Introduction: Acute pancreatitis is an infrequent but challenging cause of peritonitis in peritoneal dialysis (PD). Presentation is often indistinguishable from infectious peritonitis, interpretation of pancreatic enzymes is not straight-forward, and multiple etiologies need to be considered. Case Presentation: A 74-year-old PD patient presented with cloudy dialysate and subtle symptoms of malaise and abdominal pain. WBC was 26,000/µL, CRP was 250 mg/L, and dialysis effluent contained 1,047 leucocytes/μL (90% polymorphs). Infectious peritonitis was presumed, and antibiotic treatment started. However, dialysate cultures remained negative, effluent leucocyte count remained high, and clinical condition deteriorated. Abdominal ultrasound was unremarkable (pancreas not visible). Acute pancreatitis was diagnosed by elevated lipase level (serum: 628 U/L, dialysis fluid: 15 U/L) and CT scan. Disentangling etiological factors was challenging. The patient had gallstones, consumed alcoholic beverages, was recently on doxycycline and dialyzed with icodextrin. In addition, PD treatment itself may have been a contributory factor. Antibiotic therapy was stopped, and PD was temporarily suspended. Systemic and effluent markers of inflammation took 4 weeks to normalize. The patient did not regain his usual state of health until several weeks after discharge. Follow-up CT scan showed considerable pancreatic sequelae. Conclusion: Acute pancreatitis is an important cause of PD peritonitis. Negative dialysate cultures and unsatisfactory clinical response should trigger evaluation for acute pancreatitis and its multiple potential causes, including PD treatment itself. Serum lipase levels >3 times ULN and elevated dialysis fluid lipase can be expected. Timely performance of imaging is advisable. Prognosis can be poor, and close monitoring is recommended.

Peritonitis is a common complication of peritoneal dialysis (PD) [1]. Typical presentation comprises cloudy dialysate, elevated effluent leucocyte count, and variable degrees of abdominal pain and systemic inflammation [2]. Often, peritonitis in PD is caused by bacterial infection following touch contamination during catheter use [2]. However, enteric or culture-negative peritonitis due to acute pancreatitis might present very similar but requires very different diagnostic and therapeutic needs [3].

The contribution of this case report is to highlight and discuss three challenging aspects of acute pancreatitis in PD: first, when to look for acute pancreatitis in PD peritonitis? Second, diagnosing acute pancreatitis in PD patients, is it different? And finally, what are the causes of acute pancreatitis in PD patients?

A 74-year-old PD patient presented with cloudy dialysate and subtle symptoms of malaise and abdominal pain. For 4 days, he had been experiencing mild, non-cramping but slightly undulating, non-radiating pressing pain in the middle abdomen without exact localizability. There was no association with food intake; however, his appetite was markedly reduced. There was no nausea, heartburn, or belching, and bowel movements had been normal. He had been receiving PD treatment for 12 months as he suffered from end-stage kidney disease (ESKD) possibly due to cardiorenal syndrome and secondary focal segmental glomerulosclerosis caused by years of arterial hypertension (albumin/creatinine ratio of 0.5 g/g in spot urine). A renal biopsy had not been performed. He also suffered from coronary heart disease-induced heart failure with reduced ejection fraction. As he had considerable residual kidney function with an eGFR ranging from 7.5 to 12.3 mL/min/1.73 m2, his PD regimen consisted of a 2 L icodextrin dwell overnight with no further treatment during the day. With additional torsemide doses between 30 and 100 mg per day, normovolemia could be maintained. Seven days before presentation, he had finished a 14-day course of doxycycline due to a PD catheter exit site infection with Corynebacterium amycolatum.

On examination, his general condition was moderately reduced. He had fever (up to 38.8°C) and was hypotensive (97/63 mm Hg) and tachycardic (100 bpm). Abdominal examination was inconclusive with guarding on deep palpation being the only sign on initial presentation. There was no jaundice or Murphy’s sign. The exit site of the peritoneal catheter did not show any signs of inflammation, and an ultrasound examination of the catheter tunnel was unremarkable. Dialysis effluent appeared cloudy and contained 1,047 leucocytes/µL with 90% polymorphs. Parameters of PD treatment were otherwise unchanged. Serum white blood count was 26.000/µL (upper limit of normal [ULN] 9.600/µL), and C-reactive protein was 250 mg/L (ULN 5 mg/L) (Fig. 1). Aspartate aminotransferase (69 U/L), alanine aminotransferase (68 U/L), gamma-glutamyl transferase (125 U/L), and bilirubin (24 μmol/L) levels were mildly elevated; alkaline phosphatase (120 U/L) and serum amylase were normal. Urinalysis showed no leucocytes and no hematuria.

Fig. 1.

Course of inflammatory markers and serum lipase in relation to management. Diagnosis of PD peritonitis with CRP 250 mg/L and dialysate leucocyte count 1,047/μL. Diagnosis of acute pancreatitis via markedly elevated lipase (628 U/L, ULN 78 U/L) and abdominal CT scan. Note inflammatory markers before admission due to exit site infection treated with doxycycline. CRP, C-reactive protein.

Fig. 1.

Course of inflammatory markers and serum lipase in relation to management. Diagnosis of PD peritonitis with CRP 250 mg/L and dialysate leucocyte count 1,047/μL. Diagnosis of acute pancreatitis via markedly elevated lipase (628 U/L, ULN 78 U/L) and abdominal CT scan. Note inflammatory markers before admission due to exit site infection treated with doxycycline. CRP, C-reactive protein.

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Infectious peritonitis was presumed. Empirical antibiotic treatment was started (intraperitoneal cefazolin, loading dose 1,000 mg, 250 mg 4 times daily thereafter adding 3-day dwells with 1.5% glucose, plus gentamicin 50 mg once daily; vancomycin 2 g at day one and day four was added to our usual regimen due to the severely elevated inflammatory markers and the recent exit site infection), and the patient was admitted to hospital.

During the ensuing days, his condition deteriorated. Dialysate cultures remained negative (sampled on day 1, 4, 8, 14, 17, 28, and 36), and effluent leucocyte count remained high (Fig. 1). Clinically, no alternative inflammatory foci were identified, urinalysis was unremarkable, and blood and urine cultures remained negative. Abdominal ultrasound showed gallstones without signs of cholecystitis or obstructed bile ducts, and the pancreatic gland was not visible.

On day four, the clinical team decided to broaden the diagnostic approach as, despite broad antibiotic coverage, effluent cell count (910/μL) and C-reactive protein (202 mg/L) decreased unsatisfactorily, clinical condition did not improve, and dialysate cultures were still negative despite significant peritoneal and systemic inflammation. Differential diagnostic considerations with regard to possible causal factors of peritonitis particularly comprised inflammatory, infective, perforative, ischemic, or malignant gastrointestinal pathologies with consecutive, enteric peritonitis (e.g., appendicitis, diverticulitis, inflammatory bowel disease, abscesses, cholecystitis, pancreatitis, bowel obstruction, ischemia, colorectal cancer, or lymphoma). Diagnosis of acute pancreatitis was established on the basis of CT scan showing an enlarged pancreas surrounded by fluid collections (Fig. 2) and elevated serum lipase (628 U/L, ULN 78 IU/L) (Fig. 1). Effluent lipase level was reordered and was 15 IU/L (Table 1).

Fig. 2.

CT scan – diagnosis of acute pancreatitis. Notice enlarged pancreas with fluid collections.

Fig. 2.

CT scan – diagnosis of acute pancreatitis. Notice enlarged pancreas with fluid collections.

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Table 1.

Lipase in serum and peritoneal fluid in PD patients without acute pancreatitis as well as during an episode of acute pancreatitis according to the literature

AuthorPatients, nMean serum lipase, U/LPeritoneal fluid lipase, U/L
a Lipase in PD patients without acute pancreatitis 
Bruno et al. [4] (2000) n = 9 202 (81–460) All <10 
Masoero et al. [5] (1996) n = 28 259 (98–801), SD 177 All <10 
61%: 0–246 
29%: 247–492 
7%: 493–738 
3%: >738 
39% >ULN 
3% >3 × ULN 
Villacorta et al. [6] (2010) n = 5 (icodextrin) 70  
n = 5 (glucose) 95 
n = 10 (icodextrin) 52 
AuthorPatients, nMean serum lipase, U/LPeritoneal fluid lipase, U/L
a Lipase in PD patients without acute pancreatitis 
Bruno et al. [4] (2000) n = 9 202 (81–460) All <10 
Masoero et al. [5] (1996) n = 28 259 (98–801), SD 177 All <10 
61%: 0–246 
29%: 247–492 
7%: 493–738 
3%: >738 
39% >ULN 
3% >3 × ULN 
Villacorta et al. [6] (2010) n = 5 (icodextrin) 70  
n = 5 (glucose) 95 
n = 10 (icodextrin) 52 
AuthorEpisodes, nSerum lipase, U/LPeritoneal fluid lipase, U/L
b Lipase in PD patients during episode of acute pancreatitis 
Lankisch et al. [12] (2008)* n = 9 (in 9 patients) All episodes >3 × ULN  
Bruno et al. [4] (2000)** n = 9 (in 7 patients) Mean 5,450 (849–13,100) Median 253 (1–21.950) 
>10 in 7/9 episodes 
Quraishi et al. [13] (2005)*** n = 20 (in 20 patients) Mean 1.060  
Villacorta et al. [6] (2010) n = 10 (in 5 patients) All episodes >3 × ULN  
Our data** n = 1 628 (ULN 78) 15 
AuthorEpisodes, nSerum lipase, U/LPeritoneal fluid lipase, U/L
b Lipase in PD patients during episode of acute pancreatitis 
Lankisch et al. [12] (2008)* n = 9 (in 9 patients) All episodes >3 × ULN  
Bruno et al. [4] (2000)** n = 9 (in 7 patients) Mean 5,450 (849–13,100) Median 253 (1–21.950) 
>10 in 7/9 episodes 
Quraishi et al. [13] (2005)*** n = 20 (in 20 patients) Mean 1.060  
Villacorta et al. [6] (2010) n = 10 (in 5 patients) All episodes >3 × ULN  
Our data** n = 1 628 (ULN 78) 15 

ULN, upper limit of normal.

*6 PD patients and 14 HD patients. Only attacks without identifiable cause were included.

**One case with missing serum lipase level.

***Serum lipase levels were taken at time of admission.

Disentangling etiological factors of the acute pancreatitis was challenging. The patient had gallstones, consumed one cup of coffee with brandy daily (around 30 g of alcohol) without additional alcoholic beverages, was on long-term medication with torasemide and on doxycycline shortly before presentation, and was dialyzed with icodextrin. In addition, PD treatment itself may have been a contributory factor. Serum calcium (corrected by albumin) and serum lipids were normal; parathyroid hormone was within target range.

Antibiotic therapy was stopped at the end of day four. To exclude icodextrin as a potential cause, it was switched to a 4th dwell of glucose 1.5%. As clinical condition did not improve after 2 more days, PD treatment was paused completely (the patient had sufficient residual kidney function). Monitoring of effluent leucocyte count was continued using single 3-h glucose 1.5% dwells every other day. Intake of alcoholic beverages was stopped on admission.

The patient’s condition slowly improved. During the prolonged hospital stay, the patient suffered several complications: an episode of congestive heart failure exacerbation triggered by peritonitis-induced increased resorption of glucose dwells (4 kg weight gain in 2 days with matching considerable reductions in ultrafiltration) and tachycardic atrial fibrillation, an episode of acute gout during restoration of normovolemia, and a weight loss of 2 kg (compared to his weight at admission) due to multifactorial loss of appetite. Systemic and effluent markers of inflammation took 4 weeks to normalize (Fig. 1), and the patient did not regain his usual state of health until several weeks after discharge. Follow-up CT scan after 6 weeks showed considerable pancreatic sequelae (a pseudocyst, calcification, parenchymal necrosis, Fig. 3). Ten weeks later, PD with icodextrin was restarted without complications (Fig. 1). Long-term follow-up yielded one infective peritonitis (Staphylococcus aureus) and four further episodes of peritonitis due to acute pancreatitis despite complete cessation of alcohol consumption and cholecystectomy that was performed after the second episode of pancreatitis. The decision for cholecystectomy was based on the patient’s recurrent and increasingly debilitating episodes of pancreatitis with known gallstones and thus increased likelihood of obstruction. While intermittent bile duct obstruction due to sludge or microlithiasis remained a possible cause throughout the patient’s entire history, CT scans, endosonography, and MRCP had never been suggestive of a lithogenic (post-)obstructive etiology. Our diagnostic work-up did not reveal hypertriglyceridemia, hypercalcemia, viral hepatitis, human immunodeficiency virus, ischemia, anatomic malformations or malignancies. However, we did not evaluate genetic, functional, or in-depth infectious causes of pancreatitis. Torasemide, as a very rare possible cause of pancreatitis, was continued for volume control. Imaging studies, absence of maldigestion, and complete normalization of symptoms and lipase levels between episodes did not suggest chronic pancreatitis. After the fourth episode of pancreatitis, the patient was switched to hemodialysis, where he suffered another episode of pancreatitis 3 months later. With every episode of pancreatitis and worsening heart failure, general condition deteriorated. Cognitive performance and level of autonomy declined progressively, and the patient finally wished to discontinue kidney replacement therapy. He died 3 years after the initial episode of acute pancreatitis. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000539185).

Fig. 3.

CT scan – 6 weeks follow-up. Notice pancreatic parenchymal necrosis and pseudocyst (arrow).

Fig. 3.

CT scan – 6 weeks follow-up. Notice pancreatic parenchymal necrosis and pseudocyst (arrow).

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When to Search for Acute Pancreatitis in PD Peritonitis?

Bacterial infection is the leading cause of peritonitis in PD [1]. Peritonitis due to acute pancreatitis is considerably less frequent with only around 5.9 cases per 1,000 PD years [7]. However, acute pancreatitis-related peritonitis demands significantly different diagnostic and therapeutic strategies, and prognosis can be unfavorable [7]. Therefore, a discussion about when to search for acute pancreatitis in a PD peritonitis seems valuable. In light of our case, the following seems advisable: first, worsening clinical condition and persistent elevation or absence of considerable decrease of effluent leucocyte count beyond 3–5 days despite adequate empirical antibiotic treatment of suspected bacterial peritonitis (ideally <100/μL) [2] should trigger evaluation for alternative etiologies including acute pancreatitis. Second, lack of microbial growth from peritoneal cultures should trigger differential diagnostic considerations regarding non-infective or enteric etiologies. Third, the initial diagnostic approach should be broadened if a critical clinical condition does not allow for delayed diagnosis or treatment failure. Last, characteristic presentation of acute pancreatitis and its causes (jaundice, colored urine, belt-like abdominal pain, Murphy’s sign, etc.) should prompt evaluation for acute pancreatitis and existing risk factors for acute pancreatitis (gallstones, regular consumption of alcoholic drinks, suggestive personal, familial, or drug history, etc.) should always be given careful consideration.

Diagnosing Acute Pancreatitis in PD Patients: Is It Different?

Serum Pancreatic Enzymes

The diagnosis of acute pancreatitis in general relies considerably on elevated serum lipase levels. Although a consensus on a clear cut-off level has not been reached [8, 9], serum lipase levels of at least 3 times the ULN are considered diagnostic if clinical course and/or imaging studies are suggestive [10, 11].

The main difference in patients with CKD or ESKD is that baseline serum lipase levels are often elevated. An Italian study with 246 participants showed serum lipase levels above 3 times the ULN in 10% of HD, 3% of CKD, and 3% of PD patients [5]. A Dutch study, analyzing 241 person-years, found a mean serum lipase level in PD patients of 202 U/L ranging between 81 and 460 U/L [4] (Table 1).

However, if there is acute pancreatitis in PD patients, serum lipase level will most probably be considerably higher than the elevated baseline values (Table 1). Evidence from cohort studies and case series suggests serum lipase level above the 3 times ULN in the majority of cases: a Germany study detected 9 episodes of acute pancreatitis in 3,386 PD patients with all serum lipase levels above the 3 times ULN (one case with missing values) [12]. A Dutch case series investigated 7 PD patients with 9 episodes of acute pancreatitis and found mean serum lipase level of 5,450 U/L (range 849–13,100 U/L) [4]. A US case-control study in HD and PD patients found mean serum lipase level of 1,060 IU/L during episodes of acute pancreatitis without an identifiable cause [13]. Villacorta et al. [6] followed 213 PD patients for 13 years identifying 10 episodes of acute pancreatitis in 5 patients with serum lipase levels all exceeding the 3 times ULN cut-off.

In line with this literature, we found lipase levels well above the 3 times ULN cut-off of our laboratory (ULN = 78 IU/L), specifically 628, 404, 455, 345, and 248 IU/L at day 4, 5, 15, 23, and 29, respectively. The considerable elevation of serum lipase significantly contributed to establishing the diagnosis of acute pancreatitis.

Serum amylase plays a minor role in the evaluation of acute pancreatitis in PD. This is due to its well-known disadvantages of shorter half-life and reduced specificity compared to serum lipase. Furthermore, falsely low results due to interaction of icodextrin with the polysaccharide reagent of amylase detection assays are well described. A false decline in amylase levels of up to 90% can be seen [6, 14]. In an amylase detection assay not based on polysaccharide but on p-nitrophenol maltoheptaoside, no significant interference with icodextrin was detected [15].

Dialysate Pancreatic Enzymes

In the Dutch case series cited above, all of the randomly selected PD patients without acute pancreatitis showed dialysate amylase and dialysate lipase levels below 30 and 10 U/L, respectively. During acute pancreatitis (7 patients with 9 attacks, dialysate enzymes available from 8 attacks), dialysate amylase concentrations were 30, 30, 30, 33, 62, 130, 616 and 1,229 U/L. The authors concluded that dialysate amylase levels above 100 U/L are highly suggestive of acute pancreatitis. Dialysate lipase levels during acute pancreatitis were 1, 15, 46, 144, 361, 561, 1.336, and 21.950 U/L [4] (Table 1). It should be mentioned that PD regimen and timing of sampling substantially influence concentration of dialysate enzyme concentrations. Furthermore, very high levels of dialysate pancreatic enzymes should raise the suspicion of damage to the pancreatic duct system with pancreatic ascites. We found dialysate lipase level of 15 IU/L at day 5 which made the presence of pancreatic ascites unlikely.

Clinical Presentation

Reliably discriminating pancreatic versus infectious origins of PD peritonitis solely by clinical symptoms and signs seems impossible [3]. In addition, we are not aware of data, showing that the presentation of acute pancreatitis is different in PD versus non-PD patients. In both populations, a variety of gastrointestinal and/or systemic complaints are reported [6, 8]. In our case, symptoms and signs were non-specific and comparably subtle despite considerable pancreatic affection (CT scan) and slow clinical recovery.

Imaging Studies

As regards appropriate imaging studies, we do not see major differences between diagnostic strategies for suspected acute pancreatitis in PD and non-PD patients. Considering the diagnostic challenges of acute pancreatitis in PD peritonitis, the valuable properties of ultrasound and CT scan should be appreciated. Ultrasound, despite limitations of pancreatic visibility and its operator dependency, is readily available at the bedside and cost-effective, and can deliver valuable information, e.g., about the biliary tract. CT scan provides over 90% sensitivity and specificity and is a recommended imaging modality in the evaluation of acute pancreatitis [8, 9, 11]. If radiation or contrast agents are of concern, non-enhanced magnetic resonance imaging is an excellent alternative, providing similar sensitivity, specificity, and accuracy with advantages in detecting lithiasis and hemorrhage [11, 16]. Timely execution of imaging studies can be important as diagnosing acute pancreatitis in PD peritonitis without imaging can be a challenge. Furthermore, delayed diagnosis might be disadvantageous and edematous enlargement of the pancreatic gland may return to normal within a few days [4]. In our case, the CT scan was crucial in establishing the diagnosis.

What Are the Causes of Acute Pancreatitis in PD Patients?

PD patients seem to carry an increased risk of acute pancreatitis. Bruno et al. [4] compared the incidence of acute pancreatitis in Dutch PD patients to the incidence in the general population. Investigating 241 patient-years, a very high standardized risk ratio of 249 (95% CI: 114–473) was found. A large study from Taiwan using national health insurance data compared 9,766 PD patients to 114.386 age- and sex-matched controls and found an adjusted HR of 7.47 (95% CI: 6.48–8.62; p < 0.001) [17]. Compared to data from 18.841 HD patients, the adjusted HR was 1.41 (95% CI: 1.21–1.65). In a retrospective US study of 160 PD patients with a follow-up of 5 years, Quraishi et al. [13] found an adjusted HR of 3.94 (p = 0.006) compared to HD patients.

It is difficult to attribute the increased incidence of acute pancreatitis in PD to specific etiologic factors as most of the studies do not investigate or report risk factors or possible causes. Furthermore, the low absolute incidence of acute pancreatitis in PD limits the interpretation of the relative frequency of causes. In addition, control groups are often lacking.

Bruno et al. [4] investigated risk factors for acute pancreatitis in 7 patients suffering 9 attacks. In 4 out of the 7 patients, more than one known or potential risk factor for acute pancreatitis was present (choledocholithiasis, alcohol, hypercalcemia, hypertriglyceridemia, medication, history of transplantation, history of peritonitis, concomitant peritonitis). However, no single etiologic factor or combination of risk factors accounted for the increased incidence [4]. During a 13-year follow-up of 213 PD patients, Villacorta et al. [6] found 10 episodes of acute pancreatitis in 5 patients. Two patients suffered from cholelithiasis, one had severe hyperparathyroidism, and in the remaining two, one of whom had 6 pancreatitis episodes, no possible cause was found. Lankisch et al. [12] described 9 episodes of acute pancreatitis in 3,386 PD patients. Causes were reported to be biliary (3 patients) and alcohol-associated (1 patient). In 5 patients (56%), no etiologic factor was detected. Chen et al. [7] looked at national health insurance claims data of 67.078 HD and PD patients. Independent risk factors for acute pancreatitis in this ESKD population (HD plus PD) were being female, being elderly (>65 years old), having biliary stones or liver disease, and being on PD.

In summary, evidence of etiologic factors driving the increased incidence of acute pancreatitis in PD is scarce. It is therefore difficult to determine whether a single factor or a specific combination of causes accounts for the increased incidence of pancreatitis in PD patients.

The suggestion that PD itself could be a significant risk factor for acute pancreatitis does originate not only from the increased incidence compared to the general population and to HD patients, but also from pathophysiological considerations (high intra-abdominal pressure, high level of uremic toxins, non-physiological dialysate fluid potentially causing local toxicity/irritation, premature activation of proteolytic pancreatic enzymes, or local hypercalcemia) [4, 13]. In addition, episodes of acute pancreatitis with no identifiable risk factor other than PD are well described [6, 12]. However, further research is warranted to better understand the significance of the various PD-associated potential causes of pancreatitis.

An association between acute pancreatitis and the polyglucose PD solution icodextrin has been reported in several case reports [18‒20]. In contrast, in a large study by Wang et al. [17] investigating 9,766 PD patients, icodextrin was associated with a reduced incidence of acute pancreatitis showing an adjusted HR of 0.59 (95% CI = 0.47–0.73). However, cited results from detailed case reports cannot be neglected. Regarding our case, as clinical condition deteriorated, we opted to address any potential cause of acute pancreatitis and therefore temporarily suspended icodextrin. As re-exposure did not immediately re-trigger acute pancreatitis, and as much more likely risk factors like gallstones and alcohol were present for a prolonged period of time, we did not assume that icodextrin played a significant part in the origin of acute pancreatitis in our patient. The repeated attacks of pancreatitis in the follow-up even after performing a cholecystectomy and after stopping the alcohol intake make it more likely that PD treatment per se could have been the cause of the pancreatitis attacks. However, there was also a recurrence under hemodialysis. Genetic, auto-immune, or rare infectious etiologies were not investigated.

In summary, several population-based studies provide solid evidence that PD patients suffer from an increased incidence of acute pancreatitis. However, evidence of causal relationships is scarce. It is not known if the increased incidence is driven by a single risk factor or a combination of causes. Also, the possible impact of PD treatment itself remains to be quantified. Case studies suggest icodextrin as a risk factor for acute pancreatitis, although this observation was not confirmed in larger cohorts. With regard to our case, awareness of acute pancreatitis as an important differential diagnosis in a PD patient with peritonitis seems valuable. Timely evaluation using serum lipase level and CT scan is advisable if dialysate cultures remain negative, and clinical condition deteriorates or does not allow for treatment failure. Comparing individual patient’s lipase level in serum and dialysis fluid to the literature (Table 1) supports the diagnostic process. Finally, our case suggests that in polymorbid PD patients with acute pancreatitis, particular attention to malnutrition and adequate long-term support of convalescence are to be recommended. Recurrent episodes with inconclusive work-up warrant evaluation of less frequent etiologies.

We are grateful for the thorough work of Katrin Pellmann, who provided invaluable support with regard to peritoneal dialysis patient care.

On December 21, 2012, the Winterthur Cantonal Hospital was granted general authorization by the Federal Expert Commission on Professional Secrecy in Medical Research to disclose professional secrecy within the meaning of Article 321 of the Swiss Penal Code for research purposes in the field of medicine and healthcare. The responsible Ethics Committee for Winterthur Cantonal Hospital is the Zurich Cantonal Ethics Committee, Switzerland. Ethical approval is not required for this study in accordance with local or national guidelines. Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images on March 26, 2018, prior to his passing away.

The authors declare that there are no potential financial or non-financial competing interests with regard to evaluation, interpretation, and publication of this clinical case.

For our case report, there was no funding involved.

Simeon Schietzel was involved in clinical care of the patient and wrote the manuscript. Luzia Nigg was involved in clinical care or the patient, supplemented the clinical follow-up of the case, and reviewed the manuscript. Jane Rippin was involved in the clinical care of the patient and reviewed the manuscript.

All data which are important for the comprehensibility of the case are contained in the manuscript. Further data that support the findings of this case report are not publicly available due to content overload reasons but are available from the corresponding author upon reasonable request.

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