Diagnostic odyssey and therapeutic challenges in a renal transplant recipient with Pneumocystis jirovecii pneumonia: a case report

Introduction

Recipients of solid organ transplants (SOTs) face a significantly heightened risk of secondary infections due to prolonged corticosteroid and immunosuppressant use to prevent organ rejection. Pulmonary infections are the most prevalent among these, mainly opportunistic, and may involve mixed infections with other opportunistic pathogens (1). Pneumocystis jirovecii pneumonia (PJP) is an opportunistic pulmonary infection caused by Pneumocystis jirovecii, especially in immunocompromised individuals like patients with human immunodeficiency virus (HIV), chemotherapy recipients, and SOT recipients (2). Trimethoprim/sulfamethoxazole (TMP/SMX) is the recommended first-line treatment and prophylactic drug (2). This article reports a case of PJP that developed 4 months post-kidney transplantation in a patient who did not receive PJP prophylaxis due to documented TMP/SMX allergy. Upon admission, empirical therapy was initiated with caspofungin (a second-line anti-PJP agent). Following confirmed diagnosis, immediate TMP/SMX desensitization was performed alongside standard treatment. Throughout the clinical course, therapeutic drug monitoring (TDM) guided dose adjustments of both TMP/SMX and caspofungin. Later stages involved differential diagnosis and management of graft rejection versus infection. The patient ultimately achieved full recovery and was discharged. While PJP prophylaxis at 6 months post-transplant is now a consensus practice, implementation gaps may occur due to regional healthcare disparities or clinical decision-making variations. This case report details the management of a severe PJP infection in a TMP/SMX-allergic recipient, aiming to enhance clinical and pharmaceutical practitioners’ understanding of clinical management for such patient populations with significant pathophysiological alterations and provide practical clinical insights for similar scenarios. We present this article in accordance with the CARE reporting checklist (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-22/rc).

Case presentation

A 34-year-old male office worker was admitted to the hospital. Four months earlier, he underwent an allogeneic kidney transplant at Renji Hospital due to uremia and stage 5 chronic kidney disease (CKD). The surgery was successful, resulting in a postoperative urine output of 1,500–2,000 mL/day and a serum creatinine level of 150 µmol/L (53–115 µmol/L). Following kidney transplantation, the patient previously received postoperative prophylaxis with TMP/SMX 80/400 mg once daily for 5 days. Therapy was discontinued due to generalized rash with concomitant progressive eosinophilia (peak: 5×10⁹/L; reference range, 0.02–0.52 ×10⁹/L). Following discontinuation of TMP/SMX, the rash resolved and eosinophil count gradually returned to normal range. No further PJP prophylaxis was administered prior to this hospital admission. Postoperatively, he was maintained on long-term oral immunosuppressive therapy with tacrolimus 2 mg twice daily and mycophenolate mofetil 750 mg twice daily. At the time of transplant, prednisone 15 mg once daily was initiated, which was then tapered by 5 mg weekly until reaching a maintenance dose of 5 mg once daily. One week before admission, he developed a sore throat and dry cough following an upper respiratory illness, accompanied by occasional shortness of breath and a maximum body temperature of 39.2 ℃. The local hospital suspected influenza and empirically treated him with oseltamivir (75 mg) twice daily for 5 days. However, his symptoms did not improve. He was admitted to Renji Hospital transplant department for further evaluation and treatment. The patient had no history of diabetes, heart disease, or familial genetic disorders, and denied any history of infectious diseases, including hepatitis or tuberculosis. He reported allergies to sulfonamides and cephalosporins.

Upon admission, the physical examination showed a temperature of 39.2 ℃, a respiratory rate of 28 breaths/min, a heart rate of 98 beats/min, and blood pressure of 148/85 mmHg. Lung auscultation indicated diminished breath sounds with scattered fine crackles, but no wheezing or other notable abnormalities. Blood tests showed hemoglobin of 120 g/L (120–160 g/L), platelets of 299×10⁹/L (100–300 ×10⁹/L), white blood cells of 10.71×10⁹/L (4.0–10.0 ×10⁹/L), neutrophil percentage of 89.5% (40–75%), and absolute neutrophil count of 9.58×10⁹/L (2.0–7.5 ×10⁹/L). Infection-related markers: C-reactive protein (CRP) 43.7 mg/L (<10 mg/L), procalcitonin (PCT) 0.08 ng/mL (<0.05 ng/mL), (1,3)-β-D-glucan- 1313.4 pg/mL (<60–80 pg/mL). Respiratory virus panel, influenza virus, cryptococcal latex agglutination, and sputum smear were all negative. Immune-related markers: Absolute lymphocyte count 0.65×10⁹/L (1.1–3.2 ×10⁹/L), regulatory T cells 1.18% (5–10%), CD4⁺ Th cells 23.8% (30–60%), total T cell count 406.3 cells/µL (700–2,200 cells/µL), total Ts cell count 228.9 cells/µL (190–1,140 cells/µL), total Th cell count 154.7 cells/µL (410–1,590 cells/µL), CD4/CD8 ratio 0.68 (1.0–3.0). Arterial blood gas analysis: pH 7.303 (7.35–7.45), P/F: 206 mmHg (>300 mmHg), PCO₂ 42 mmHg (35–45 mmHg), HCO₃⁻ 22.1 mmol/L (22–28 mmol/L), BE −3.1 mmol/L (−2.0 to +2.0 mmol/L), lactate 2.6 mmol/L (0.9–1.7 mmol/L). Diffuse infiltrates are observed along the hilar regions in both lungs in Chest computed tomography (CT) (Figure 1).

Figure 1 Chest CT imaging on day 1. Diffuse infiltrates are observed along the hilar regions in both lungs. CT, computed tomography.

After admission, the patient underwent renal ultrasound, which showed no elevation in the renal vascular resistance index. The tacrolimus concentration was 5.2 ng/mL. Laboratory tests indicated low absolute lymphocyte count, suggesting an immunosuppressed state. Therefore, tacrolimus and mycophenolate mofetil were discontinued, and methylprednisolone 40 mg once daily was initiated. Oxygen was administered via a face mask at 8 L/min, and anti-infective therapy with levofloxacin 500 mg once daily and caspofungin 50 mg once daily was initiated immediately for suspected PJP. However, the patient’s etiological tests like cytomegalovirus and Epstein-Barr virus DNA, sputum culture, blood culture, and serum galactomannan, all came back negative during the first four days after admission. The patient’s febrile course was characterized by sustained peak temperatures of 39.5 ℃ (103.1 ℉) without diurnal variation, while his oxygenation index decreased from 130 to 80 mmHg, and his respiratory rate increased from 28 to 35 breaths/min. A repeat chest CT scan indicated worsening pulmonary infiltrates (Figure 2).

Figure 2 Chest CT imaging on day 4. The chest CT shows bilateral diffuse interstitial changes with increased exudation compared to before. CT, computed tomography.

On the fourth night of hospitalization, the patient was unable to lie flat, exhibited significant shortness of breath, and presented with a predominantly dry cough without sputum or hemoptysis. Consequently, he was transferred from the general ward to the intensive care unit (ICU), and his oxygen delivery was upgraded to a high-flow nasal cannula (HFNC). On the sixth day of hospitalization, fiberoptic bronchoscopy with bronchoalveolar lavage was performed. Specimens were submitted for Gomori methenamine silver staining, as well as metagenomic next-generation sequencing (mNGS) of whole blood and bronchoalveolar lavage fluid (BALF). All results indicated the presence of Pneumocystis jirovecii (Figure 3), with 523 reads found in the blood sample and 17,593 reads in the BALF sample. Pneumocystis jirovecii was confirmed via mNGS of blood and BALF. Consequently, the patient was diagnosed with PJP.

Figure 3 The patient underwent a fiberoptic bronchoscopy examination. (A) Bronchoscopy revealed extensive congestion and edema of the airway mucosa. (B) Giemsa staining demonstrated Pneumocystis jirovecii cysts.

The patient reported a history of sulfonamide allergy, although the specifics were not detailed. A rapid sulfonamide desensitization test was successfully conducted under the supervision of a clinical pharmacist (refer to Table 1 for the protocol). The patient was subsequently administered TMP/SMX 240/1,200 mg per dose, three times daily, and levofloxacin was discontinued.

During hospital days six through nine, the patient continued to exhibit a persistent fever with daily peaks of 39.5 ℃ (103.1 ℉), accompanied by a marked increase in respiratory rate to 45 breaths/min. Bedside chest X-rays indicated worsening pulmonary infiltrates, prompting the initiation of non-invasive positive pressure ventilation at 14/8 cmH₂O. The patient’s oxygenation index decreased to 60 mmHg, while the peak serum concentration of SMX was 78.348 mg/mL, below the normal range of 100–150 mg/mL. On hospital day ten, the dosage of TMP/SMX was escalated to 320/1,600 mg administered orally four times daily. During hospital days 10 to 17, serial bedside chest radiographs continued to indicate progressive pulmonary infiltrates (Figure 4). Concurrently, the patient developed refractory hypoxemia necessitating endotracheal intubation and invasive mechanical ventilation (IMV). The subsequent peak concentration of SMX was 144.763 mg/mL, achieving the target level.

Figure 4 Serial portable chest radiographs from days 6 to 16.

The patient’s inadequate response to treatment was attributed to: (I) prolonged use of corticosteroids and immunosuppressants, resulting in persistent immune suppression, necessitating enhancement of the patient’s immune status; (II) rapidly progressing respiratory failure with impaired oxygenation correction. PJP frequently causes spontaneous pneumothorax and mediastinal emphysema, requiring appropriate respiratory support techniques and increased respiratory assistance.

On hospital day 19, the treatment regimen was escalated to veno-venous extracorporeal membrane oxygenation (VV-ECMO) coupled with IMV. Methylprednisolone 40 mg was administered intravenously once daily, and TMP 320 mg was given orally four times daily. The peak TMP/SMX concentration under VV-ECMO was 98.45 mg/mL, which was below the target level. Caspofungin 70 mg was administered intravenously once daily. Thymalfasin 1.6 mg was given intramuscularly once daily, but the lymphocyte count did not increase significantly. On hospital day 23, the thymalfasin dosage was increased to 1.6 mg twice daily.

On hospital day 24, the patient developed ventilator-associated pneumonia (VAP) due to carbapenem-resistant Pseudomonas aeruginosa. The endotracheal tube was removed, and the patient was transitioned to VV-ECMO combined with HFNC for respiratory support. Intravenous piperacillin-tazobactam [sensitive, minimal inhibitory concentration (MIC) 4 mg/mL] at 4.5 g every 6 hours and amikacin (sensitive, MIC 2 mg/mL) at 800 mg once daily were administered. After 28 days of hospitalization, the patient was successfully liberated from VV-ECMO. Five days post-decannulation, oxygen therapy was de-escalated to face mask delivery. Following four additional days of observation in the step-down unit, the patient was transferred to the general ward. Given the immunocompromised status, a graded sulfamethoxazole de-escalation protocol was implemented to reduce relapse risk, transitioning to maintenance prophylaxis with TMP/SMX 160/800 mg orally three times daily. After one week of this regimen, the dosage was tapered to TMP/SMX 160/800 mg twice daily. The patient remained clinically stable throughout this period and is now pending discharge.

On hospital day 46, the patient developed recurrent fever with temperatures peaking at 38.3 ℃ (100.9 ℉) persisting for 3 days. He did not exhibit shortness of breath, back pain, or abdominal pain. Urine output was 1,200–1,500 mL/day, slightly reduced from previous levels. Lung auscultation indicated decreased breath sounds with scattered fine wet rales, but no wheezing. The heart rhythm was regular, and the abdomen was soft without tenderness. Chest CT demonstrated improvement in pulmonary infiltrates (Figure 5). Bedside ultrasound revealed an enlarged transplanted kidney with a high resistance index. Repeated immune markers showed: absolute lymphocyte count at 0.27×10⁹/L, CD3⁺ Th cells at 83.1%, CD4⁺ Th cells at 51.7%, absolute T cell count at 224.4 cells/µL, absolute Ts cell count at 82.3 cells/µL, absolute Th cell count at 139.6 cells/µL, and a CD4/CD8 ratio of 1.70. The patient’s serum creatinine level was 346 µmol/L. Sonographic evaluation revealed normo-sized kidneys with unremarkable vascular resistive indices. Percutaneous renal biopsy was deemed clinically unwarranted. The whole blood trough concentration of tacrolimus was quantified at 1.8 ng/mL. The recurrent fever was attributed to organ rejection, and the patient was treated with intravenous methylprednisolone 200 mg every 12 hours for 3 days, along with oral tacrolimus 2 mg twice daily.

Figure 5 Chest CT imaging on day 45. It demonstrated improvement in pulmonary infiltrates during episodes of recurrent fever. CT, computed tomography.

The patient’s temperature normalized, and urine output increased to 1,500–2,000 ml/day. Serum creatinine decreased to 150 µmol/L. On hospital day 58, the patient was discharged in stable condition following comprehensive recovery, with prescriptions for tacrolimus 2 mg every 12 hours, mycophenolate mofetil 0.75 g every 12 hours, and prednisolone 10 mg once daily, all administered orally (Figure 6).

Figure 6 Treatment timeline. HFNC, high-flow nasal cannula; ICU, intensive care unit; LFNC, low-flow nasal cannula; LVX, levofloxacin; NIV, noninvasive ventilation; TMP/SMX, trimethoprim/sulfamethoxazole; VV-ECMO, veno-venous extracorporeal membrane oxygenation.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

PJP primarily affects immunocompromised hosts and represents the most common opportunistic infection and cause of acute respiratory failure in patients with HIV (3). However, with the increasing prevalence of solid organ transplantation in recent years, the incidence of PJP in this population has risen steadily (4). Kidney transplant recipients are at high risk for PJP due to long-term immunosuppressive therapy. Epidemiological studies indicate that among patients without prophylaxis, PJP incidence ranges from 5–15% (5,6), predominantly occurring 3–6 months post-transplant (the peak immunosuppression phase), with mortality rates reaching 12–43% (7,8). Consequently, the Branch of Organ Transplantation of the Chinese Medical Association guidelines mandate TMP/SMX prophylaxis during months 1–6 after solid organ transplantation (9). However, due to confirmed TMP/SMX hypersensitivity, PJP prophylaxis was not administered in this patient. Characteristic symptoms include progressive dyspnea, nonproductive cough, fever, and hypoxemia, with radiographic findings typically showing bilateral diffuse ground-glass opacities (9). Prognosis critically depends on early diagnosis: prompt initiation of TMP/SMX treatment increases survival rates to >90%, whereas delayed therapy may lead to respiratory failure or death. Survivors may develop sequelae such as pulmonary fibrosis (9). Major risk factors include: CD4⁺ T-lymphocyte count <200 cells/µL, intensive immunosuppressive regimens (e.g., antithymocyte globulin or high-dose corticosteroids), prior PJP history, concurrent cytomegalovirus infection, and acute rejection within 6 months post-transplant (9,10).

The diagnosis of PJP depends on clinical symptoms, imaging, pathogen detection, and serology. Typical chest CT findings show bilateral or diffuse ground-glass opacities (11). In non-HIV patients, early imaging findings may be subtle, making pathogen detection crucial for diagnosis. Traditional PJP detection methods involve microscopic examination of lower respiratory tract specimens for trophozoites and cysts using Grocott’s methenamine silver or toluidine blue staining, both highly sensitive (3). mNGS is increasingly used in PJP diagnosis for its sensitivity, efficiency, and rapid turnaround time (11). Serological tests, including β (1,3)-D-glucan and CD4⁺ T cell counts, also assist in diagnosing PJP (12). In this case, the patient exhibited a sore throat, dry cough, and fever 4 months post-kidney transplantation, with no improvement following empirical antibacterial therapy. The patient rapidly progressed to respiratory failure, consistent with the clinical course documented in the literature. Chest imaging, immune monitoring, and pathogen detection in lower respiratory tract and blood samples confirmed a diagnosis of PJP.

TMP/SMX continues to be the primary treatment for PJP (13). TMP and SMX inhibit dihydrofolate reductase and dihydrofolate synthetase, respectively, thereby blocking tetrahydrofolate metabolism and exerting a bacteriostatic effect. For moderate to severe PJP, intravenous administration is advised, transitioning to oral therapy once the patients’ condition stabilizes and gastrointestinal function is restored (14).

For adult patients with a creatinine clearance exceeding 30 mL/min, the recommended dosage is TMP 15–20 mg/kg/day and SMX 75–100 mg/kg/day, administered in 3 or 4 divided doses either intravenously or orally, over a period of 3 weeks (15). As TMP/SMX is the most effective treatment for PJP, if a patient has an unclear history of sulfonamide allergy, desensitization is recommended. However, if the patient has a severe allergy history, such as Stevens-Johnson syndrome or toxic epidermal necrolysis, TMP/SMX or desensitization therapy should not be used (16). The patient self-reported a sulfonamide allergy with unclear details. To prevent severe allergic reactions, our department, guided by a clinical pharmacist, implemented a stepwise incremental desensitization protocol prior to administering the conventional therapeutic dose (see Table 1 for the specific process). Desensitization therapy must be conducted under inpatient or outpatient observation, with approximately 180 mL of water consumed after each dose of TMP/SMX. The use of glucocorticoids and antihistamines should be avoided during desensitization (16).

A position paper jointly published in Intensive Care Medicine (ICM) by the European Society of Intensive Care Medicine (ESICM), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), International Association of Therapeutic Drug Monitoring and Clinical Toxicology (IATDMCT), and International Society of Antimicrobial Chemotherapy (ISAC) in 2020 does not advocate routine TDM of TMP/SMX. However, TDM becomes imperative in critically ill patients due to altered pathophysiology, hemodynamic instability, and the effects of extracorporeal life support devices such as ECMO (17). For this patient with microbiologically confirmed PJP but suboptimal therapeutic response, TMP/SMX concentration monitoring was warranted to evaluate pharmacokinetic/pharmacodynamic (PK/PD) target achievement. TDM may enhance clinical efficacy and minimize adverse reactions (17). This approach aligns with critical care standards for severe infection management. Hughes recommends a target Cmax of 100–150 mg/L for sulfonamides in the treatment of PJP (18). A retrospective analysis of 60 PJP patients identified initial Cmax levels outside the target range as risk factors for clinical failure and 28-day all-cause mortality (19). In this case, following desensitization, the patient received oral TMP/SMX at 240/1,200 mg three times a day for 3 days. However, the daily maximum body temperature remained at 39.5 ℃, the peak respiratory rate was 45 breaths/min, and the oxygenation fraction was 60 mmHg. The peak concentration of SMX was 78.348 mg/mL, below the target blood concentration. Consequently, the dosage of TMP/SMX was increased to 320/1,600 mg four times daily orally, resulting in a steady-state peak concentration of 144.763 mg/mL.

Second-line treatments for PJP include combinations such as primaquine with clindamycin, pentamidine, dapsone, and atovaquone. Reports also suggest using echinocandins in combination. Caspofungin, the most common echinocandin antifungal, disrupts fungal cell wall structure, causing PJ cyst rupture and inhibiting hyphae formation. It acts rapidly, reducing cyst load but not inhibiting trophozoite formation. Caspofungin was significantly less effective in second-line treatment than in first-line treatment in terms of both the mortality rate and response rate, so it is not recommended alone (20-22). Furthermore, a study of 248 HIV patients with PJP showed that caspofungin combined with TMP/SMX had higher response rates, in-hospital survival, and lower all-cause mortality compared to TMP/SMX alone (23). Consequently, the patient received a first-line regimen of TMP/SMX and caspofungin, achieving synergistic anti-PJP effects and favorable outcomes. However, large-sample prospective studies are needed to confirm true efficacy. Additionally, severe PJP patients often require comprehensive treatment. Glucocorticoids are effective in reducing pulmonary edema and exudation, demonstrating proven efficacy in HIV patients with PJP (24). For non-HIV PJP patients, treatment should be individualized based on the patient’s specific condition (25,26). A meta-analysis by Ding et al. indicated that glucocorticoids significantly decrease mortality in non-HIV PJP patients with hypoxemia. Consequently, prednisone is recommended for acute PJP cases with PaO₂ <70 mmHg (27).

Two critical limitations existed in this case management. (I) Failure in PJP prophylaxis: during the high-risk period (6 months post-kidney transplant), secondary prophylaxis (e.g., clindamycin plus primaquine) should have been initiated given the patient’s TMP/SMX allergy (20). The absence of any prophylactic intervention substantially elevated the risk of PJP infection. (II) Delayed recommencement of immunosuppression: postponed assessment for restarting immunosuppressants directly triggered allograft rejection. Transplant recipients require dynamic balancing of antimicrobial and immunomodulatory therapies; delayed evaluations risk irreversible complications.

Conclusions

PJP is a prevalent infection during the early post-operative period in kidney transplant recipients, typically occurring within 1–6 months post-surgery. Diagnosis necessitates a combination of clinical symptoms, imaging, pathogen identification, and laboratory tests for prompt treatment. Treatment strategies should be promptly adjusted based on changes in the patient’s clinical symptoms, alongside immune indicators and sulfonamide drug concentration monitoring, to ensure individualized and precise treatment, thereby achieving satisfactory clinical outcomes.

Acknowledgements

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-22/rc

Peer Review File: Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-22/prf

Funding: This work was supported by the Project of the Key Laboratory of Multiple Organ Failure, Ministry of Education (Nos. 2023KF07 and 2024KF03) and the Key Laboratory of Intelligent Pharmacy and Individualized Treatment in Huzhou City (No. HZKF-20240101).

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-22/coif). Y.Y. serves as the Editor-in-Chief of Journal of Emergency and Critical Care Medicine from September 2024 to August 2026. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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