Abstract
Perinephric myxoid pseudotumor of fat (PMPF) is a rare and highly heterogeneous disease consisting of mature fat, myxoid stroma with spindled or stellate stromal cells histologically. Here, we present 2 cases of PMPF occurring in an allograft and a native kidney, and a systematic review that included 120 previously reported cases was subsequently conducted. Notably, 89% of PMPF cases with documented medical history had comorbidities. The most common comorbidities were urologic neoplasm (45%), chronic kidney disease (23%), allograft kidney (16%), and urinary tract obstruction (5%). We propose a classification of PMPF based on comorbidities and discovered that patients with concomitant urologic neoplasm or obstruction tended to have significantly smaller tumors, and active surveillance of PMPF after treating the primary disease might be an appropriate approach. In contrast, for patients with kidney transplants, chronic kidney disease, or no identifiable primary disease, the tumors were generally larger; therefore, surgical intervention should be considered. Regardless of the classification method used, for tumors exhibiting a slow growth rate, active surveillance should be considered. Our findings aimed to facilitate more accurate differential diagnosis and optimize treatment options.
Index Words: allograft kidney, chronic kidney disease, perinephric myxoid pseudotumor of fat, urinary tract obstruction, urologic neoplasm
Pseudosarcomatous fibroblastic/myofibroblastic proliferation in perinephric adipose tissue was first described by Tanas et al,1,2 who reported an unexpectedly high incidence of up to 20% in a consecutive case series. In 2019, Dashti et al3 introduced the term perinephric myxoid pseudotumor of fat (PMPF) and proposed that it may be associated with nonneoplastic renal diseases. To date, approximately over 100 PMPF cases have been reported globally, nearly all sporadic. Typically, PMPF lacks specific symptoms beyond compression, with similarities to both benign and malignant fat-containing tumors. As a very rare disease, standardized treatment guidelines do not exist. Pathology is the gold standard for the diagnosis of PMPF.
Given the rarity, diagnostic complexity, and clinical implications of PMPF, we present 2 new cases at our institution and retrospectively review 120 published cases, aiming to elucidate clinicopathologic features, propose a new classification, and identify diagnostic pitfalls.
Methods
Ethical approval was waived because no new research on humans or animals was conducted. Informed consent was obtained in accordance with institutional guidelines.
The PubMed database was systematically searched for all English articles through February 2025, using the keywords “PMPF” or “perinephric myxoid pseudotumor of fat.” When analyzing comorbidities, patients with a history of kidney transplantation who developed PMPF were analyzed separately from those with chronic kidney disease (CKD).
Results
Case 1
A 54-year-old male with a history of immunoglobulin A nephropathy, kidney transplantation 21 years ago, and subsequent graft failure (2017) on hemodialysis was admitted in December 2024 for an incidentally discovered lower abdominal mass present for 1 year. Positron emission tomography/computed tomography (PET/CT) revealed a mass with mildly heterogeneous fluorodeoxyglucose uptake (SUVmax 3.95) in the allograft area (Fig 1A-C). Biopsy revealed a spindled mesenchymal tumor with low cellularity and inflammatory infiltrates, but well-differentiated liposarcoma could not be radiologically excluded. Follow-up CT demonstrated interval growth from 16.0 cm × 10.0 cm (July 2024, Fig 1D and E) to 16.5 cm × 11.1 cm (December 2024, Fig 1F and G).
Figure 1.
Case 1(A) Positron emission tomography/computed tomography (PET/CT) scan suggested a mass with a mildly inhomogeneous increase in glucose metabolism with an maximum standardized uptake value of 3.95. PET/CT images in axial, coronal, and sagittal planes showed a hypermetabolic lesion in the allograft kidney, suggesting high metabolic activity. (B) Corresponding noncontrast CT scan images in axial, coronal, and sagittal views demonstrated the anatomic structure of the renal mass with heterogeneous density. (C) Fused PET/CT scan images in axial, coronal, and sagittal planes clearly localized the hypermetabolic activity to the mass observed on CT scan, providing both metabolic and anatomic correlation. (D) Axial T1-weighted images in July 2024 suggested a 15.0 cm × 10.0 cm × 16.0 cm mass with a slightly hypointense signal. (E) Axial T2-weighted images with fat saturation showed that the mass was hyperintense. (F) Enhanced CT scan in December 2024 showed an increased size of 16.5 cm × 11.1 cm of the mass in the arterial phase. (G) Enhanced CT scan in December 2024 (venous phase). (H) The gross specimen of the tumor was irregularly shaped, with a maximum diameter of about 17 cm, and a grayish, partly mucoid cut surface. (I) The tumor showed expansive growth with an intact capsule and no clear infiltrative border (Δ) (hematoxylin and eosin, scale bar = 1.25 mm). (J) The tumor is mainly composed of adipocytes, myxoid stroma with spindled or stellate stromal cells (hematoxylin and eosin, scale bar = 200 μm). (K) Spindle-shaped tumor cells are arranged in bundles, with long oval nuclei, uniform chromatin, and with no nuclear pleomorphism or atypia (hematoxylin and eosin, scale bar = 100 μm). (L) Immunohistochemistry showed CD34 positive (scale = 200 μm). (M) Desmin is weakly positive. (N) Murine double minute 2 negative (scale bar = 200 μm). (O) S100 negative (scale bar = 200 μm).
Surgery was recommended after discussion by a multidisciplinary team because of the tumor’s size, growth, and uncertain malignancy. The patient underwent allograft nephrectomy plus right iliac lymph node dissection in December 2024.
The irregular mass measured up to 17 cm (Fig 1H). Microscopically, it had an intact capsule without infiltration and consisted mainly of adipocytes, myxoid stroma, and spindle or stellate stromal cells with no nuclear pleomorphism or pathologic nuclear atypia (Fig 1I and J). Spindle-shaped tumor cells were arranged in bundles (Fig 1K). All 6 lymph nodes showed reactive hyperplasia. Immunohistochemistry was positive for smooth muscle actin, CD34, desmin (weak), CD117, P16, and CD10 but negative for epithelial (pan-cytokeratin), neural (S100), melanocytic (human melanoma black 45), and negative for tumor-specific markers, including estrogen receptor, P53, cyclin-dependent kinase 4, signal transducer and activator of transcription 6, mucin 4, and murine double minute 2 homolog (MDM2), thereby excluding these differential diagnoses (Fig 1L-O). Fluorescence in situ hybridization revealed no MDM2 gene amplification and no significant monoallelic loss of Rb1, supporting the final diagnosis of PMPF.
Case 2
A 43-year-old male was incidentally found with a 1.9 cm × 1.6 cm fat-density nodule anterior to the upper right ureter without hydronephrosis (Fig S1A). He had no other comorbidities. A follow-up CT scan 1 month later showed no significant size change (Fig S1B). The mass was resected and appeared gray-yellow with a smooth, lobulated surface. Immunohistochemistry staining was positive for CD34, S100, and MDM2, focally positive for cyclin-dependent kinase 4, and negative for P16, smooth muscle actin, human melanoma black 45, Melan-A (melanocytic marker), and transcription factor E3 (tumor-specific marker). Fluorescence in situ hybridization revealed no MDM2 gene amplification or CDK4 gene amplification. The final diagnosis was PMPF.
Retrospective Review of 120 PMPF Cases
Basic Clinical Characteristics
We analyzed 120 patients from 15 studies and the 2 present cases3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 2, 15, 16 (Tables S1 and S2). PMPF was more frequently seen in males (76.40%, 68/89), with an average age of 66.51 years (Table 1). Lesions occurred throughout the retroperitoneum, most commonly in native or allograft kidney, and nearly half were multiple masses (44.44%, 16/36). Among all patients (N=120), biopsy was performed in 47 patients (39.2%, 47/120); PMPF was correctly diagnosed in 42 cases (89.4%, 42/47) (including 6 cases that underwent biopsy alone, and 8 cases subsequently underwent surgical management), while failed biopsy cases (10.64%, 5/47) all required subsequent surgery. Overall, 65 patients (54.17%, 65/120) underwent surgery, most commonly nephroureterectomy (36.92%, 24/65). Interestingly, 31 patients were incidentally diagnosed during renal tumor surgery. The pathologic features of PMPF are summarized in Table S3.
Table 1.
Baseline Characteristics of All Patients With Perinephric Myxoid Pseudotumor of Fat
| Features | Case/Value (Mean ± SD) | Percentage |
|---|---|---|
| Chief complaint | ||
| Incidental (including transplant evaluation) | 6 | 50.00 |
| Pain or discomfort | 4 | 33.33 |
| Hematuria/microhematuria | 2 | 16.67 |
| Underlying renal disease | ||
| Renal transplantation | 15 | 12.50 |
| Chronic kidney disease | 21 | 17.50 |
| Urologic neoplasm | 42 | 35.00 |
| Obstruction | 5 | 4.17 |
| No underlying renal disease | 10 | 8.30 |
| NA | 27 | 22.50 |
| Gender | ||
| Male | 68 | 76.40 |
| Female | 21 | 23.60 |
| Age, y | 66.51 ± 12.67 | |
| Lateral | ||
| Left kidney | 18 | 32.14 |
| Allograft kidney | 15 | 26.79 |
| Right kidney | 10 | 17.86 |
| Bilateral | 8 | 14.29 |
| Periureter | 3 | 5.36 |
| Pelvic | 2 | 3.57 |
| Tumor burden | ||
| Single | 20 | 55.55 |
| Multiple | 16 | 44.44 |
| Size of the largest mass | 5.17 ± 5.57 cm | |
| Other complication | ||
| DM | 11 | 9.17 |
| Cancer (except for urologic cancer) | 5 | 4.17 |
| HTN | 5 | 4.17 |
| Renal cyst | 4 | 3.33 |
| BPH | 4 | 3.33 |
| PKD | 2 | 1.67 |
| Biopsy | ||
| Diagnostic | 42 | 89.36 |
| Nondiagnostic | 5 | 10.64 |
| Procedure | ||
| Nephroureterectomy | 24 | 33.80 |
| Nephrectomy | 15 | 21.13 |
| Resection | 12 | 16.90 |
| Allograft nephrectomy | 9 | 12.68 |
| Biopsy | 6 | 8.45 |
| Excision | 4 | 5.63 |
| Partial nephrectomy | 1 | 1.41 |
| Latent vs overt manifestationa | ||
| Type 1 (overt type) | 75 | 62.50 |
| Type 2 (latent type) | 31 | 25.83 |
| NA | 14 | 11.67 |
| Follow-up | 13.0 (3.0, 30.5) mo | |
| Survival outcome | ||
| ANED | 31 | 25.83 |
| DOC | 16 | 13.33 |
| AWOD | 4 | 3.33 |
| NA | 69 | 57.50 |
Abbreviations: ANED, alive with no evidence of disease; AWOD, alive with other disease; BPH, benign prostate hyperplasia; DM, diabetes mellitus; DOC, died of other causes; HTN, hypertension; NA, not applicable/not available; PKD, polycystic kidney disease; SD, standard deviation.
Cases with clinical symptoms or imaging changes were defined as overt; those detected using pathology without clinical symptoms or detectable using imaging were defined as latent.
Comorbidities of PMPF
Notably, among patients with available medical histories (n=93), 89.24% of patients (83/93) presented with documented comorbidities: urologic neoplasm (42/83, 50.6%), CKD (21/83, 25.3%), kidney allograft (15/83, 18.1%), and urinary tract obstruction (5/83, 6.0%). Differential analysis revealed that patients with comorbid tumors were significantly older than those with comorbid kidney allograft (Table 2, Fig S2A), and tumor size was significantly smaller in patients with urologic neoplasm or obstruction (Fig S2B).
Table 2.
Differential Analysis of Underlying Renal Diseasea
| Variable | Renal Transplantation (n=6) | Chronic Kidney Ddisease (n=14) | Urologic Neoplasm (n=28) | Obstruction (n=5) | No Underlying Renal Disease (n=10) | P Value |
|---|---|---|---|---|---|---|
| Age, y, mean ± SD | 55.00 ± 7.92 | 69.36 ± 12.44 | 71.50 ± 10.78 | 60.75 ± 12.97 | 67.33 ± 12.20 | 0.021 |
| Size of largest mass, cm, mean ± SD | 7.60 ± 3.39 | 8.27 ± 4.80 | 1.75 ± 2.01 | 1.96 ± 2.28 | 8.30 ± 5.96 | <0.001 |
| Gender, n (%) | 0.276 | |||||
| Female | 2 (33.33) | 1 (7.14) | 8 (28.57) | 2 (40.00) | 1 (10.00) | |
| Male | 4 (66.67) | 13 (92.86) | 20 (71.43) | 3 (60.00) | 9 (90.00) | |
| Tumor burden, n (%) | 0.446 | |||||
| Single | 1 (16.67) | 5 (35.71) | 0 (0.00) | 0 (0.00) | 1 (10.00) | |
| Multiple | 5 (83.33) | 5 (35.71) | 2 (7.14) | 1 (20.00) | 3 (30.00) |
Abbreviations: SD, standard deviation.
A total of 63 cases with complete data were included in the statistical analysis.
Classification of PMPF
Based on the initial imaging results of PMPF (n=106), patients can be classified into 2 subtypes (Table S4):
-
(1)
Type 1 (overt type, CKD/healthy-dominant subtype) (n=75, 70.8%): tumors detected using imaging and characterized by concomitant CKD, kidney transplantation, or no comorbidities, usually with larger tumor size (mean, 8.05 cm);
-
(2)
Type 2 (latent type, mass-effect/obstruction subtype) (n=31, 29.3%): patients whose tumors were incidentally discovered during pathologic evaluation for other diseases and associated with urologic neoplasms or obstruction with smaller tumors (mean 1.23 cm, Fig S2C).
Subtype distribution differed significantly across comorbidity groups (Fig S2D), with further analyses of native/allograft kidney, tumor burden, and comorbid tumors shown in Tables S5-S7.
Discussion
PMPF is extremely rare, with approximately 120 cases reported worldwide. Diagnosis based on imaging alone is challenging because of its heterogeneity, ranging from single or multiple, unilateral or bilateral, cystic or solid lesions.1,5,6,9,14 Magnetic resonance imaging provides superior enhancement evaluation compared with CT.5 All reported cases showed T2 hyperintensity, with variable T1 signal (hypointense or isointense).5,6,9,14 For patients with kidney failure, contrast-enhanced ultrasound can help differentiate solid from cystic masses via enhancement patterns.6,9 Fluorine-18 fluorodeoxyglucose PET/CT demonstrating low uptake in PMPF may help differentiate it from hypermetabolic malignancies like liposarcoma, suggesting it is not significantly hypermetabolic.5,14,17 Monitoring tumor growth rate helps differentiate PMPF from malignant retroperitoneal liposarcoma. Although variable, PMPF growth typically exceeds that of most renal tumors but remains slower than liposarcomas (Fig S2E). Radiologic misdiagnosis may occur because PMPF extensively infiltrates renal sinusoidal adipose tissue rather than forming isolated nodules,7 suggesting its true incidence is likely underreported.
Pathologic examination is the gold standard when imaging is inconclusive. Immunoglobulin G4–positive plasma cells, MDM2 amplification, and DNA damage-inducible transcript 3 fluorescence in situ hybridization help exclude immunoglobulin G4–related disease, liposarcoma, and mucinous liposarcoma, respectively.1, 2, 3,18 In about 10% of previously reported cases, biopsy failed to diagnose PMPF, resulting in repeated biopsy procedures or switching to resection.
Although the exact etiology of PMPF remains unknown, its pathogenesis is widely believed to be related to renal inflammation or neoplasia.7 Our study found that nearly 90% of patients had comorbid conditions involving nephrologic or urologic diseases, possibly due to cytokines, chemokines, and growth factors secreted by tumor cells acting on stromal fibroblasts, which promote changes in the extracellular matrix to form myxoid stroma.11 A possible association with immunosuppressive therapy should also be considered because patients with the “overt” type were often comorbid with CKD or had histories of renal transplantation, commonly involving immunosuppression,19 highlighting the need for regular monitoring in individuals under immunosuppressive therapy.
Notably, PMPF arising in renal transplants often demonstrates distinct growth and imaging patterns compared with the native kidneys. First, patients with allograft renal PMPF were typically younger, with tumors presenting as an infiltrative mass involving the renal sinus of the transplanted kidney, especially the transplant vessels, and less frequently the perirenal space, without identifiable fat.5 Notably, PMPF manifests much later than typical posttransplant malignancies, occurring more than 20 years after transplantation in 3 of 4 reported cases.20 These findings suggest that PMPF may have a longer latency than typical posttransplant malignancies, highlighting the importance of long-term abdominal imaging surveillance in kidney recipients even after graft failure.
Although PMPF is indolent and does not affect overall survival, its management must consider both the primary disease and the tumor growth rate. Tumors classified as the “overt” type are typically large at diagnosis with rapid growth, often necessitating proactive surgery. However, many cases in this category are associated with CKD, so surgical planning should carefully consider renal function preservation. “Latent” PMPF management focuses on primary diseases. Active surveillance may be considered as a treatment option for PMPF alone, following benign renal tumor protocols with CT scans every 3-6 months initially, then annually. Finally, regardless of the type, biopsy has high but imperfect accuracy for diagnosing PMPF (Fig 2).
Figure 2.
Overview of 2 subtypes of perinephric myxoid pseudotumor of fat (PMPF). Significant differences between the 2 subtypes of patients in terms of the size of the largest mass and underlying renal disease. Among the ‘overt’ type, there are different imaging manifestations between the native kidney and the allograft PMPF. This classification method may guide the selection of treatment regimens.
In summary, this study proposed a PMPF classification into clinical subtypes to guide management, warranting future research for further elucidation.
Conclusion
PMPF is a rare benign condition frequently associated with comorbidities. Based on the initial imaging presentation, we propose a 2-subtype classification: type 1 (overt subtype), characterized using larger, faster-growing tumors often requiring surgery, and type 2 (latent subtype), consisting of smaller incidental lesions suitable for active surveillance.
Article Information
Authors’ Full Names and Academic Degrees
Xu Shi, MD, Yuxi He, MD, Xiuya Zhou, MD, Zhang Zhang, MD, Ling Nie, MD, Xingming Zhang, MD, and Hao Zeng, MD
Author Contributions
XS and YH participated in research design and in the performance of the research. ZZ and LN participated in the pathological diagnosis of this case. XZ and HZ participated in research design and in the performance of the research. Each author contributed important intellectual content during manuscript drafting or revision and accepts accountability for the overall work by ensuring that questions pertaining to the accuracy or integrity of any portion of the work are appropriately investigated and resolved.
Support
None.
Financial Disclosure
The authors declare that they have no relevant financial interests.
Acknowledgments
We sincerely thank the patients for consenting to share their clinical information in this case report.
Data Sharing
The data supporting the findings of this study are provided in the supplementary materials accompanying the article. All data have been deidentified to protect patient privacy. Additional details derived from published literature are openly available in the public domain and can be accessed through the cited references within the article. No new software, custom code, or algorithms were developed for this study.
Patient Protections
The authors declare that they have obtained informed consent from the patients reported in this article for publication of the information about them that appears within this Case Report.
Peer Review
Received July 08, 2025. Evaluated by 2 external peer reviewers, with direct editorial input from an Associate Editor and the Editor-in-Chief. Accepted in revised form September 23, 2025.
Footnotes
Complete author and article information provided before references.
Figure S1. Radiographic data of case 2.
Figure S2. Classification, comorbidities, and tumor growth rate of PMPF.
Table S1. Clinical Features of Allograft Kidney in Patients With PMPF
Table S2. Clinical Features of Native Kidney in Patients With PMPF.
Table S3. Overview of the Pathologic Features of Previously Reported PMPF Cases
Table S4. Differential Analysis of Latent Versus Overt Manifestation
Table S5. Differential Analysis of Native/Allograft Kidney
Table S6. Differential Analysis of Tumor Burden
Table S7. Differential Analysis of Different Comorbid Tumor Types
Contributor Information
Xingming Zhang, Email: jarmin@scu.edu.cn.
Hao Zeng, Email: kucaizeng@163.com.
Supplementary Material
Figures S1 and S2; Tables S1-S7
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Associated Data
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Supplementary Materials
Figures S1 and S2; Tables S1-S7