rare condition. Among all cases of acute renal failure, the incidence of renal cortical necrosis was 3.8% in one of the study in North India. Till date, only eight cases of bilateral cortical necrosis following acute pancreatitis were reported in the literature. We report a case of a 27-year-old male patient with abdominal pain, nausea and vomiting since 2 days duration and anuria since 24 h. Serum amylase and lipase were raised, and elevated serum creatinine was noted on admission. Contrast-enhanced computed tomography scan of the abdomen revealed changes of acute pancreatitis with hypoenhancement of renal cortex compared to medulla on both sides (reverse rim sign-stronger enhancement of the renal medulla compared to cortex), suggest an acute renal cortical necrosis.
Keywords: Acute pancreatitis, acute renal failure, bilateral renal cortical necrosis, reverse rim sign
|How to cite this article:|
Dave KD, Patel RB, Patel BJ, Solanki SM, Shah BK. A rare entity of acute bilateral cortical renal necrosis following acute pancreatitis. Med J DY Patil Univ 2015;8:540-2
|How to cite this URL:|
Dave KD, Patel RB, Patel BJ, Solanki SM, Shah BK. A rare entity of acute bilateral cortical renal necrosis following acute pancreatitis. Med J DY Patil Univ [serial online] 2015 [cited 2022 Jul 5];8:540-2. Available from: https://www.mjdrdypu.org/text.asp?2015/8/4/540/160833
| Introduction|| |
Acute bilateral renal cortical necrosis following acute pancreatitis is extremely rare condition. Among all cases of acute renal failure, the incidence of renal cortical necrosis was 3.8% in one of the study in North India.  Till date, only eight cases of bilateral cortical necrosis following acute pancreatitis were reported in the literature. 
| Case Report|| |
A 27-year-old male patient presented with abdominal pain, nausea and vomiting since 2 days duration and anuria since 24 h. Patient was conscious and oriented. All vitals were stable on admission. Pulse was 116-b/min and blood pressure was 140/90 mm of Hg. On the blood, examination increased white blood cell counts (26390/c.mm), elevated serum amylase (1779 U/L), lipase (1106 U/L) and elevated serum creatinine (4.43 mg%) was noted. Subsequently after 3 days serum creatinine was 7.43 mg%.
On ultrasonography examination, the study revealed changes of acute pancreatitis in form of diffusely bulky hypoechoic pancreas. Edema and thickening of peripancreatic fat planes and mesentry with surrounding fluid collection. Both kidneys appeared normal in size and echotexture. No evidence of hydronephrosis or hydroureter noted. Cortico-medullary differentiation was well maintained.
Contrast-enhanced abdominal computed tomography scan revealed evidence of the diffusely bulky pancreas measuring 41 mm in head, 35 mm in body and 39 mm in the tail region [Figure 2]. Pancreas showed homogenous enhancement. No evidence of areas of necrosis within it. There was edema and thickening of peripancreatic fat planes with mild peripancreatic and lesser sac collection [Figure 2]. There was hypoenhancement of the renal cortex compared to medulla on both sides (reverse rim sign-stronger enhancement of the renal medulla compared to the cortex) [Figure 1], [Figure 3], [Figure 4]. Findings suggestive of acute renal cortical necrosis. Mild to moderate ascites, and mild left sided pleural effusion was also noted. The findings were suggestive of acute pancreatitis with acute renal cortical necrosis.
|Figure 1: Contrast-enhanced coronal section of computed tomography of the abdomen showing diffuse hypoenhancement of cortex as compared medulla in both the kidneys (arrow)|
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|Figure 2: Contrast-enhanced computed tomography of the abdomen showing the diffusely bulky pancreas with surrounding oedema and thickening of peripancreatic fat planes with mild peripancreatic and lesser sac collection|
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|Figure 3: Contrast-enhanced computed tomography of the abdomen showing diffuse hypodense areas in the cortex surrounded by the capsular enhancement in both the kidneys (arrow)|
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|Figure 4: Contrast-enhanced axial section of computed tomography of the abdomen showing diffuse hypoenhancement of cortex as compared medulla in both the kidneys (arrow)|
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| Discussion|| |
Acute renal cortical necrosis is common following obstetrics complications and accounts for 56.6% of cases.  Other nonobstetrics causes include snakebite, hemolytic uremic syndrome and postrenal transplant rejection accounts for 43.4% of cases.  Among the nonobstetrics causes pancreatitis accounts for only 3.8% of all causes.
The exact pathophysiology is uncertain. It is an irreversible form of acute tubular necrosis.  Though it is consider that diminished arterial perfusion secondary to vascular spasm or microvascular injury in cortex occurs secondary to the release of vasoactive or cytotoxic substances in cases of pancreatitis, which leads to acute cortical necrosis. 
Patient with acute cortical necrosis commonest presentation is anuria in 70-80% cases. Some presents with oliguria. Patient can also present with flank pain, hematuria and fever.
Ultrasonography is usually the first modality. Both kidneys can be normal or enlarged in size following cortical necrosis. Sometimes renal cortex may appear typically hypoechoic. Computed tomography scan is the best modality for diagnosis. The characteristic finding on contrast-enhanced computed tomography scan is lack of the renal cortical enhancement.  Other findings include the presence of medullary enhancement and absent renal excretion.  On computed tomography typical appearance of reverse rim sign which is stronger enhancement of the renal medulla compared to cortex suggestive of cortical necrosis is seen.  At later stages, thin cortical or tram lines calcification can be seen on the radiograph. Magnetic resonance imaging (MRI) has a limited role in diagnosing renal cortical necrosis. Though it can show low signal intensity areas affecting the inner renal cortex and the columns of Bertin on both T1- and T2-weighted sequences. Sometimes swelling of both kidneys can be seen on MRI. Renal scanning by diethylenetriaminepentaacetic acid scanning reveals markedly diminished perfusion with delayed or no function. Renal scan is the imaging technique of choice to diagnose renal cortical necrosis in transplant kidneys or if contrast-enhanced computed tomography scanning is unavailable. Although the diagnosis is best confirmed by renal biopsy. Renal biopsy also helps in prognosis also. 
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]