Summary
Gastric mucosal calcinosis is a rare condition identified on biopsies undertaken during oesophagogastroduodenoscopy. Metastatic gastric mucosal calcinosis is gastric calcium deposition in the context of an abnormal biochemical environment, usually detected on routine biopsies or postmortem incidentally. A man in his late 70s on regular haemodialysis, with a history of end-stage kidney failure secondary to immunoglobulin A nephropathy, presented with a 3-month history of upper gastrointestinal symptoms including vomiting, abdominal fullness and weight loss. Medical history included extensive coronary artery calcification and refractory secondary hyperparathyroidism. An oesophagogastroduodenoscopy with biopsies demonstrated gastric mucosal deposits of calcium. There are no prevalence or outcome data reported for gastric mucosal calcinosis; it may be underdiagnosed. This case suggests that gastric mucosal calcinosis was a plausible contributor to the patient’s symptoms and should be considered in people with known vascular and soft tissue calcification risk factors, although the association does not establish causation.
Keywords: Endoscopy, Chronic renal failure, Dialysis, Renal transplantation, Fluid electrolyte and acid-base disturbances
Background
Gastric mucosal calcinosis is a rare condition identified on biopsies undertaken during oesophagogastroduodenoscopy. It may be further classified into dystrophic, metastatic, iatrogenic and idiopathic subtypes.1 Metastatic is the most common subtype and is defined as the deposition of calcium salts in the stomach related to an abnormal biochemical environment, including hypercalcaemia, hyperphosphataemia and an elevated calcium-phosphate product. It is therefore associated with the disordered mineral metabolism seen in people with kidney failure.2
Case presentation
A man in his late 70s, well known to the renal team with end stage kidney failure secondary to immunoglobulin A (IgA) nephropathy, presented with a 3-month history of nausea, vomiting two to three times per week, early satiety, abdominal pain, abdominal feeling of fullness and 3 kg weight loss. On examination, there was a feeling of fullness in his upper abdomen that was thought may represent a mass. The renal team referred the patient to gastroenterology for investigation of a possible malignancy.
Medical history
He had presented to a nephrologist in his mid-40s, and a diagnosis of IgA nephropathy was made on renal biopsy. He commenced renal replacement therapy with peritoneal dialysis in his early 60s. He received a renal transplant a few years later; this failed after 6 months, and an attempt at further peritoneal dialysis was unsuccessful. He had been receiving in-centre haemodialysis, 4 hours, three times a week for 15 years. He was well dialysed with an arteriovenous fistula with a transonic flow of >1000 mL/min and a urea reduction ratio of 0.75. He had longstanding hyperphosphataemia and hyperparathyroidism for which he was taking non-calcium-based phosphate binders to reduce intestinal phosphate absorption, the vitamin D analogue alfacalcidol to increase serum calcium and suppress parathyroid hormone secretion and the calcimimetic cinacalcet to enhance calcium-sensing receptor activity and further suppress parathyroid hormone levels. He had been a participant in a clinical trial for 7 years receiving 60 000 units of colecalciferol every fortnight with no record of vitamin D toxicity. He also had a history of ischaemic heart disease, atrial fibrillation and heart failure with reduced ejection fraction.
Investigations
At the time of symptom onset, serum corrected calcium was 2.41 mmol/L (9.64 mg/dL; normal 2.05–2.55 mmol/L or 8.5–10.5 mg/dL), serum phosphate was 1.31 mmol/L (4.1 mg/dL; normal 0.80–1.50 mmol/L or 2.5–4.5 mg/dL) and parathyroid hormone was elevated at 79.5 pmol/L (750 pg/mL; normal 1.6–6.9 pmol/L, 14–72 pg/mL). He was not diabetic, and a glycated haemoglobin was 28 mmol/mol (<40 mmol/mol). There was no history of calciphylaxis or skin involvement. A CT scan of the patient’s abdomen and pelvis showed no primary malignancy or evidence of distant metastatic disease. An oesophagogastroduodenoscopy showed Barrett’s oesophagus, irregular looking mucosa in the gastric body and antrum (figures 1 and 2) and irregular folds at pyloric region. The endoscopist obtained biopsies of these sites.
Figure 1. Oesophagogastroduodenoscopy image demonstrating irregular looking mucosa in the gastric body.
Figure 2. Oesophagogastroduodenoscopy image demonstrating irregular looking mucosa in the gastric body.
The pathology report demonstrated crystalline material within the lamina propria (figure 3), consistent with gastric mucosal calcinosis in the context of end stage kidney disease.
Figure 3. Pathology image of gastric mucosa stained using H&E. Arrows demonstrate areas of crystalline material within the lamina propria.
Outcome and follow-up
When vomiting was initially reported, a side effect of the oral calcimimetic cinacalcet was suspected, and this medication was changed to intravenous etelcalcetide, given at each haemodialysis session. This maintained calcimimetic therapy while avoiding a possible oral medication-related contributor to nausea and vomiting; the change preceded the histological diagnosis and was not intended as a specific treatment for gastric mucosal calcinosis. While serum corrected calcium was within the normal range at the onset of abdominal symptoms, this became elevated over the following 3 months, and in response, alfacalcidol was stopped to reduce calcium loading. The patient’s calcium returned to within the normal range. The etelcalcetide dose was increased after 2 months because the parathyroid level remained elevated, with the aim of improving control of secondary hyperparathyroidism. Parathyroidectomy was considered but not pursued, as the risks were judged to outweigh the potential benefits for this patient.
From a symptom management basis, most treatment was non-pharmacological. Following a dietitian review, small and regular meals were encouraged which resulted in an increased appetite and an improvement in vomiting symptoms. Despite this, the patient initially suffered from ongoing weight loss, and in response, nutritional supplement drinks were started. Because these measures occurred alongside changes to chronic kidney disease-mineral and bone disorder (CKD-MBD) therapy, the relative contribution of each intervention to symptom improvement cannot be determined.
He is followed up in haemodialysis clinic where his serum calcium, phosphate, parathyroid level and vitamin D levels are routinely checked (table 1), and he is receiving ongoing dietitian support. Five months after the diagnosis (and 8 months after the initial symptom onset), he reported significant improvement in symptoms. His most recent parathyroid level was improved at 56.8 pmol/L (535 pg/mL; normal 1.6–6.9 pmol/L, 14–72 pg/mL). His serum albumin at presentation was 40 g/L and was consistently within our reference range of 35–50 g/L. His dry weight had decreased from 82.5 kg at symptom onset to 76.5 kg at time of writing, though had stabilised. This correlates to a reduction in body mass index (BMI) from 25.7 kg/m² to 23.9 kg/m². No formal functional gastrointestinal assessment or repeat oesophagogastroduodenoscopy was undertaken; therefore, the mechanism of the symptoms and any change in the mucosal calcification was not objectively assessed.
Table 1. Trend of serum corrected calcium, serum phosphate and parathyroid hormone over time.
| Time point | Corrected calcium (2.05–2.55 mmol/L) | Phosphate (0.80–1.50 mmol/L) | Parathyroid hormone (1.6–6.9 pmol/L) |
|---|---|---|---|
| −3 months | 2.47 | 2.15 | 63.6 |
| −2 months | 2.36 | 1.83 | 22.6 |
| −1 month | 2.37 | 1.92 | 34.6 |
| Presentation | 2.41 | 1.31 | 79.5 |
| +1 month | 2.54 | 1.26 | – |
| +2 months | 2.48 | 1.52 | 54.5 |
| +3 months | 2.60 | 1.33 | 42.6 |
| +4 months | 2.68 | 1.56 | 48.5 |
| +5 months | 2.38 | 2.01 | 56.4 |
| +6 months | 2.16 | 1.40 | – |
| +7 months | 2.40 | 1.74 | – |
| +8 months | 2.33 | 1.79 | 61.0 |
| +9 months | 2.36 | 1.72 | 56.8 |
Discussion
There are no prevalence or outcome data reported for gastric mucosal calcinosis. Existing literature on gastric mucosal calcinosis is largely confined to individual case reports. Gastric mucosal calcinosis has been reported as rarely being associated with symptoms and is a rare incidental biopsy finding on oesophagogastroduodenoscopy when alternate diagnoses are searched for or on postmortem investigations.1 3 In this patient, the clinical context led us to believe that gastric mucosal calcinosis was a plausible contributor to the patient’s symptoms. However, although CT and endoscopy did not identify malignancy or another major structural explanation, alternative causes were not fully excluded and causation cannot be established from a single case.
Our patient had longstanding hyperphosphataemia prior to diagnosis. In the presence of hyperphosphataemia and altered mineral metabolism seen in secondary hyperparathyroidism, hydroxyapatite crystals (a primary form of calcium phosphate) can nucleate and form in the extracellular matrix of the gastric mucosa (figure 4), consistent with the calcium deposition identified in our biopsy samples.4 This mechanism provides biological plausibility for an association with symptoms but does not prove causation.
Figure 4. Pathophysiology of gastric mucosal calcinosis.12.
Like vascular and soft tissue calcifications, there are no proven treatments for gastric mucosal calcinosis; clinical management is targeted at managing risk factors. The 2017 Kidney Disease: Improving Global Outcomes (KDIGO) guideline recommends maintaining serum phosphate towards the normal range, avoiding hypercalcaemia and maintaining parathyroid hormone levels between two and nine times the upper limit of normal.5 These recommendations relate to CKD-MBD generally rather than gastric mucosal calcinosis specifically and were applied to manage the underlying biochemical risk factors.
Evidence that gastric mucosal calcium deposition can be reversed by correcting the abnormal biochemical markers implicated in its pathophysiology is limited, although some case reports describe apparent improvement6 7; treatment efficacy has not been established. In this patient, a normal serum calcium level for many years did not protect from mucosal deposits; recent research supports the notion that serum calcium is not a reliable indicator of calcium balance.8 9 Discontinuation of active vitamin D analogues and initiation or optimisation of calcimimetic treatments are associated with improved outcomes in other soft tissue and vascular calcification disorders, namely, calciphylaxis.10 Although this evidence cannot be directly extrapolated to gastric mucosal calcinosis, it informed our approach to reducing calcium loading and controlling secondary hyperparathyroidism. This treatment approach, together with dietary guidance and nutritional supplementation, was followed by symptom improvement in the presented case. The clinical course is consistent with gastric mucosal calcinosis being a possible contributor, but because multiple interventions were introduced, improvement cannot be attributed to any single treatment, the absence of repeat endoscopy or functional gastrointestinal assessment also limits objective assessment of treatment impact.
Upper gastrointestinal symptoms are common in people with kidney failure.11 This case suggests that gastric mucosal calcinosis should be considered as a possible contributor and differential diagnosis in people with known vascular and soft tissue calcification risk factors. Its identification should be interpreted alongside the clinical context and continued assessment for alternative causes.
Learning points.
Gastric mucosal calcinosis is a rare diagnosis seen in people with chronic kidney disease and may be clinically relevant in patients with upper gastrointestinal symptoms.
It is rarely an incidental finding on histopathological analysis; identification in a symptomatic patient supports an association but does not establish causation.
While there are no proven condition-specific treatments, increased awareness of gastric mucosal calcinosis may improve diagnosis and guide management of CKD-MBD risk factors and supportive care; improvement after combined interventions cannot be attributed to one treatment.
Normocalcaemia alone does not exclude calcium deposition in tissues; serum calcium is a poor marker of calcium balance.
In patients presenting with upper gastrointestinal symptoms and a history of risk factors such as hyperphosphataemia and elevated parathyroid hormone, gastric mucosal calcinosis should be considered as a possible contributor and differential diagnosis while alternative causes are assessed.
Acknowledgements
The writers of this manuscript would like to give special thanks to Dr. Leonid Semkin and Dr. Sacha Moore. Dr. Semkin assisted with obtaining images of pathology slides and imparting information with regard to staining techniques used. Dr. Moore created the pathophysiology figure contained in the manuscript (figure 4) using BioRender (Moore, S. (2025) https://BioRender.com/yqptarl).
Footnotes
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Provenance and peer review: Not commissioned; externally peer reviewed.
Patient consent for publication: Consent obtained from next of kin.
References
- 1.Dincay D, Atay K, Hatemi I, et al. Mucosal gastric calcinosis in a hypocalcaemic patient. Prz Gastroenterol . 2017;12:70–1. doi: 10.5114/pg.2016.61885. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Gorospe M, Fadare O. Gastric mucosal calcinosis: clinicopathologic considerations. Adv Anat Pathol. 2007;14:224–8. doi: 10.1097/PAP.0b013e31805048ea. [DOI] [PubMed] [Google Scholar]
- 3.Reyes JVM, Seen T, Al-Khazraji A, et al. Recurrent Dyspepsia Secondary to Gastric Mucosal Calcinosis GMC. Am J Gastroenterol. 2021;116:S1296. doi: 10.14309/01.ajg.0000786108.27369.76. [DOI] [Google Scholar]
- 4.Kosoru V, Mohammed A, Kapoor R, et al. Metastatic Calcinosis of Gastric Mucosa. J Investig Med High Impact Case Rep. 2020;8:1–5. doi: 10.1177/23247096209400482. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Kidney Int Suppl (2011) 2017;7:1–59. doi: 10.1016/j.kisu.2017.04.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Gurala D, Almoussawi H, Haddad FG, et al. S3015 A Case of Gastric Mucosal Calcinosis. Am J Gastroenterol. 2020;115:S1589–90. doi: 10.14309/01.ajg.0000714108.12993.f6. [DOI] [Google Scholar]
- 7.Nayak HK, Mohindra S, Iqbal S, et al. Gastric Mucosal Calcinosis Mimicking Malignancy. Am J Gastroenterol. 2016;111:1380. doi: 10.1038/ajg.2016.274. [DOI] [PubMed] [Google Scholar]
- 8.Shroff R, Lalayiannis AD, Fewtrell M, et al. Naturally occurring stable calcium isotope ratios are a novel biomarker of bone calcium balance in chronic kidney disease. Kidney Int. 2022;102:613–23. doi: 10.1016/j.kint.2022.04.024. [DOI] [PubMed] [Google Scholar]
- 9.Evenepoel P, Jørgensen HS, Bover J, et al. Recommended calcium intake in adults and children with chronic kidney disease-a European consensus statement. Nephrol Dial Transplant. 2024;39:341–66. doi: 10.1093/ndt/gfad185. [DOI] [PubMed] [Google Scholar]
- 10.Seethapathy H, Brandenburg VM, Sinha S, et al. Review: update on the management of calciphylaxis. QJM. 2019;112:29–34. doi: 10.1093/qjmed/hcy234. [DOI] [PubMed] [Google Scholar]
- 11.Karahan D, Şahin İ. Comparison of gastrointestinal symptoms and findings in renal replacement therapy modalities. BMC Nephrol. 2022;23:261. doi: 10.1186/s12882-022-02893-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Moore S. Created in BioRender. 2025 https://BioRender.com/yqptarl Available.