Elevated Serum Creatinine as a Marker of Pancreatic Necrosis in Acute Pancreatitis

Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, UPMC Presbyterian Hospital, University of Pittsburgh School of Medicine, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
The American Journal of Gastroenterology (Impact Factor: 10.76). 01/2009; 104(1):164-70. DOI: 10.1038/ajg.2008.66
Source: PubMed


Pancreatic necrosis is a serious complication of acute pancreatitis. The identification of simple laboratory tests to detect subjects at risk of pancreatic necrosis may direct management and improve outcome. This study focuses on the association between routine laboratory tests and the development of pancreatic necrosis in patients with acute pancreatitis.
In a cohort of 185 patients with acute pancreatitis prospectively enrolled in the Severity of Acute Pancreatitis Study, patients with contrast-enhanced computerized tomography performed were selected (n=129). Serum hematocrit, creatinine, and urea nitrogen on admission and peak values within 48 h of admission were analyzed. The volume of intravenous fluid resuscitation was calculated for each patient.
Of 129 patients, 35 (27%) had evidence of pancreatic necrosis. Receiver operating characteristic curves for pancreatic necrosis revealed an area under the curve of 0.79 for admission hematocrit, 0.77 for peak creatinine, and 0.72 for peak urea nitrogen. Binary logistic regression yielded that all three tests were significantly associated with pancreatic necrosis (P<0.0001), with the highest odds ratio, 34.5, for peak creatinine. The volume of intravenous fluid resuscitation was similar in patients with and without necrosis. Low admission hematocrit (< or =44.8%) yielded a negative predictive value of 89%; elevated peak creatinine (>1.8 mg/dl) within 48 h yielded a positive predictive value of 93%.
We confirm that a low admission hematocrit indicates a low risk of pancreatic necrosis (PNec) in patients with acute pancreatitis. In contrast, an increase in creatinine within the first 48 h is strongly associated with the development of PNec. This finding may have important clinical implications and warrants further investigation.

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    • "Some of them are: a) the Acute Physiology, Age and Chronic Health Evaluation (Apache II) [4] [7] [9] [14]; b) Structured Interview of Reported Symptoms (SIRS) [4] [9]; c) the Ranson score [4] [7] [9]; d) Bedside index for severity in AP (BISAP) (blood urea nitrogen >25mg/dl, impaired mental status, Systemic inflammatory response syndrome, age >60 years and pleural effusions) [2] [3] [15]; e) The Harmless Acute Pancreatitis Score (HAPS) (no rebound tenderness and/ or guarding, normal hematocrit and normal serum creatinine level) allows rapid identification of patients who present mild AP in 98% of cases; f) CT severity index (CTSI) based on local complications and percentage of pancreatic necrosis seen on a CT scan [2] [4] [5] [17] [18]. Various laboratory tests and biomarkers for predicting AP outcome have been described: a) elevated C-reactive protein (CRP) [1] [4] [13] [14] [19] [20]; b) elevated hematocrit (Ht) [5] [7] [14] [21] [22]; and c) high serum creatinine, as a doubtful predictor of pancreatic necrosis [23] [24]. Some of the recently described individual markers of severity include procalcitonin [25] [26] [27], urinary trypsinogen activation peptide, intra-abdominal hypertension (>15mmHg) [7], angiogenic factors [28] and interleukins (IL-6 and IL-8) [29]. "
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    Expert review of gastroenterology & hepatology 09/2009; 3(4):435-44. DOI:10.1586/egh.09.27 · 2.42 Impact Factor
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