Does peritoneal dialysis predispose a diabetic patient to icodextrin-induced peritonitis?

Roman Fiedler1, Ingeborg Schneider2, Joerg Buchmann3, Bernd Osten1 and Thomas Langer4

1 Department of Nephrology and 2 Institute of Clinical Chemistry, Martin-Luther-University, Halle-Wittenberg, Halle, Germany 3 Institute of Pathology, Martha-Maria-Hospital Halle-Doelau, Halle, Germany 4 Department of Nephrology, St Elisabeth-Hospital Halle, Germany Email: roman.fiedler{at}medizin.uni\|[hyphen]\|halle.de

Sir,

The application of icodextrin solution is established in peritoneal dialysis (PD), especially in patients with loss of peritoneal ultrafiltration. Despite its effectiveness and safety in PD therapy, incompatibility or allergic reactions have been reported for icodextrin [15]. A sterile, icodextrin-associated peritonitis in diabetic PD patients has been frequently observed [3,5]. In the case we report, icodextrin induced a sterile peritonitis in a diabetic PD patient.

Case.

A 39-year-old male patient with end-stage renal disease due to type 1 diabetes had been treated since November 1997 with continuous ambulatory peritoneal dialysis (CAPD), applying four exchanges of 2 l each of glucose solution per day. In May 1999, his renal function declined and PD was subsequently increased to six exchanges per day. Starting in July 2000, to avoid caloric overload, icodextrin was used as overnight dwell instead of 3.86% glucose solution. In May 2001, peritonitis was diagnosed first by a cloudy outflow of dialysate. The patient had no other clinical symptoms such as fever, abdominal pain, purulent exit site, or tunnel infection. He reported dilute stools 2 days previously. At the onset of peritonitis, microscopic and microbiological analysis of the PD effluent revealed an increased cell count (557/µl) but no bacteria or fungi. During the course of several intraperitoneal and oral antibiotic treatments, the levels of proinflammatory marker cells (557–2491/µl), interleukin (IL)-6 (4232–11842 pg/ml), immunoglobulin (Ig)-G (0.15–0.25 g/l), protein loss (protein 1.4–3.4 g/l, albumin 0.9–1.9 g/l), and activation of coagulation (thrombin–antithrombin III complex) were markedly elevated in the PD effluent. Despite intensified antibiotic therapy the PD effluent remained cloudy. Based on further negative microbiological tests and only moderate elevations of blood leukocytes (<=12.3 GPt/l) and serum C-reactive protein (<=52 mg/l) we considered a connection between icodextrin and peritonitis. Therefore, on day 11, overnight exchanges with icodextrin were stopped. In the following 3 days, dialysate concentrations of inflammatory markers and protein loss decreased to normal values. To confirm the relationship between icodextrin and peritonitis, icodextrin was given again on day 22 with the patient's consent, and the inflammatory response monitored. The next day there again appeared a cloudy effluent with an increased cell count (baseline/re-exposure: 57/587/µl) and IL-6 (39/2086 pg/ml) in the dialysate. Microscopic and microbiological examination of the effluent demonstrated a decrease in the ratio of monocytes (from 71 to 45%) and lymphocytes (from 29 to 20%), an increase of neutrophiles (from 0 to 30%) and eosinophiles (from 0 to 5%), but no evidence of bacteria or fungi. An immediate allergic reaction (type I) could be excluded (Ig E <=19 kU/l). Four days after the single-dose re-exposure to icodextrin all parameters reverted to normal.

Comments.

Icodextrin solution can induce a sterile peritonitis in PD patients. Diabetic patients seem to be especially predisposed to an inflammatory reaction after icodextrin therapy—vide the frequent case reports. But the genesis of the peritonitis is not wholly clear. As in the examination of Reichel [5], in our case a neutrophilic zytotoxic peritonitis is predominant, in contrast to the icodextrin-associated lymphocyte stimulation in the case report of Heering [3]. If the unspecific immunological reaction (elevated neutrophilic reaction and IL-6 levels) is a consequence of an undetected infection, which only manifests in the presence of icodextrin, or of a preliminary stage of lymphocyte stimulation due to a type III allergic reaction against it, icodextrin should be further investigated.

References

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