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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2015  |  Volume : 26  |  Issue : 1  |  Page : 56-60
Acute kidney injury in severe acute pancreatitis: An experience from a tertiary care center


1 Central Research Laboratory, Sri Aurobindo Institute of Medical Sciences, Indore, India
2 Department of Nephrology, Sri Aurobindo Institute of Medical Sciences, Indore, India
3 Department of Medicine, Sri Aurobindo Institute of Medical Sciences, Indore, India

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Date of Web Publication8-Jan-2015
 

   Abstract 

Acute kidney injury (AKI) is an important cause of morbidity and mortality in severe acute pancreatitis (SAP). We aimed in our study to explore the risk factors of AKI in patients with SAP and assess the prognosis of patients with SAP and AKI. This is a retrospective study consisting of analysis of outcome and complications encountered in 72 severe acute pancreatitis patients admitted to a tertiary care center at Indore, India, from May 2011 to April 2012. We encountered 14 AKI cases in the SAP study patients. There was a significant association of diabetes and alcohol with AKI in patients with SAP. Alcohol was found to be an independent significant risk factor for AKI in SAP. All the eight patients with SAP who expired had AKI. None of the patients of SAP without AKI expired during the study. We conclude that the patients with SAP with AKI have a greater mortality rate as compared with the SAP patients without AKI.

How to cite this article:
Kumar R, Pahwa N, Jain N. Acute kidney injury in severe acute pancreatitis: An experience from a tertiary care center. Saudi J Kidney Dis Transpl 2015;26:56-60

How to cite this URL:
Kumar R, Pahwa N, Jain N. Acute kidney injury in severe acute pancreatitis: An experience from a tertiary care center. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2019 Dec 10];26:56-60. Available from: http://www.sjkdt.org/text.asp?2015/26/1/56/148734

   Introduction Top


Acute pancreatitis (AP) is a sudden inflammation of the pancreas characterized clinically by severe upper abdominal pain, and it may be associated with nausea, vomiting, diarrhea, fever and chills, hemodynamic instability, tachycardia and respiratory distress. [1] Most of the AP patients have a self-limited course, but it may become worse in about 15-20% with progression to multiple organ dysfunction or local complications including necrosis, pseudocyst and abscesses, and then called severe acute pancreatitis (SAP). [2]

Acute kidney injury (AKI) is a known complication of SAP. Despite the availability of intensive care, AKI is one of the most common causes of death in patients with SAP. [3],[4],[5],[6],[7],[8],[9]

The mechanism of AKI that occurs in patients with SAP remains unclear and may involve many factors. However, there is a lack of reports about the risk factors for AKI in patients with SAP, especially in central India. We aimed in our study to determine the risk factors associated with AKI in SAP patients.


   Patients and Methods Top


All patients admitted to the tertiary care center in Indore, India, with SAP were recruited for the study from May 2011 to April 2012. Diagnosis of AP was made if two of the following three features were present: (1) abdominal pain characteristic of acute pancreatitis, (2) serum amylase and/or lipase ≥3 times the upper limit of normal and (3) characteristic findings of acute pancreatitis on computerized tomography (CT) scan. The patients were classified as having SAP based on the presence of persistent systemic inflammatory response syndrome (SIRS) and/or developing organ failure for >48 h. [10] SIRS was defined by the presence of two or more of the following criteria for >48 h: Pulse >90 beats/min, rectal temperature < 36°C or >38°C, white blood count < 4000 or >12,000 per mm 3 and respirations >20/min or PCO 2 < 32 mm Hg. Organ failure was defined as shock-systolic pressure < 90 mm Hg, PaO2 ≤60 mm Hg, creatinine >2.0 mg/L after rehydration and gastrointestinal bleeding >500 mL/ 24 h.

Patients with AP due to surgery, inflammatory bowel disease, stoma, trauma, cancer, short bowel and chronic pancreatitis with exacerbation were excluded from the study.

The data of the patients were recorded in specially designed forms, which included age, gender, symptoms at presentation, the peak of the serum amylase and lipase levels, local and systemic complications, ultrasound scan findings, local and systemic complications and requirement of hemodialysis.

AKI was defined and classified according to the RIFLE (Risk, Injury, Failure, Loss, and End-stage) criteria based on urine production < 400 mL/d or serum creatinine level >2 mg/dL.


   Statistical Analysis Top


Statistical Package for Social Science (SPSS) version 20.0 was used for data analysis. Results were presented as mean ± standard deviation for quantitative variables and percentages for qualitative variables. Student's "t" test was used to assess the difference of the quantitative variables in the study groups. Significance between distributions of frequencies of qualitative variables between the study groups was assessed by the χ 2 test. Multinomial logistic regression analysis was performed to determine the independent effect of the variables on the disease.


   Results Top


A total of 72 (58 male and 14 female) patients who satisfied the inclusion and exclusion criteria were recruited for the study. The mean age of the patients was 37.5 ± 14.8 years (14-74 years). The cause of pancreatitis was alcohol intake in 24 (33.33%) patients, cholelithiasis in 18 (25%) patients and necrotizing pancreas in 15 (20.8%) patients. The cause of pancreatitis in the remaining patients was unknown. Diabetes mellitus was present in 34 (47.2%) patients, whereas hypertension and hepatomegaly were reported in eight (11.11%) and 19 (26.3%) patients, respectively. Twenty (27.77%) patients had a previous history of AP. The mean serum amylase and lipase levels were 1290 ± 1930 U/L and 2781 ± 4322 U/L, respectively.

The patients were treated conservatively with IV fluids, antibiotics (such as carbapenem, quinolone, piperacillin and trazobactum) and analgesics.

Of the 72 patients with SAP, 14 (19.4%) had AKI, hemodialysis was required in 10 patients with AKI, while four patients completely recovered without dialysis. SIRS was observed in 12 of 14 (85%) of the SAP and AKI patients. Nine patients with SAP with AKI developed shock (systolic pressure < 90 mm Hg) during their hospitalization, while no patients with SAP without AKI developed shock. Ten patients with SAP and AKI developed sepsis during the course of the disease.

We found no significant difference in terms of past history of pancreatitis, occurrence of hepatomegaly, cholelithiasis and hypertension in the development of AKI in the SAP cases. Although the differences were not statistically significant, the patients with diabetes, hypertension and hepatomegaly had a higher risk of development of AKI in SAP [Table 1]. We found that diabetes and alcohol were significantly associated with AKI in the SAP patients. With the multinomial logistic regression analysis, we found that alcohol was an independent risk factor for AKI in the SAP patients [Table 2].
Table 1: Clinical characteristics in severe acute pancreatitis (SAP) with and without acute kidney injury (AKI).

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Table 2: Independent prognostic factors in a multinomial logistic regression analysis.

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Of 72 patients, eight patients expired during the course of the treatment, of whom six (75%) patients developed multiple organ failure; no SAP patient without AKI died during the study period.


   Discussion Top


AKI is one of the most common complications in patients with SAP. Its incidence rateranges from 14% to 42% in previous studies. [3],[4],[5],[6],[7],[8],[9] In our study, the incidence rate of AKI was 19.4%, which is consistent with the incidence reported in the medical literature. Compañy et al reported that age positively correlated with the prognosis of SAP; [3] however, in our study, we found that age was an insignificant risk factor for AKI in patients with SAP, and our results were compatible with the study of Li et al. [11]

The causes for AKI in the patients with SAP can be multifactorial. The exact mechanism for pancreatitis-related renal failure is not yet well established, but studies have shown that systemic inflammation, cytokine production, free radicals and other factors influencing the microcirculation play a role. Li et al [11] assessed the multivariate risk factors that would predict the outcome and reported that age, history of kidney disease and abdominal compartment syndrome were independent prognostic factors. [8]

Alcohol was a significant risk factor for AKI in SAP in our study. Previous studies found that alcohol consumption increased the risk of kidney failure by initiating and/or promoting atherogenic risk factors, such as high blood pressure, [12],[13] hyperuricemia, [14] insulin resistance [15] and diabetes. [16],[17]

The prognosis of the patients with SAP and AKI is extremely guarded. In our study, when AKI occurred in the patients with SAP, the incidence of sepsis increased to 71.4% (P = 0.001) and the mortality rate was high (57.1%); the rate of infection in SAP ranged from 19% to 70% according to previous reports. [4],[18]

In conclusion, patients with SAP have a higher risk of developing AKI that is associated with high mortality. Our study suggests that this concept may be true and future studies to evaluate the various therapeutic interventions are warranted.


   Acknowledgment Top


The authors are thankful to the Chairman, Sri Aurobindo Institute of Medical Sciences, Indore for providing infrastructure facilities.

Conflict of interest: None

Source of Funding: None

 
   References Top

1.
Imrie CW. Acute pancreatitis: Overview. Eur J Gastroenterol Hepatol 1997;9:103-5.  Back to cited text no. 1
    
2.
Swaroop VS, Chari ST, Clain JE. Severe acute pancreatitis. JAMA 2004;291:2865-8.  Back to cited text no. 2
    
3.
Ljutić D, Piplović-Vuković T, Raos V, Andrews P. Acute renal failure as a complication of acute pancreatitis. Renal Fail 1996;18:629-33.  Back to cited text no. 3
    
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Compañy L, Sáez J, Martínez J, et al. Factors predicting mortality in severe acute pancreatitis Pancreatology 2003;3:144-8.  Back to cited text no. 4
    
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Kong L, Santiago N, Han TQ, Zhang SD. Clinical characteristics and prognostic factors of severe acute pancreatitis. World J Gastroenterol 2004;10:3336-8.  Back to cited text no. 5
    
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Halonen KI, Leppaniemi AK, Puolakkainen PA, et al. Severe acute pancreatitis: Prognostic factors in 270 consecutive patients. Pancreas 2000;21:266-71.  Back to cited text no. 6
    
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Isenmann R, Rau B, Beger HG. Early severe acute pancreatitis: Characteristics of a new subgroup. Pancreas 2001;22:274-8.  Back to cited text no. 7
    
8.
Herrera Gutiérrez ME, Seller Pérez G, de La Rubia De Gracia C, Chaparro Sánchez MJ, Nacle López B. Acute renal failure profile and prognostic value in severe acute pancreatitis. J Med Clin 2000;115:721-5.  Back to cited text no. 8
    
9.
Tzovaras G, Parks RW, Diamond T, Rowlands BJ. Early and long-term results of surgery for severe necrotising pancreatitis. J Dig Surg 2004;21:41-6.  Back to cited text no. 9
    
10.
Banks PA, Freeman ML. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006;101:2379-400.  Back to cited text no. 10
    
11.
Li H, Qian Z, Liu Z, Liu X, Han X, Kang H. Risk factors and outcome of acute renal failure in patients with severe acute pancreatitis. J Crit Care 2010;25:225-9.  Back to cited text no. 11
    
12.
Marmot MG, Elliott P, Shipley MJ, et al. Alcohol and blood pressure: The INTERSALT Study. BMJ 1994;308:1263-7.  Back to cited text no. 12
    
13.
Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men: A randomized controlled trial. Hypertension 1985;7:707-13.  Back to cited text no. 13
[PUBMED]    
14.
Nishimura T, Shimizu T, Mineo I, et al. Influence of daily drinking habits on ethanolinduced hyperuricemia. Metabolism 1994;43:745-8.  Back to cited text no. 14
    
15.
Knip M, Ekman AC, Ekman M, Leppäluoto J, Vakkuri O. Ethanol induces a paradoxical simultaneous increase in circulating concentrations of insulin-like growth factor binding protein-1 and insulin. Metabolism 1995;44:1356-9.  Back to cited text no. 15
    
16.
Holbrook TL, Barrett-Connor E, Wingard DL. A prospective population-based study of alcohol use and non-insulindependent diabetes mellitus. Am J Epidemiol 1990;132:902-9.  Back to cited text no. 16
    
17.
Brancati FL, Whelton PK, Randall BL, Neaton JD, Stamler J, Klag MJ. Risk of end-stage renal disease in diabetes mellitus: A prospective cohort study of men screened for MRFIT. Multiple Risk Factor Intervention Trial. JAMA 1997;278:2069-74.  Back to cited text no. 17
    
18.
Rau B, Steinbach G, Gansauge F, Mayer JM, Grünert A, Beger HG. The potential role of procalcitonin and interleukin 8 in the prediction of infected necrosis in acute pancreatitis. Gut 1997;41:832-40.  Back to cited text no. 18
    

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Correspondence Address:
Dr. Neeraj Jain
Department of Medicine, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh
India
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DOI: 10.4103/1319-2442.148734

PMID: 25579716

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    Tables

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    Abstract
   Introduction
   Patients and Methods
   Statistical Analysis
   Results
   Discussion
   Acknowledgment
    References
    Article Tables
 

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