Diffuse Large B-cell Lymphoma in a Patient With Refractory Perinephric Fluid Collection and Pleural Effusion: A Case Report

Abstract

Perinephric fluid collections have a broad differential diagnosis and may be difficult to characterize by imaging or fluid analysis. Diffuse large B-cell lymphoma (DLBCL) typically presents as mass-like lesions in nodal or extranodal sites but may rarely present as isolated fluid collections. We report a 53-year-old woman with acute right flank pain after minor trauma. Imaging showed a large right perinephric fluid collection extending into the retroperitoneum and pleural cavity without an identifiable mass. Fluid studies and lymphangiography did not identify a clear underlying etiology. Despite intervention for persistent high-output drainage, the patient developed prolonged fever and was ultimately diagnosed with DLBCL following biopsy of a newly developed cheek lesion. This case highlights an atypical presentation of DLBCL in a patient with a persistent perinephric fluid collection and underscores the importance of considering malignancy in unexplained, refractory fluid collections.

Introduction

Perinephric spaces consist of the anterior and posterior pararenal, perirenal, and subcapsular compartments, where fluid may accumulate due to several pathological conditions, including hemorrhagic, purulent, serous, urinary, lymphatic, or pancreatic fluid collections. Although these collections can be detected using CT or ultrasound, differentiating their underlying causes based on imaging alone is often challenging [1,2].

Fluid analysis may assist in determining the origin of fluid collections and guide management [3]. However, even with combined radiologic and biochemical evaluation, the underlying etiology may remain indeterminate in certain cases.

In such situations, systemic diseases, including hematologic malignancies, should be considered. Diffuse large B-cell lymphoma (DLBCL) is one of the most common non-Hodgkin lymphomas and is characterized by marked clinical and biological heterogeneity, with frequent extranodal involvement and the ability to affect virtually any organ system. Presentations may range from nodal masses to diffuse infiltrative disease or, rarely, atypical non-mass-forming manifestations [4,5].

This case highlights the diagnostic challenge of persistent perinephric fluid collections with an initially unclear etiology in a patient subsequently diagnosed with DLBCL.

Case presentation

Initial presentation

A 53-year-old woman presented to the emergency department with sudden, right-sided flank pain on April 22. She reported receiving water spa sessions three days prior to symptom onset, during which water jets were directed at her flank region. She denied fever, weight loss, night sweats, gross hematuria, or gastrointestinal symptoms, although she reported generalized fatigue. She had no significant past medical history and no family history of lymphoma or leukemia. She had worked as a press operator in the printing industry for more than 20 years. There was no history of hepatitis B, hepatitis C, human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), or human T-lymphotropic virus type 1 (HTLV-1). She was in otherwise good health and was not taking any regular medications. Initial blood tests were unremarkable. Contrast-enhanced computed tomography (CECT) of the abdomen revealed a right perinephric fluid collection with bilateral retroperitoneal and pelvic fluid collections, without contrast extravasation or abnormal enhancement (Figure 1).

Figure 1. Axial contrast-enhanced CT performed after double-J stent placement showing a right perinephric fluid collection (white arrow).

A moderate right-sided pleural effusion with associated atelectatic changes was also noted (Figure 2).

Figure 2. Coronal CT image showing right pleural effusion with lower lobe atelectasis (yellow arrow) and heterogeneous left renal cortical changes (white arrow).

The cortical findings were nonspecific at the time of presentation.

No lymphadenopathy was identified. A traumatic urinoma was initially speculated due to the presumed injury, and a double-J stent was placed.

Initial management and diagnostic evaluation

Ten days later, the patient developed dyspnea and returned for evaluation. Laboratory investigations, including complete blood count, basic metabolic panel, liver function tests, and urinalysis, were all unremarkable. Imaging showed persistent fluid collections. Thoracentesis revealed low pleural fluid protein (0.5 g/dL; exudative threshold >3 g/dL) and LDH (46 U/L; exudative threshold >200 U/L), suggesting a transudative pattern [6]. Cytology was negative for malignancy.

Refractory high-output drainage

Due to persistent fluid accumulation, a perinephric pigtail drainage catheter was placed, and the double J stent was removed on May 9. Fluid analysis showed a creatinine level of 0.41 mg/dL with a corresponding serum creatinine of 0.41 mg/dL (fluid-to-serum ratio = 1; fluid creatinine > serum creatinine or fluid creatinine ≥30 mg/dL suggests urinary leak). Triglyceride was <10 mg/dL, below the threshold for chylous effusion (>100 mg/dL). Protein was elevated at 112 g/L, higher than values typically seen in transudative or uncomplicated infectious effusions (>10 g/L), consistent with a protein-rich fluid collection [7]. Given the high protein content, a non-chylous lymphatic origin was speculated, but subsequent lymphangiography demonstrated no evidence of leakage. The patient continued to produce high-output drainage (>1500 mL/day) for several weeks. Therefore, sclerotherapy and glue injection were performed, reducing output to approximately 300 mL/day. Follow-up imaging demonstrated interval changes in the fluid collections with fibrotic changes consistent with post-sclerotherapy effects (Figure 3).

Figure 3. Follow-up CT after sclerotherapy showing interval renal and perirenal changes.

Follow-up CT after sclerotherapy demonstrates interval changes in fluid collections with post-sclerotherapy fibrotic changes (yellow arrow) and heterogeneous renal cortical changes (white arrows), as compared with Figure 2. These findings were later reviewed after the diagnosis of diffuse large B-cell lymphoma in conjunction with FDG-PET/CT (Figure 4).

FDG-PET/CT: fluorodeoxyglucose-positron emission tomography/computed tomography

Figure 4. FDG-PET/CT demonstrating multifocal hypermetabolic lesions.

FDG-PET/CT images showing abnormal radiotracer uptake in multiple sites. A hypermetabolic focus is seen in the left renal cortex (white arrow) and in the right perirenal region corresponding to the prior intervention site (yellow arrow). Additional hypermetabolic lesions are present in the left cheek, left nasal cavity, left cervical lymph nodes, and left adrenal gland (not shown).

FDG-PET/CT: fluorodeoxyglucose-positron emission tomography/computed tomography

Persistent fever

Since June 6, the patient has developed intermittent low-grade fever. Drain culture grew Acinetobacter species sensitive to carbapenems, and the drain was removed due to minimal fluid production after sclerotherapy. Despite appropriate antimicrobial therapy, the patient continued to experience intermittent low-grade fever over the following months. Repeated evaluation, including infectious, autoimmune, and hematologic investigations, remained unrevealing, and bone marrow biopsy showed no evidence of malignancy.

During hospital admission for persistent fever of unclear origin in late October, the fever was noted to be more prominent in the afternoon and evening. At the same time, the patient reported a painless, enlarging nodule over her left cheek over the preceding weeks. An inflammatory nuclear imaging study demonstrated increased uptake in the left cheek region, which was further supported by single-photon emission computed tomography (SPECT). Fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) performed on November 9 revealed areas of increased uptake in the left cheek, left nasal cavity, left cervical lymph nodes, left adrenal gland, left renal cortex, and right perirenal region (Figure 4).

Final diagnosis

Excisional biopsy of the left cheek lesion was performed, and histopathological examination on November 21 confirmed diffuse large B-cell lymphoma, non-germinal center B-cell subtype. Immunohistochemistry revealed tumor cells positive for CD20, bcl-2, bcl-6, and MUM1 and were negative for CD3, CD10, CD5, CD30, HHV8, cyclin D1, and EBV. The proliferative index was high, with a Ki-67 of approximately 90%, and c-MYC was expressed in 30% of tumor cells.

An ENT evaluation was also performed due to a hypermetabolic focus on PET/CT in the left nasal cavity. A corresponding nasal lesion was identified, and a biopsy of this lesion confirmed DLBCL, concordant with the cheek lesion

The Ann Arbor staging was III at the time of diagnosis. The patient subsequently received six cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin hydrochloride (hydroxydaunorubicin), vincristine sulfate (Oncovin), and prednisone) chemotherapy over four months with intrathecal prophylaxis due to extranodal involvement of the facial region and concern for increased risk of central nervous system dissemination. She achieved remission following initial therapy. However, disease recurrence occurred approximately eight months later, requiring allogenic hematopoietic stem cell transplantation. She ultimately died from complications of septicemia one year after the transplant. The clinical course is summarized in Figure 5.

Figure 5. Timeline summarizing clinical presentation, diagnostic workup, interventions, and final diagnosis.

LDH, lactate dehydrogenase; WBC, white blood cell; NOS, not otherwise specified

Discussion

Why this case is unusual

This case is notable for presenting with a large perinephric fluid collection extending into the retroperitoneal and pleural cavities, associated with acute flank pain following a minor traumatic event. Initial imaging showed no discrete mass or lymphadenopathy, and fluid analysis demonstrated low creatinine and triglyceride levels with elevated protein content and negative cytology. Despite persistent drainage, no definitive structural or biochemical source was identified, making early diagnosis challenging.

Differential diagnosis

The differential diagnosis evolved over time. Urinoma was initially considered but became unlikely due to the absence of contrast extravasation and low fluid creatinine. Chylous leakage was also excluded, given the low triglyceride levels [5]. Lymphangiography was performed because non-chylous lymphatic leakage was suspected based on the high protein content and imaging findings. However, it failed to demonstrate a leak, and the mechanism underlying the persistent high-yield drainage remained unclear. Infection later developed, but did not fully explain the persistent drainage or clinical course. Malignancy was not initially suspected, given the absence of a discrete mass and nonspecific imaging findings, although it remained in the broader differential diagnosis in a refractory clinical course. These competing considerations reflect the diagnostic complexity of the case and the limitations of conventional imaging and fluid analysis in establishing a definitive diagnosis.

Atypical presentation of DLBCL

DLBCL is one of the most common non-Hodgkin lymphomas and typically presents with nodal or extranodal masses [6]. However, rare cases have been reported in which lymphoma presents predominantly as effusions without detectable masses, leading to delayed diagnosis [7].

The renal involvement of lymphoma is rare, accounting for approximately 0.7% of extranodal lymphomas, and often presents as renal masses or infiltrative disease [8,9]. Review of CT imaging demonstrated subtle heterogeneous left renal cortical attenuation (Figures 2, 3), which is nonspecific and may be seen in a variety of infiltrative or inflammatory conditions. These findings were not diagnostic at the time of presentation and lacked specificity for a definitive etiology [10]. Subsequent FDG-PET/CT (Figure 4) demonstrated multifocal hypermetabolic lesions involving the left renal cortex, cheek, cervical lymph nodes, adrenal gland, and right perirenal region, with biopsies of the cheek and nasal cavity lesions confirming DLBCL.

Based on these findings, tissue diagnosis from the kidney or retroperitoneal region may have been considered in retrospect. However, invasive diagnostic approaches were not pursued due to the absence of a discrete mass and the initial clinical suspicion of benign etiologies.

Conclusions

This case highlights an unusual clinical course of DLBCL in a patient with a refractory perinephric fluid collection of initially unclear etiology. At presentation, no discrete mass or systemic features suggestive of malignancy were present, which contributed to diagnostic difficulty. The diagnosis was ultimately established following evaluation for fever of unknown origin. Although a causal relationship between the perinephric fluid collection and the underlying lymphoma could not be determined, clinicians should consider a broad differential diagnosis for persistent perinephric fluid collections that do not respond to standard management, even when imaging and fluid analysis are nonspecific.