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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2018  |  Volume : 29  |  Issue : 5  |  Page : 1211-1215
Bilateral renal cortical necrosis following acute pancreatitis - A rare complication of a common disease


Department of Nephrology, Government T. D. Medical College, Alappuzha, Kerala, India

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Date of Submission09-Oct-2017
Date of Decision26-Dec-2017
Date of Acceptance27-Dec-2017
Date of Web Publication26-Oct-2018
 

   Abstract 

Acute renal cortical necrosis is a rare cause of intrinsic acute kidney injury (AKI) which is commonly associated with obstetric complications such as placental abruption and some serious systemic disorders such as hemolytic-uremic syndrome, sepsis, severe burns, and snake bite. Acute pancreatitis is an extremely rare cause of renal cortical necrosis, and only less than 10 cases are reported in the literature. Here, we present a 24-year-old male presented with features of acute pancreatitis and oliguric AKI. His pancreatic enzymes were above 1000 IU/mL at admission. He was initiated on hemodialysis. Percutaneous renal biopsy done at 4th week of illness showed features of diffuse renal cortical necrosis. Contrast-enhanced computed tomography demonstrated hypoattenuation of cortex compared to medulla consistent with renal cortical necrosis. He developed complications such as acute necrotic collection, pleural effusion and retinal detachment in addition to renal cortical necrosis which was managed conservatively. Since there was no improvement in the renal function now, he is being evaluated for renal transplantation.

How to cite this article:
Anandan AK, Balachandran P, Chowksey A, Sankaranarayanan G, Samuel U. Bilateral renal cortical necrosis following acute pancreatitis - A rare complication of a common disease. Saudi J Kidney Dis Transpl 2018;29:1211-5

How to cite this URL:
Anandan AK, Balachandran P, Chowksey A, Sankaranarayanan G, Samuel U. Bilateral renal cortical necrosis following acute pancreatitis - A rare complication of a common disease. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2018 Dec 16];29:1211-5. Available from: http://www.sjkdt.org/text.asp?2018/29/5/1211/243968

   Introduction Top


It is well known that severe acute pancreatitis can be complicated by intrinsic renal failure. In most of these situations, acute tubular necrosis is the actual etiology of renal failure and the kidneys recover completely with supportive care. Acute renal cortical necrosis is considered as very rare event complicating acute pancreatitis and only few case reports are available in the literature. Our patient with typical severe acute pancreatitis presented with this very rare complication and his clinical radiological and histological features were very characteristic.


   Case Report Top


A 24-year old male, manual laborer by profession presented to our hospital with complaints of severe upper abdominal pain and multiple episodes of vomiting for two days. He gave a history of regular ethanol consumption for the past three years, and his last consumption was two days before the onset of the symptoms. History revealed no other significant comorbidities in the past. On examination, the patient was conscious, oriented. He was tachypneic, afebrile, pulse rate was 88 beats/min, and blood pressure was 120/80 mm Hg. General examination was unremarkable. His abdomen was diffusely tender with guarding over the epigastrium and bowel sounds were sluggish. There was no evidence of ascites clinically. Respiratory system examination showed reduced breath sounds over the left lower thorax with stony dullness. Other system examination was essentially normal.

His initial evaluations were carried out under the surgery department to find out the cause for the acute abdomen. Preliminary investigations ruled out bowel perforation. Blood investigations revealed highly elevated serum lipase and amylase (serum amylase 2750 u/mL and serum lipase 1850 u/mL). Renal function was deranged with a serum creatinine of 4 mg/dL. Total leukocyte count was slightly increased with neutrophil predominance. Ultrasonogram of the abdomen showed bulky pancreas and evidence of the left-sided pleural effusion. Blood glucose and electrolytes including calcium and magnesium were within normal limits at admission.

He was maintained nil per oral with intravenous fluids along with antibiotics and supportive care. Even though he reported symptomatic improvement by the next day, his urine output dropped to less than 50 mL over 24 h despite maintaining adequate hydration. A diagnosis of anuric acute kidney injury secondary to acute tubular necrosis was made, and he was supported with hemodialysis (HD). Serum amylase and lipase normalized over the next two weeks, but urine output did not improve and he was maintained on alternate day HD. As there was no improvement in the renal function with supportive care we wanted to revise our initial diagnosis and hence further evaluation was planned. A percutaneous renal biopsy was performed after three weeks of the onset of illness, and it was reported as diffuse acute cortical necrosis [Figure 1] and [Figure 2].
Figure 1: The light microscopy with H&E stain showing features of complete necrosis of the visualized glomerular tufts (arrows).

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Figure 2: H and E staining under light microscopy showing tubular necrosis also (arrow).
Renal biopsy report
Light microscopy
Multiple section from single corticomedullary core stained with H and E, PAS, MT, and Silver show 21 glomeruli. Cortex reveals necrosis which shows ghost outline of glomeruli and proximal convoluted tubule. A few distal tubule in the cortex and medulla appear viable. No viable glomeruli noted in the core.
Immunofluorescence studies.
Tissues for IF also show cortical necrosis.
Medulla appears viable.


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His hospital course was complicated by recurrence of abdominal pain with re-elevation in serum amylase and lipase during the 4th week illness. CT scan of the abdomen was done to look for any cause for recurrent pancreatitis. Scan showed acute necrotic collection in the pancreas with bilateral pleural effusion and basal atelectasis [Figure 3], [Figure 4], [Figure 5]. He improved with conservative management. After four weeks into the illness, he developed visual disturbance and was detected to have exudative retinal detachment again responded to conservative management. Since there was no improvement in the renal function he is now being worked up for live related kidney transplantation.
Figure 3: The corticomedullary phase of contrast-enhanced computed tomography abdomen showing absence of contrast uptake by the cortex. A collection can also be observed toward the tail of pancreas (arrow).

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Figure 4: The nephrographic phase of contrastenhanced computed tomography abdomen showing reduced uptake of contrast in the cortex compared to the medulla. The hypo-enhancing cortex is seen as a thin rim (arrow) in the periphery.

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Figure 5: The delayed phase of contrastenhanced computed tomography showing the absence of excretion of contrast into the pelvicalyceal system.

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   Discussion Top


Renal cortical necrosis (RCN) was first described by Juhal Renoy in the year 1886.[1] It is responsible for about 2% of intrinsic acute kidney injury. Obstetric emergencies such as placental abruption, postpartum hemorrhage, septic abortion, and amniotic fluid embolism account for the majority of the cases. A study from India showed that 56.6% of the RCN is pregnancy-related.[2] With the improvement in obstetric care the incidence has come down. In India, the incidence has decreased from 20% to 30% of obstetric acute kidney injury to 5% over the past two decades.[3] The etiology of nonobstetric RCN includes hemolytic uremic syndrome, viperine snake envenomation, renal allograft rejection, sepsis, severe burns, acute pancreatitis, shock, diabetic ketoacidosis, severe abdominal trauma, drugs, etc. A peak occurs in infancy when severe dehydration in the setting of diarrheal disease, congenital heart disease, fetomaternal transfusion, perinatal asphyxia, severe hemolytic disease, and sepsis leads to RCN.[4] Acute pancreatitis is a rare cause of RCN with only less than 10 cases reported in the literature. It was responsible for 3.8% of the cases in a study from the northern part of India.[5]

The most commonest presentation is absolute anuria in around 70–80% of the patients. RCN results in ischemic necrosis of all components of the renal cortex extending to the column of Bertin. It is associated with markedly diminished renal perfusion, intense vasospasm, and microvascular injury. It shares many similarities with the generalized Schwartzman reaction induced by endotoxin.[6]

Plain abdominal X-ray can identify calcification as thin cortical shells or tram lines, but these changes take at least four to six weeks to appear.[7] Ultrasonogram may be normal or show increase in the kidney size and very rarely shows hypoechoic renal cortex.[8] In contract-enhanced CT the typical finding is lack of renal cortical enhancement. The presence of medullary enhancement and absence of renal excretion are the other findings. Stronger enhancement of the medulla compared to cortex which is known as reverse rim sign also indicates RCN.[9] Hence, contrastenhanced computed tomography (CECT) is a very useful tool for the early diagnosis of RCN. Magnetic resonance imaging has limited role in the diagnosis although it can detect renal swelling and low-signal changes in T1- and T2-weighted in inner renal cortex and the columns of Bertin. DTPA renogram can detect diminished renal perfusion and absence or low renal function. It is useful in transplant renal cortical necrosis and under situations when CECT cannot be performed.[8]

Renal biopsy is considered as the gold standard investigation in RCN and it also has prognostic significance. Light microscopy can demonstrate the necrosis of all the elements of the cortex and sparing thin rim of cortex under the renal capsule, juxtamedullary cortex, and medulla. RCN is classified into focal, minor, patchy, gross and confluent forms which differ in the extent of involvement.[10] Patchy form of the disease may regain some renal function compared to diffuse form. Small surviving population of juxtamedullary nephrons gradually undergo adaptive changes and contribute to glomerular filtration rate. These nephrons may not be picked up in needle biopsy.[1]

The prognosis is very often grim with nearly all patients end up in renal replacement therapy after variable period. Majority of diffuse RCN will not regain renal function whereas patchy cortical necrosis shows some improvement in renal function but gradually progress to the stage of end-stage renal disease. Although the only curative treatment is renal transplantation, dialysis-free survival up to 12 years has been reported in India.[5]

Conflict of interest: None declared.

 
   References Top

1.
Bloom R, Swenson RS, Coplon NS. Acute renal cortical necrosis. Variable course and changing prognosis. Calif Med 1973;119:1-5.  Back to cited text no. 1
    
2.
Prakash J, Vohra R, Wani IA, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: A single-centre experience of 22 years from Eastern India. Nephrol Dial Transplant 2007; 22:1213-7.  Back to cited text no. 2
    
3.
Prakash J, Singh VP. Changing picture of renal cortical necrosis in acute kidney injury in developing country. World J Nephrol 2015;4: 480-6.  Back to cited text no. 3
    
4.
Campbell AC, Henderson JL. Symmetrical cortical necrosis of the kidneys in infancy and childhood. Arch Dis Child 1949;24:269-85.  Back to cited text no. 4
    
5.
Chugh KS, Jha V, Sakhuja V, Joshi K. Acute renal cortical necrosis – A study of 113 patients. Ren Fail 1994;16:37-47.  Back to cited text no. 5
    
6.
Cisse MM, Ka EF, Seck SM, et al. Obstetric cortical renal necrosis, even reality in the tropics. J Nephrol Ther 2014;4:156.  Back to cited text no. 6
    
7.
Oram S, Ross G, Pell L, Winterler J. Renal cortical calcification after snake bite. Am Heart J 1964;67:714-5.  Back to cited text no. 7
    
8.
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.  Back to cited text no. 8
  [Full text]  
9.
Yudin A. Cortical rim sign and reversed rim sign. Metaphorical Signs in Computed Tomography of Chest and Abdomen. Switzerland: Springer International Publishing; 2014. p. 139.  Back to cited text no. 9
    
10.
Kennedy C, Khilji S, Dorman A, Walshe J. Bilateral renal cortical necrosis in meningococcal meningitis. Case Rep Nephrol 2011; 2011:274341.  Back to cited text no. 10
    

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Correspondence Address:
Dr. Arun Karat Anandan
Department of Nephrology, Government T. D. Medical College, Alappuzha, Kerala
India
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DOI: 10.4103/1319-2442.243968

PMID: 30381522

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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