Saudi Journal of Kidney Diseases and Transplantation

CASE REPORT
Year
: 2020  |  Volume : 31  |  Issue : 6  |  Page : 1395--1398

Bilateral renal cortical necrosis in a child with acute pancreatitis


Vybhav Venkatesh1, Aradhana Aneja1, Aditi Kumar1, Raja Ramachandran2, Sadhna Bhasin Lal1,  
1 Division of Pediatric Gastroenterology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Nephrology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Sadhna Bhasin Lal
Division of Paediatric Gastroenterology, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
India

Abstract

Bilateral renal cortical necrosis (RCN) as a cause of acute kidney injury is very rare in the pediatric population. Progression to end-stage renal disease is seen virtually in every patient with RCN. There are many causes for the occurrence of cortical necrosis in children, with severe pancreatitis being a rarity. In this report, we describe a child with severe acute pancreatitis complicated by bilateral RCN.



How to cite this article:
Venkatesh V, Aneja A, Kumar A, Ramachandran R, Lal SB. Bilateral renal cortical necrosis in a child with acute pancreatitis.Saudi J Kidney Dis Transpl 2020;31:1395-1398


How to cite this URL:
Venkatesh V, Aneja A, Kumar A, Ramachandran R, Lal SB. Bilateral renal cortical necrosis in a child with acute pancreatitis. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2021 Apr 14 ];31:1395-1398
Available from: https://www.sjkdt.org/text.asp?2020/31/6/1395/308353


Full Text



 Introduction



Renal cortical necrosis (RCN) due to acute pancreatitis is a rare complication in children. Obstetric complications, septic abortion, severe gastroenteritis, snake envenomation, septicemia, and very rarely severe pancreatitis are among the reported causes of cortical necrosis. It is extremely rare in children as such and only eight cases have been reported in the literature to date. We report an 11-year-old girl who presented with severe acute pancreatitis complicated by bilateral RCN.

 Case Report



Written informed consent for the publication of this case was obtained from the patient’s guardian.

An 11 -year-old girl presented to us with pain abdomen radiating to back and vomiting for four days. There was no history of trauma/ drug intake/fever. There was a strong family history of pancreatitis on the paternal side. She was also oliguric for three days before presentation. She was conscious and oriented with stable vitals on admission. She did not receive any fluid therapy before presentation during the initial four days of illness. The pulse rate was 116/min and blood pressure was 110/80 mm of Hg. The abdomen was tender on examination and there was no organomegaly. There were no signs of dehydration or fluid overload. Blood investigations revealed increased white blood cell counts (14700/μl), elevated serum amylase (1904 U/L), lipase (989 U/L), and severe acute kidney injury (AKI) (serum creatinine 5.8 mg/dL). There was no improvement in renal functions and she rapidly progressed to anuria over 6 h after admission. She initially received normal maintenance fluid as per the body weight and later, was changed to the anurie regimen (400 mL/m2/day plus the previous urine output volume). On the ultrasonography examination of the abdomen, the pancreas was bulky and heterogeneous in echotexture. Both kidneys were normal-sized but had altered cortical echogenicity. Since she had organ dysfunction in the form of stage three AKI according to the KDIGO criteria persisting for >48 h, she was classified to have severe acute pancreatitis as per revised Atlanta classification.[1] The cause of AKI considered was intrinsic injury probably because of acute tubular necrosis from prolonged prerenal AKI. She was initiated on hemodialysis in view of anuria, acidosis, and electrolyte disturbances on day 2 of her hospital stay. She developed new-onset fever spikes on day 3 of her hospital stay. A possibility of infected pancreatic necrosis was considered and she underwent a contrast-enhanced computed tomography scan of the abdomen which revealed bilateral cortical hypodense areas surrounded by capsular enhancement in both kidneys-the “cortical rim sign,” characteristic of cortical necrosis [Figure 1] shows the cortical rim sign). Furthermore, there were edematous pancreas with necrotic areas and a peri-pancreatic fluid collection. A final diagnosis of bilateral RCN as the cause of AKI complicating acute necrotizing pancreatitis was made. She underwent percutaneous catheter drainage of the necrotic collection along with intravenous antibiotics in renal modified doses and was continued on hemodialysis due to anuric AKI. In view of strong family history and other causes of acute pancreatitis being ruled out, genetic testing for hereditary pancreatitis was performed in the child and it revealed a pathogenic heterozygous mutation in the PRSS1 gene (c.86A>T-p.Asn29Ile). She recovered from acute pancreatitis but was oliguric throughout the hospital stay. She remained dialysis-dependent and at the time of discharge after six weeks of hospital stay, she had a urine output of 0.3–0.4 mL/kg/h on diuretics.{Figure 1}

 Discussion



Acute pancreatitis in children is on the rise. The etiology includes trauma, infections, drug-induced, and biliary causes, but largely remains idiopathic. Though pancreatitis tends to be mild in children, few subset of patients develop severe pancreatitis with complications.[2] RCN is a rare, severe, and often irreversible form of acute tubular necrosis. Its incidence is high in developing nations. In a study from this institute, the incidence of RCN was 3.8% of all patients dialyzed for AKI over a 28-year period.[3] Etiology includes obstetric complications such as septic abortion, hemolytic uremic syndrome, snake bite, severe dehydration following gastroenteritis, septic shock, and abdominal trauma.[4] Only eight cases of bilateral RCN following acute pancreatitis have been described in the literature.[5]

AKI is a well-known complication of acute pancreatitis. Hypovolemia, amylase from injured pancreas leading to impaired renal microcirculation, abdominal compartment syndrome, vascular endothelial injury through the circulating mediators among others contribute to the kidney injury.[6] Endotoxins and reactive oxygen species lead to necrosis and apoptosis. Increased vascular permeability as a result of inflammatory cytokine release leads to fluid sequestration in the abdomen and raises intra-abdominal pressure leading to decreased renal perfusion.[7] Endothelin, a potent vasoconstrictor is postulated in the pathogenesis leading to renal damage and subsequent RCN, because both renal hypoperfusion and endothelial injury stimulate the release of endothelin from vascular endothelial cells. RCN results from renal arterial hypo-perfusion which is the final common pathogenic pathway resulting in ischemic cortical necrosis.[8] The diagnosis can be established by CT scan which shows a lack of renal cortical enhancement, presence of medullary enhancement, and absent renal excretion. Renal biopsy, though helpful in prognostication must be avoided since the diagnosis can be made based on imaging findings itself. Failure of complete recovery and prolonged periods of oligo-anuria are seen in many cases.[9] Fluid sequestration in the abdomen and systemic inflammatory response would be the likely mechanism of renal injury in the setting of acute pancreatitis. Adequate fluid management during the first 24-h of acute pancreatitis episode is crucial to prevent complications. The recent European Pancreatic Club guidelines on the management of pediatric pancreatitis recommend early aggressive fluid management at a rate of >1.5–2 times the maintenance rate of IV fluids in the first 24 h.[10] This case has been reported due to the rarity of the complication and also to highlight the importance of fluid management in the initial phase of acute pancreatitis in children.

 Conclusion



Appropriate fluid management is crucial in the initial phase of acute pancreatitis in children. Meticulous monitoring during the initial 48 h of an episode of acute pancreatitis would help in detecting organ dysfunction early and prevent disastrous complications like RCN.

Conflict of interest: None declared.

References

1Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: Revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-11.
2Abu-El-Haija M, Kumar S, Szabo F, et al. Classification of acute pancreatitis in the pediatric population: Clinical report from the NASPGHAN pancreas committee. J Pediatr Gastroenterol Nutr 2017;64:984-90.
3Chugh KS, Jha V, Sakhuja V, Joshi K. Acute renal cortical necrosis – A study of 113 patients. Ren Fail 1994;16:37-47.
4Prakash 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.
5Goffin EJ, Coche EE, Lambert MJ. The case: Acute renal failure following necrotico-hemorrhagic pancreatitis. Kidney Int 2008;74: 975-6.
6Petejova N, Martinek A. Acute kidney injury following acute pancreatitis: A review. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2013;157:105-13.
7Pupelis G, Plaudis H, Zeiza K, Drozdova N, Mukans M, Kazaka I. Early continuous veno-venous haemofiltration in the management of severe acute pancreatitis complicated with intra-abdominal hypertension: Retrospective review of 10 years’ experience. Ann Intensive Care 2012;2 Suppl 1:S21.
8Prakash J, Singh VP. Changing picture of renal cortical necrosis in acute kidney injury in developing country. World J Nephrol 2015;4: 480-6.
9Rodríguez PM, Morales E, Sánchez Á, Milla M, Martínez MA, Praga M. Cortical necrosis: An uncommon cause of acute renal failure with a very poor outcome. Nefrologia 2017;37: 339-41.
10Párniczky A, Abu-El-Haija M, Husain S, et al. EPC/HPSG evidence-based guidelines for the management of pediatric pancreatitis. Pancreatology 2018;18:146-60.