Renal transplantation
Complications: Infection
Pneumocystis Jirovecii Pneumonia in Renal Transplant Recipients: A National Center Experience

https://doi.org/10.1016/j.transproceed.2013.02.107Get rights and content

Abstract

Background

Pneumocystis jirovecii pneumonia (PCP) represents an important cause of morbidity and mortality in kidney transplant recipients. In recent years an increasing number of PCP outbreaks have been reported worldwide.

Patients and Methods

We performed a retrospective study including the demographic, clinical, laboratory, and therapeutic parameters of all renal transplant recipients with PCP in Slovenia during the period from January 1, 2006, to December 31, 2011.

Results

At the end of the 2011, 13/601 (2.2%) kidney transplant recipients followed in our center experienced PCP. The median time from transplantation to development of disease was 17 months (range, 3–148). Three recipients had PCP during the first year after transplantation because of early trimethoprim and sulfamethoxazole (TMP-SMX) discontinuation; in 3, it was related to acute graft rejection treatment; and in 6, to cytomegalovirus (CMV) infection. Pneumocystis jirovecii was microbiologically confirmed in 10 recipients. In 10 of 13 patients serum concentrations of lactic acid dehydrogenase (LDH) were increased. In addition, serum concentrations of beta-d-glucan was determined in 9 cases was elevated in each one.

Conclusion

The incidence of PCP was low, most probably owing to prolonged (12 months) TMP-SMX prophylaxis. Premature TMP-SMX discontinuation in the first year after transplantation, treatment of graft rejection and CMV infection seemed to be risk factors for PCP. Elevated serum beta-d-glucan concentration was a better noninvasive indicator of P jirovecii infection than elevated serum LDH concentration. In cases with no microbiological conformation, beta-d-glucan and LDH concentrations were helpful to establish the diagnosis of PCP for early treatment.

Section snippets

Methods

This single-center, retrospective clinical study included all PCP cases from January 1, 2006, to December 31, 2011. TMP-SMX prophylaxis (80 mg/400 mg) was administered for 12 months after transplantation. The demographic, clinical, laboratory, and therapeutic parameters were retrospectively collected from the hospital's electronic and paper medical records.

Serum concentrations of creatinine, calcium, C-reactive protein (CRP), and lactate dehydrogenase (LDH) as well as the numbers of leukocytes

Results

As of December 31, 2011, 601 kidney transplant recipients were being followed in our center. From January 1, 2006, to December 31, 2008, we did not observe any proven PCP. From January 1, 2009, to December 31, 2011, we diagnosed PCP in 13 recipients (2.2%): 8 men and 5 women of overall mean age 49 ± 4 years. At the time of diagnosis, 12 recipients were prescribed cyclosporine or tacrolimus, mycophenolate mofetil, and methylprednisolone and 1, monotherapy with cyclosporine. All subjects had

Discussion

Over the last 3 years, the PCP incidence among our renal transplant recipients has increased, an observation consistent with reports from other transplant centers.1, 2, 3, 4, 5 Our observations may be explained by the large number of renal transplant recipients worldwide, their altered immunosuppressive status owing to newer drugs, better compliance and regular follow-up within hospital settings, combined with an higher rate of encounters and potential interhuman transmission of P jirovecii.5

References (18)

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