Published online Nov 27, 2026. doi: 10.4240/wjgs.124761
Revised: August 3, 2026
Accepted: September 9, 2026
Published online: November 27, 2026
Processing time: 141 Days and 20.1 Hours
Gastric metastasis of renal cell carcinoma (RCC) is rare clinically, often presenting with a prolonged interval (median 7-10 years) between initial diagnosis and meta
We report a 70-year-old man with advanced clear cell RCC (ccRCC) who developed gastric metastasis 10 years after initial radical nephrectomy. After adju
For advanced RCC, gastric metastasis should remain part of differential diagnosis even in the absence of gastrointestinal symptoms.
Core Tip: Gastric metastasis from renal cell carcinoma is exceedingly rare, with a median latency of 7-10 years after nephrectomy, making it prone to diagnostic oversight. We report a 70-year-old man who developed gastric fundus metastasis 10 years after radical nephrectomy for clear cell renal cell carcinoma. Despite a suspicious computed tomography finding misread as food residue three months earlier, the lesion was confirmed by endoscopic biopsy and resected via robot-assisted wedge gastrectomy. This case underscores that even without gastrointestinal symptoms, gastric metastasis must remain on the differential for advanced renal cell carcinoma patients with prior distant metastases.
- Citation: Gao TZ, Zheng CZ, Zhu KK, Wu XN, He CY, Lou YM, Liu XS. Gastric metastasis from renal cell carcinoma with a 10-year interval: A case report. World J Gastrointest Surg 2026; 18(11): 124761
- URL: https://www.wjgnet.com/1948-9366/full/v18/i11/124761.htm
- DOI: https://dx.doi.org/10.4240/wjgs.124761
Renal cell carcinoma (RCC) accounts for approximately 90% of all kidney cancers and represents the most common renal malignancy[1]. According to the Global Burden of Disease Study 2021, an estimated 387800 new cases of kidney cancer were diagnosed and 161200 deaths occurred worldwide in 2021, with the age-standardized incidence continuing to rise (average annual percent change +0.15% from 2000 to 2021)[2,3]. In China, kidney cancer incidence has nearly tripled over the past three decades, from 1.38 per 100000 in 1990 to 4.62 per 100000 in 2021, with approximately 65800 new cases annually[4]. Approximately half of all RCC patients present with metastatic lesions at initial diagnosis or during the disease course. The most prevalent metastatic sites include the lungs, lymph nodes, bones, liver, adrenal glands, and brain[5]. The prognosis of RCC metastasis varies: Patients with metastases to the liver, brain, or pleura exhibit the shortest median overall survival (OS) (< 18 months), whereas those with metastases to endocrine organs (pancreas, thyroid, and adrenal glands) have a more favorable prognosis (median OS > 27 months). Among the various target organs for late-stage RCC metastasis, gastric metastasis is rare, with a reported incidence of 0.2%-0.8% and typically manifests several years after nephrectomy (median interval approximately 6.7 years)[6]. Here, we report a case of gastric metastasis from RCC that was managed with robot-assisted surgical intervention, aiming to enhance the understanding of this disease entity and reduce the incidence of misdiagnosis.
A 70-year-old male was asymptomatic and was referred after a routine follow-up positron emission tomography (PET)/computed tomography (CT) revealed a mass in the gastric fundus. He denied nausea, vomiting, abdominal pain, abdominal distension, hematemesis, melena, or altered bowel habits.
The patient had been undergoing regular postoperative surveillance at our hospital without any specific complaints. The current PET/CT in June 2025 revealed a soft tissue density mass in the gastric fundus with mildly increased 18F-fluorodeoxyglucose (18F-FDG) uptake, representing a new finding compared with prior imaging studies and raising suspicion for metastasis. Following endoscopic biopsy with histopathological confirmation, the patient was admitted with a diagnosis of secondary gastric malignancy consistent with metastatic clear cell RCC (ccRCC) in August 2025.
The overall clinical timeline is illustrated in Figure 1. Ten years prior, he underwent radical nephrectomy for pathologically confirmed right RCC and received interleukin-2 as postoperative adjuvant therapy. In December 2021, he was diagnosed with recurrent RCC in the left renal pelvis and underwent partial nephrectomy. Postoperatively, he was prescribed oral pazopanib for a consecutive 12-month course and maintained regular follow-up thereafter. A whole-body PET/CT scan with 18F-FDG suggested recurrent left pelvic RCC (Figure 2A), complicated by suspicious metastatic lesions in the retroperitoneum (Figure 2B) and lungs (Figure 2C) during routine follow-up in December 2022. Consequently, he received penpulimab combined with axitinib as second-line therapy in January 2023. A follow-up re-evaluation in December 2023 revealed complete resolution of all recurrent and metastatic lesions. However, during this period, the patient developed hypocortisolism and hypothyroidism. After a comprehensive assessment of the patient’s clinical status, penpulimab injection and axitinib were discontinued.
The patient had a smoking history of > 30 years but had been abstinent for 10 years. There was no history of malignant tumors in three generations on either side of the family. There was no occupational exposure history. The patient had no known drug allergies.
On admission, vital signs were: Body temperature, 36.7 °C; pulse, 85 beats/minute; respiratory rate, 15 breaths/minute; blood pressure, 94/55 mmHg. Physical examination revealed a flat abdomen with several old surgical scars. The abdomen was soft and nontender, without rebound tenderness or guarding. The liver and spleen were not palpable below the costal margin, and no abdominal masses were detected. Examination of other systems was unremarkable.
Laboratory investigations revealed that tumor markers, including a-fetoprotein, carcinoembryonic antigen, carbohydrate antigen (CA) 125, CA19-9, ferritin, and prostate-specific antigen, were all within normal limits. Serum creatinine was 140 μmol/L and uric acid was 561 μmol/L; other hepatic and renal function parameters were unremarkable. Lymphocyte subset analysis showed an absolute lymphocyte count (CD45+) of 1465 cells/μL, an absolute T lymphocyte count of 781 cells/μL, an absolute helper/inducer T lymphocyte count (CD3+, CD4+) of 368 cells/μL, and an absolute B lymphocyte count (CD19+) of 87 cells/μL; all mildly decreased relative to the reference ranges.
During the patient’s regular follow-up in June 2025, whole-body PET/CT with 18F-FDG uptake measurement revealed a soft tissue density mass in the gastric fundus, which showed slightly increased FDG uptake (Figure 3A). A retrospective review of the prior regular outpatient follow-up records revealed that a suspicious patchy opacity in the gastric fundus had already been detected by CT in March 2025. At that time, the radiologist’s interpretation was possible food residue. This new lesion was confirmed to be gastric metastasis from RCC by endoscopy, which revealed a spherical mass approximately 4 cm in diameter in the gastric fundus (Figure 3B). On gastroscopy performed on July 5, 2025, the lesion appeared as an elevated mass with superficial erosion and friable mucosa prone to bleeding. Abdominal magnetic resonance imaging with diffusion-weighted imaging and contrast enhancement on July 23, 2025 confirmed a gastric fundus mass consistent with metastatic disease (Figure 3C). Pathological analysis of the biopsy specimens showed mucosal erosion accompanied by proliferation of granulation tissue, and typical cell clusters with clear cytoplasm were observed in the stroma, leading to a preliminary diagnosis of metastatic RCC (Figure 4A). A comprehensive immunohistochemical panel was performed on the biopsy specimen. Pathological immunohistochemical staining revealed positivity for PAX-8, CA IX, and CD10, and negativity for cytokeratin (CK) 7, which strongly supported the diagnosis of metastatic ccRCC.
A multidisciplinary team (MDT) consultation was convened to address two critical clinical questions: (1) Whether surgical resection of the gastric lesion was justified in the context of metastatic disease; and (2) How to safely manage the patient’s immunotherapy-related endocrinopathy perioperatively.
Endocrinology consultants evaluated the patient’s immunotherapy-induced adrenal insufficiency (basal cortisol < 1.0 μg/dL) and hypothyroidism. They recommended switching from oral prednisone to hydrocortisone (morning 20 mg, afternoon 10 mg) and emphasized the necessity of perioperative intravenous stress-dose hydrocortisone (100 mg every 8 hours) to prevent adrenal crisis. This endocrine optimization was a prerequisite for safe surgical intervention and directly enabled the subsequent resection.
A pathologist reviewed the gastric biopsy and performed an extended immunohistochemical panel: CK (pan)+, PAX-8+, vimentin+, CD10+, CA IX+, CK7-, CDX2-, TTF-1-, GATA-3-, and P40-. The combined immunophenotype (PAX-8+/CA IX+/CD10+/CK7-) was fully diagnostic of metastatic ccRCC and definitively excluded primary gastric adenocarcinoma, neuroendocrine tumor, and pulmonary metastasis, confirming that the lesion represented isolated oligometastasis rather than a second primary malignancy.
A radiologist characterized the gastric lesion as a well-circumscribed, 4.0 cm × 3.1 cm mass arising from the gastric fundus with predominant intraluminal protrusion. Critically, no perigastric lymphadenopathy, retroperitoneal disease, or other visceral metastases were identified. Cross-sectional imaging confirmed complete radiographic resolution of previously documented pulmonary metastases following systemic therapy. The solitary nature and accessible location of the lesion rendered it amenable to wedge resection.
A medical oncologist reviewed the patient’s treatment history, which comprised multiline systemic therapy including sunitinib, axitinib, and nivolumab plus cabozantinib. They noted that all nongastric metastatic sites had achieved durable disease control. The progressive gastric lesion thus represented an oligoprogressive site amenable to local therapy, while the remainder of the disease remained controlled. The team recommended surgical metastasectomy followed by continuation of immune checkpoint inhibitor (ICI) maintenance therapy (sintilimab).
The surgical decision was to integrate the above assessments. The MDT concluded that: (1) The gastric lesion was a resectable solitary oligometastasis with no competing visceral disease; (2) Perioperative endocrine risks could be mitigated through a structured steroid replacement protocol; and (3) Complete resection offered the potential for prolonged disease-free intervals consistent with the oligometastasectomy paradigm. Robot-assisted wedge gastrectomy with a 2-cm negative margin was planned, with close postoperative endocrinology co-management.
Postoperative pathological examination of the resected specimen confirmed gastric metastatic ccRCC (Figure 4B). Immunohistochemical staining of the surgical specimen demonstrated positivity for PAX-8, CA IX, and CD10, and negativity for CK7 (Figure 4C). The immunohistochemical profile of the gastric lesion demonstrated PAX-8 positivity, which is a lineage-specific transcription factor of renal tubular epithelium and is almost never expressed in primary gastric adenocarcinoma. Diffuse membranous carbonic anhydrase (CA) IX positivity indicated aberrant activation of the von Hippel-Lindau (VHL)/hypoxia-inducible factor-α (HIF-α) pathway; a molecular hallmark of ccRCC. CD10 positivity further supported proximal nephron origin. CK7 negativity effectively ruled out gastric, pancreatobiliary, and pulmonary adenocarcinoma, which are typically CK7-positive. The combined immunohistochemistry signature of PAX-8+/CA IX+/CD10+/CK7- established the diagnosis of metastatic ccRCC and definitively excluded primary gastric adenocarcinoma, which would be expected to show a PAX-8-/CA IX-/CK7+ immunophenotype[7-11] (Table 1).
| Marker | Result (this case) | ccRCC (typical) | Gastric adenocarcinoma (typical) | Diagnostic implication |
| PAX-8 | + | + | - | Establishes renal lineage; excludes gastric primary |
| CA IX | + | + | - | ccRCC molecular hallmark; VHL/HIF pathway activation |
| CD10 | + | + | - | Supports proximal nephron origin |
| CK7 | - | - | + | Rules out gastric, pancreatobiliary, pulmonary origin |
The gastric fundus is anatomically situated in the left upper quadrant beneath the left hemidiaphragm. Surgical access to this region is technically challenging due to the cephalad-to-caudad operative trajectory required for tumor resection. In the present case, robot-assisted laparoscopy was selected over conventional laparoscopy because of the following advan
In August 2025, the patient underwent robot-assisted laparoscopic wedge resection of the stomach with adhesiolysis. Preoperative workup, including infectious disease screening, blood typing, complete blood count, coagulation profile, and hepatic and renal function tests, revealed no surgical contraindications. Intraoperative endoscopic localization identified the tumor at the gastric fundus, measuring approximately 4 cm × 2 cm with intraluminal growth and dense adhesions to the omentum secondary to prior abdominal surgery. Following adhesiolysis, the lesion was excised with a 2-cm circumferential margin using an ultrasonic scalpel. The gastric wall defect was closed with 3-0 absorbable sutures and reinforced with a PSE45 stapling device and a continuous seromuscular barbed suture layer. The specimen was retrieved in an extraction bag, and the procedure was completed without intraoperative complications.
Postoperatively, the patient received prophylactic antibiotics, acid suppression, gastroprotective agents, multimodal analgesia, intravenous fluid replacement, and nutritional support. Abdominal drainage output was 200 mL, 80 mL, and 50 mL on postoperative days 1, 2, and 3, respectively, with a serosanguinous appearance and an appropriate downward trend without evidence of active hemorrhage. The nasogastric tube was removed on postoperative day 4 following the return of bowel function (flatus on postoperative day 3). Oral liquid diet was initiated on postoperative day 7 and was well tolerated. Serial hemoglobin measurements showed no clinically significant postoperative bleeding (preoperative hemoglobin: 9.4 g/dL; postoperative day 1: 8.2 g/dL; postoperative day 6: 8.9 g/dL). By postoperative day 10, the abdominal drainage volume had decreased to < 10 mL/day for three consecutive days, confirming the absence of anastomotic leakage. No clinical signs of gastric outlet obstruction, delayed gastric emptying, or anastomotic dehiscence were observed throughout hospitalization. The patient was discharged on postoperative day 11 with an uneventful recovery. Histopathological examination of the resected specimen confirmed metastatic ccRCC with negative surgical margins (R0).
The patient recovered well postoperatively and was discharged on postoperative day 11 as scheduled. He subsequently received sintilimab 200 mg every 3 weeks as maintenance immunotherapy. At the time of the most recent visit on June 15, 2026, the patient had completed 13 cycles of immunotherapy and remained clinically well with an Eastern Cooperative Oncology Group performance status of 0.
Serial CT surveillance was performed postoperatively. At 4 months (December 2025), CT demonstrated expected post-gastrectomy changes and identified a new left mesenteric nodule, warranting enhanced CT follow-up. At 10 months (June 2026), this nodule remained stable in size with enhancement without progression, and no local recurrence was observed at the gastric resection bed (Figure 5). Given the absence of a validated serum tumor marker for ccRCC, tumor markers were not routinely monitored.
Endocrine function was reassessed on September 18, 2026 and revealed morning serum cortisol of 3.32 μg/dL (reference: 6.02-18.4) and adrenocorticotropic hormone (ACTH) < 1.5 pg/mL (reference: 7.2-63.3), confirming persistent secondary adrenal insufficiency secondary to prior ICI therapy. The patient is continuing with oral hydrocortisone replacement (20 mg in the morning and 10 mg in the afternoon).
At 16 months after metastasectomy, the patient remains progression-free at the gastric site. The radiographically stable mesenteric nodule is under close surveillance, and maintenance immunotherapy with endocrine replacement is ongoing.
This case presents several clinically instructive features of gastric metastasis from ccRCC: (1) A protracted latency of 10 years from initial nephrectomy; (2) An initial false-negative radiological interpretation leading to a 3-month diagnostic delay; (3) Successful robot-assisted metastasectomy following structured perioperative endocrine optimization for ICI-induced adrenal insufficiency; and (4) Sustained disease control with postoperative single-agent programmed death protein (PD)-1 inhibitor maintenance.
Gastric metastasis of RCC remains rare clinically, with a reported incidence of 0.2%-0.8% and a median latency of approximately 6.7 years following nephrectomy[12]. The prolonged interval between primary diagnosis and metachronous gastric metastasis, which may extend beyond 10 years as in the present case, poses a significant risk of diagnostic oversight. In our patient, a suspicious gastric fundus opacity was detected on routine CT in March 2025 but was interpreted as possible food residue by the radiologist. Importantly, the patient remained asymptomatic throughout this period, with no gastrointestinal bleeding, nausea, anorexia, or hemoglobin decline. The lesion was subsequently confirmed on PET/CT in June 2025, yet the initial misinterpretation of the March 2025 CT contributed to a 3-month delay before definitive histopathological diagnosis. This case emphasizes that suspicious gastric lesions detected on routine surveillance CT, even in asymptomatic patients with a history of RCC, should not be dismissed as benign findings, and warrant prompt further evaluation with contrast-enhanced CT, endoscopic examination, or PET/CT to establish a definitive diagnosis.
The molecular mechanisms underlying the gastric tropism of ccRCC remain incompletely understood; however, several lines of evidence suggest a multi-step process. First, the hallmark biallelic inactivation of the VHL tumor suppressor gene in ccRCC leads to constitutive stabilization of HIF-α, which in turn transcriptionally upregulates a repertoire of pro-angiogenic factors — including vascular endothelial growth factor, platelet-derived growth factor, and CA IX — creating a hypervascular tumor phenotype that facilitates hematogenous dissemination. Second, dysregulation of the PI3K/AKT, Ras/MAPK, and Wnt/β-catenin signaling pathways drives epithelial-mesenchymal transition, extracellular matrix remodeling, and enhanced invasive capacity, enabling circulating tumor cells to extravasate and colonize distant organs[6]. Third, the gastric submucosa, with its rich vascular plexus, may provide a permissive microenvironment for metastatic seeding through metabolic adaptation, immune evasion mediated by PD-ligand (PD-L) 1 upregulation, and exosome-mediated intercellular communication[6]. In the present case, gastric metastasis occurred after detection of pulmonary metastases, consistent with the predominantly hematogenous dissemination pattern of ccRCC.
RCC encompasses endoscopic resection, surgical metastasectomy, systemic therapy [tyrosine kinase inhibitors (TKIs) and ICIs], stereotactic body radiotherapy (SBRT), and palliative care[13]. The choice of treatment should be guided by metastatic burden, the patient’s performance status, and biological behavior of the disease. Endoscopic resection, including endoscopic submucosal dissection (ESD), is feasible for small, superficial lesions confined to the submucosal layer without evidence of other organ involvement. A recent case demonstrated durable local control with ESD over a 7-year follow-up period[14]. Surgical metastasectomy, when complete (R0) resection is achievable, represents the only potentially curative local therapy. A systematic review of nonsystemic treatments for metastatic RCC demonstrated that complete metastasectomy significantly improves OS and progression-free survival compared with incomplete or no metastasectomy[13,15]. For polymetastatic or surgically unresectable disease, systemic therapy with ICI-TKI combinations (e.g., pembrolizumab plus axitinib -KEYNOTE-426) or dual ICI regimens (e.g., nivolumab plus ipilimumab) has become the first-line standard of care, with significant survival benefits over sunitinib monotherapy[16,17]. SBRT offers an effective noninvasive alternative for local control of oligometastatic lesions, with durable palliation and disease control comparable to surgical approaches in selected patients[15]. In contrast, palliative care remains the mainstay for patients with poor performance status or widely disseminated disease who are not candidates for definitive local or systemic therapy
At the time of gastric metastasis detection in this patient, comprehensive restaging with PET/CT revealed no evidence of hypermetabolic activity or tumor progression in other systemic organs, supporting a diagnosis of oligometastatic disease. The treatment course of this patient is distinctive and merits individualized discussion. Prior to the diagnosis of gastric metastasis, the patient had received multiline systemic therapy, including sunitinib, axitinib, and nivolumab plus cabozantinib. This achieved durable disease control at all nongastric sites and complete radiographic resolution of previously documented pulmonary metastases. The progressive gastric lesion thus represented an instance of oligoprogression: A solitary site of progression in the context of otherwise controlled systemic disease[18]. In this scenario, surgical resection of the oligoprogressive lesion followed by continuation of the existing systemic regimen is a recognized strategy to delay escalation or switching of systemic therapy. Accordingly, the patient underwent robot-assisted wedge gastrectomy with curative intent, followed by maintenance immunotherapy with sintilimab (a PD-1 inhibitor) at 200 mg every 3 weeks. The choice of sintilimab rather than re-initiation of the prior ICI-TKI combination reflected the favorable disease control achieved before surgery, and a deliberate strategy to minimize cumulative toxicity while preserving immunosurveillance. This individualized approach, discontinuation of TKI after disease control, local resection of the oligoprogressive site, and postoperative single-agent ICI maintenance, differs from the continuous combination therapy of pivotal trials such as KEYNOTE-426, and represents a clinically pragmatic application of the oligometastasis/oligoprogression framework.
A critical aspect of this case that warrants particular emphasis is the perioperative management of ICI-related endocrine adverse events. The patient had developed secondary adrenal insufficiency (morning cortisol < 1.0 μg/dL) and hypothyroidism as a consequence of prior immunotherapy. ICI-induced hypophysitis with secondary adrenal insufficiency is a well-recognized but potentially life-threatening complication, occurring in 0.5%-3% of patients receiving anti-PD-1/PD-L1 therapy, and can persist indefinitely even after ICI discontinuation[19,20]. In the perioperative setting, unrecognized adrenal insufficiency carries a significant risk of adrenal crisis triggered by surgical stress, which is associated with mortality rates of up to 25% if untreated[19,20]. In this case, the endocrinology consultation proactively established a structured perioperative steroid coverage protocol. The patient’s baseline oral hydrocortisone replacement (20 mg in the morning and 10 mg in the afternoon) was escalated to 40 mg in the morning and 20 mg in the afternoon beginning 5 days preoperatively. Concurrently, levothyroxine was increased from 75 μg to 125 μg daily to ensure adequate thyroid hormone reserve. This endocrine optimization directly enabled the safe conduct of major abdominal surgery, and the patient experienced no hemodynamic instability, electrolyte disturbances, or adrenal crisis throughout the perioperative period. It emphasizes the indispensability of integrating endocrinology expertise into the surgical planning of patients on long-term immunotherapy.
This study had several limitations: As a single case report, its generalizability is inherently limited; long-term (> 5-year) survival data are not yet available; continuous monitoring of serum cortisol, ACTH, and thyroid function during the postoperative immunotherapy period was not systematically performed, and the long-term trajectory of ICI-induced endocrine dysfunction in this patient therefore remains incompletely characterized; and molecular biomarker characterization (e.g., PD-L1 expression and VHL mutation status) of the metastatic tissue was not performed, representing important directions for future investigation.
This case demonstrates that gastric metastasis from ccRCC can occur after a prolonged latency of up to 10 years following nephrectomy, and may present without gastrointestinal symptoms, highlighting the importance of long-term surveillance imaging. Histopathological confirmation via endoscopic biopsy with a comprehensive immunohistochemical panel (PAX-8, CA IX, CD10, and CK7) is essential for distinguishing metastatic ccRCC from primary gastric adenocarcinoma and guiding treatment. For advanced RCC patients with a history of distant metastasis, gastric imaging abnormalities should be closely scrutinized during long-term follow-up, regardless of gastrointestinal symptoms. Suspicious gastric lesions on routine surveillance CT should not be dismissed as benign findings without further evaluation with contrast-enhanced CT, endoscopy, or PET/CT. For patients with isolated gastric oligometastasis and well-controlled systemic disease, robot-assisted surgical resection with postoperative ICI maintenance therapy is a feasible strategy following MDT evaluation. This approach requires a protocol for perioperative management of immunotherapy-related endocrine adverse events with mandatory preoperative endocrinology consultation.
We thank the Department of Gastrointestinal Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine for providing the case. We also thank the Departments of Radiology, Endocrinology, Pathology, Surgical Oncology, and Thoracic Surgery for their valuable opinions during the diagnostic and therapeutic process.
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