scholarly journals THU0421 TUMOR-INDUCED OSTEOMALACIA: DATA FROM A MONOCENTRIC EXPERIENCE ON 16 PATIENTS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 448.2-449
Author(s):  
C. Crotti ◽  
F. Bartoli ◽  
M. Manara ◽  
P. A. Daolio ◽  
F. Zucchi ◽  
...  
Keyword(s):  
Functional Imaging ◽  
Serum Alkaline Phosphatase ◽  
Fibroblast Growth Factor 23 ◽  
Diagnostic Delay ◽  
The Body ◽  
Definitive Treatment ◽  
Surgical Removal ◽  
Tumor Biopsy ◽  
Pet Ct ◽  
Fgf 23

Background:Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome due to a phosphaturic tumor, which overproduces fibroblast growth factor-23 (FGF-23), causing hyperphosphaturia, hypophosphoremia, low 1,25(OH)2VitD3and osteomalacia. Locating the tumor is critical, because lesions are typically small, benign mesenchymal tumors, anywhere in the body; the delay between onset of symptoms and diagnosis ranges from 2.5–28 years. Surgical removal is the only effective therapeutic approach.Objectives:To retrospectively evaluate patients affected by TIO, investigating clinical management and disease outcome.Methods:We retrospectively collected data of patients affected by TIO referred to a tertiary Rheumatology Center between Sep 2000 and Jan 2020.Results:We included 16 patients with a definite diagnosis of TIO, mean age±standard deviation 62.4±14.6 yrs, 56.2% females, mean age at symptoms onset 48.0±14.3 yrs (53.8±13.1 at diagnosis). Mean diagnostic delay between symptoms onset and tumor detection was 6.8±6.4 yrs. All patients complained bone pain, muscle weakness, and fractures before diagnosis of TIO. Biochemical findings were: mean serum Phosphorus (PS) 1.4±0.4 mg/dL (reference range (RR) 2.5-4.6), mean serum Calcium 9.4±0.7 mg/dL (RR 8.4-10.2), mean serum 1,25(OH)2VitD330.5±23.4 ng/L (RR 25-86). Intact-FGF-23 was dosed in 9 patients, always resulting elevated: mean 396.6±707.3 pg/mL (RR 25-45). PTH was increased in 30% of cases, while serum alkaline phosphatase was increased in 87.5%. 24h-Urine Phosphorus (PU) was increased in only 13% of patients, but, when renal phosphate wasting by tubular reabsorption of phosphate (TRP) was calculated, PU resulted increased in all.Tumor was localized in all cases (Fig.1) and were localized in bone and soft tissue, by using functional imaging, followed by anatomical techniques. Before the introduction in routinely practice of68Ga-DOTATATE-PET-CT in 2013, Octreoscan-SPECT/CT and18F FDG-PET were used as imaging modalities. Since 2013, diagnostic delay consistently reduced, from 8.6±8.3 yrs (7 patients) to 4.5±2.6 yrs (9 patients), confirming higher diagnostic accuracy of68Ga-DOTATATE-PET-CT.Figure 1.13 patients underwent surgery; in two cases surgery was not possible due to tumor location, so pharmacological support with phosphate supplements and calcitriol was started; a patient underwent to TC-guided radiofrequency ablation. After surgery, 7 patients experienced a complete remission, 3 had a persistence of the disease, and 3 an overtime relapse, even after a longstanding normalization of PS (6 years). After surgical tumor removal, PS significantly increased in few days (from 1.36±0.39 to 2.9±1.1, p=0.0001), while iFGF-23 levels tended to rapidly decreased (from 396.6±707.3 to 62.8±78.4). Before the introduction of68Ga-DOTATATE-PET-CT, 6 patients underwent to imaging-guided closed biopsy to confirm tumor localization; by using68Ga-DOTATATE-PET-CT only 2 subjects had closed biopsy. Furthermore, in our population only patients who had biopsy to detect the lesion (7 patients) had relapses compared to patients who did not.Conclusion:To our knowledge, this is the widest European cohort of patients affected by TIO reported in the last two decades. We confirm an important delay between symptoms onset and diagnosis. To locate tumor, a stepwise approach is recommended, starting with a thorough medical history and physical examination, followed by functional imaging, preferring68Ga-DOTATATE-PET-CT. Tumor biopsy is not recommended due to the potential cell spilling. Surgery is considered the only definitive treatment, aiming to a wider excision. Active surveillance is always needed, due to the possible relapses, even after a long period of complete clinical and biochemical remission.Disclosure of Interests: :Chiara Crotti: None declared, Francesca Bartoli: None declared, Maria Manara Consultant of: Consultant and/or speaker for Eli-Lilly, MSD, Sanofi-Genzyme, Novartis, Alfa Wasserman and Cellgene, Speakers bureau: Consultant and/or speaker for Eli-Lilly, MSD, Sanofi-Genzyme, Novartis, Alfa Wasserman and Cellgene, Primo Andrea Daolio: None declared, Francesca Zucchi: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB, Luigi Sinigaglia: None declared, Massimo Varenna: None declared

scholarly journals Fibroblast Growth Factor 23-Producing Phosphaturic Mesenchymal Tumor with Extraordinary Morphology Causing Oncogenic Osteomalacia

Medicina ◽  
2020 ◽  
Vol 56 (1) ◽  
pp. 34
Author(s):  
Cornelia Then ◽  
Evelyn Asbach ◽  
Harald Bartsch ◽  
Niklas Thon ◽  
Christian Betz ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Olfactory Neuroblastoma ◽  
Mesenchymal Tumor ◽  
Fibroblast Growth ◽  
Phosphaturic Mesenchymal Tumor ◽  
Oncogenic Osteomalacia ◽  
Pet Ct ◽  
Fgf 23

A possible cause of hypophosphatemia is paraneoplastic secretion of fibroblast growth factor 23 (FGF-23). Tumors secreting FGF-23 are rare, mostly of mesenchymal origin, usually benign, and may be located anywhere in the body, including hands and feet, which are often not represented in conventional imaging. A 50-year-old woman presented with diffuse musculoskeletal pain and several fractures. Secondary causes of osteoporosis were excluded. Laboratory analysis revealed hypophosphatemia and elevated alkaline phosphatase, parathyroid hormone, and FGF-23. Thus, oncogenic osteomalacia due to neoplastic FGF-23 secretion was suspected. FDG-PET-CT and DOTATATE-PET-CT imaging demonstrated no tumor. Cranial MRI revealed a tumorous mass in the left cellulae ethmoidales. The tumor was resected and histopathological examination showed a cell-rich tumor with round to ovoid nuclei, sparse cytoplasm, and sparse matrix, resembling an olfactory neuroblastoma. Immunohistochemical analysis first led to diagnosis of olfactory neuroblastoma, which was later revised to phosphaturic mesenchymal tumor. Following the resection, FGF-23 and phosphate levels normalized. In conclusion, we here describe a patient with an FGF-23-secreting phosphaturic mesenchymal tumor with an unusual morphology. Furthermore, we emphasize diagnostic pitfalls when dealing with FGF-23-induced hypophosphatemia.

scholarly journals Peptide Receptor Radionuclide Therapy for a Phosphaturic Mesenchymal Tumor

2020 ◽  
Vol 13 (3) ◽  
pp. 1373-1380
Author(s):  
Simon Häfliger ◽  
Ann-Katrin Seidel ◽  
Eric Schoch ◽  
Jan Reichmann ◽  
Damian Wild ◽  
...  
Keyword(s):  
Radionuclide Therapy ◽  
Fibroblast Growth Factor 23 ◽  
Somatostatin Receptors ◽  
Peptide Receptor Radionuclide Therapy ◽  
Mesenchymal Tumor ◽  
Surgical Removal ◽  
Phosphaturic Mesenchymal Tumor ◽  
Peptide Receptor ◽  
Wasting Syndrome ◽  
Fgf 23

Tumor-induced osteomalacia is a very rare paraneoplastic syndrome. It can be caused by phosphaturic mesenchymal tumor (PMT), a generally benign tumor that produces fibroblast growth factor 23 (FGF-23), which can cause a severe renal phosphate wasting syndrome. Upon complete surgical removal of the tumor, FGF-23 normalizes and the osteomalacia is cured. In cases in which surgery is not feasible, radiofrequency ablation (RFA) is the treatment of choice. We describe a case with a PMT situated in the sacrum, in close proximity to the sacral plexus. Both surgery and RFA were considered potentially nerve damaging. Since the tumor showed expression of somatostatin receptors, we opted for a peptide receptor radionuclide therapy (PRRT) with <sup>177</sup>Lu-DOTATOC. However, the therapy did not show the expected success, since the FGF-23 level had even temporarily increased. The patient was then successfully treated with RFA. A partial remission of the tumor was achieved and FGF-23 levels nearly normalized. Despite some severe neurological side effects, the patient showed a remarkable clinical improvement, with no symptoms of osteomalacia within a few weeks.

scholarly journals AB0922 BUROSUMAB (ANTI-FGF23 MONOCLONAL ANTIBODY) IN THE TREATMENT OF A PATIENT WITH RECURRENT TUMOR INDUCED OSTEOMALACIA.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1762.3-1762
Author(s):  
C. Crotti ◽  
F. Zucchi ◽  
P. Messa ◽  
R. Caporali ◽  
M. Varenna
Keyword(s):  
Monoclonal Antibody ◽  
Vitamin D ◽  
Great Trochanter ◽  
Fibroblast Growth Factor 23 ◽  
Well Being ◽  
Hypophosphatemic Rickets ◽  
Imaging Evaluation ◽  
Left Femur ◽  
Pet Ct ◽  
Fgf 23

Background:Tumor-induced Osteomalacia (TIO) is a rare paraneoplastic syndrome caused by tumoral overproduction of fibroblast growth factor 23 (FGF23), resulting in hyperphospaturia, hypophosphatemia and osteomalacia. Surgery is the only curative treatment, but tumor can locally recur, even after years from primary surgery. Furthermore, some tumors cannot be removed by surgery due to their location.Objectives:To describe a case of a 53-year-old woman affected by recurrent TIO after three surgical attempts of removal treated with Burosumab.Methods:We describe the case of a 53 years old woman with TIO treated with Burosumab, an anti-FGF-23 monoclonal antibody at present approved for X-linked hypophosphatemic rickets only.Results:A 46-year-old Caucasian female was referred to our Bone Unit after experiencing several fractures in different sites. She reported being in good health until three years prior consultation. At the time of symptoms onset, she experienced a progressive muscle pain, enabling her to stand for a long period. During imaging evaluation for atraumatic fracture of right great trochanter, the MRI abdomen and18FDG- PET-CT showed a metabolic pre-sacral lesion. She unsuccessfully underwent to an exploratory laparotomy of that lesion. Then, she suffered from atraumatic intertrochanteric fracture of right femur, surgically treated, and after 3 months, she had an insufficiency dyaphiseal fracture of the left femur, surgically treated. Furthermore, she experienced several ribs fractures. At the time of first evaluation, lab works showed: serum-Phosophate (PS) 1.2 mg/dL (reference range (RR) 2.5-4.5 mg/dL), urinary-phosphate of 24h (PU) 842 mg/24h, alkaline phosphatase (ALP) 565 UI (RR<300), 1,25(OH)2vitamin D327 ng/L (RR 25-86.5), PTH 24 (RR<75 pg/mL), intact-FGF-23 117 (RR 25-45 pg/mL), normal serum and 24h-urinary Calcium. Patient underwent to68Ga-DOTATATE-PET-CT that showed a pre-sacral lesion, who was studied with MRI and CT before surgery. In 2013 patient underwent surgical excision of the pre-sacral region. After 18 months of well-being, patient complained worsening of articular pain and muscle weakness, and further ribs fractures. Another68Ga-DOTATATE-PET-CT reported a relapse of the previous pre-sacral lesion (32x12x47 mm) with an increase of FGF-23levels (54.6 pg/mL). Even the subsequent surgery was not able to remove the tumor. Since 2015, patient was maintained in phosphorus supplements and 1,25(OH)2vitamin D3, but PS levels never normalized. We asked for compassionate use of Burosumab and, after ethical committee approval, in September 2019 she was started on Burosumab, at a dose of 30 mg per month (0.3 mg/kg). At baseline, she had PS 1.2 mg/dL, PU 1874 mg/24h, TRP 25.96%. After two months, she improved in pain symptom (VAS reduction from 65 to 12 mm), which allow her to walk and stand without crutches. She did not normalize her PS levels (1.3 mg/dL), while PU reduced to 1000 mg/24h. We titred Burosumab dose at 40 mg per month (0.6 mg/kg) and patient is still under therapy, waiting for next blood works.Conclusion:This is the first European patient affected by TIO treated with Burosumab. Burosumab could be a promising therapy in the medical treatment of TIO refractory or not eligible for definitive surgery. Further data are needed to standardize the proper dose regimen.Disclosure of Interests:Chiara Crotti: None declared, Francesca Zucchi: None declared, Piergiorgio Messa: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB, Massimo Varenna: None declared

scholarly journals A Case of Tumor-Induced Osteomalacia: Finding the Culprit Acetabular Tumor and Successful Resection with a Novel Hip Joint-Preserving Surgery

2021 ◽  
Vol 11 (3) ◽  
Author(s):  
Christie G. Turin ◽  
Robert J. Wilson ◽  
Ciera Mangone ◽  
Karen Rosenspire ◽  
Jessica Berman ◽  
...  
Keyword(s):  
Case Report ◽  
Surgical Technique ◽  
Functional Imaging ◽  
Hip Joint ◽  
Bone Mineralization ◽  
Fibroblast Growth Factor 23 ◽  
Surgical Removal ◽  
Joint Preserving Surgery ◽  
Surgical Cure ◽  
Paraneoplastic Disorder

Introduction: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic disorder caused by tumors that produce fibroblast growth factor 23 (FGF23) resulting in phosphate wasting and inadequate bone mineralization. Complete resection of the tumor can be curative. However, these tumors are typically difficult to find anatomically due to small size and location. Case Report: We present the case of a patient who presented for evaluation of recurrent fractures and hypophosphatemia in the setting of elevated FGF23 suggestive of TIO. 68Gallium-DOTATATE revealed multiple somatostatin avid lesions in several ribs, left acetabulum, sacrum, right tibia, and feet, some of which appeared with fracture on computed tomography scan, initially concerning for metastatic disease. However, the lesion in acetabulum was considered the culprit tumor given its remarkably higher maximum standard uptake values. Complete surgical removal of the FGF23-secreting tumor led to cure of this disease. Conclusion: This case report highlights the challenges with functional imaging differentiating fractures from the culprit lesion and reports on a novel surgical technique that allowed for surgical cure while preserving the hip joint. Keywords: Hypophosphatemia, osteomalacia, tumor, functional imaging, surgical technique.

scholarly journals Prolonged Hypophosphatemia and Intensive Care After Curative Surgery of Tumor Induced Osteomalacia: A Case Report

2021 ◽  
Vol 12 ◽  
Author(s):  
Eeva M. Ryhänen ◽  
Camilla Schalin-Jäntti ◽  
Niina Matikainen
Keyword(s):  
Intensive Care ◽  
Case Report ◽  
Muscle Weakness ◽  
Correct Diagnosis ◽  
Fragility Fractures ◽  
The Body ◽  
Definitive Treatment ◽  
Surgical Removal ◽  
Diagnostic Laboratory ◽  
Work Up

IntroductionRare FGF23-producing mesenchymal tumors lead to paraneoplastic tumor-induced osteomalacia (TIO) presenting with phosphate wasting, hypophosphatemia, chronic hypomineralization of the bone, fragility fractures and muscle weakness. Diagnosis of TIO requires exclusion of other etiologies and careful search for a mesenchymal tumor that often is very small and can appear anywhere in the body. Surgical removal of the tumor is the only definitive treatment of TIO. Surgical complications due to chronic hypophosphatemia are not well recognized.Case DescriptionThe current case describes severe fragility fractures in a 58-year-old woman, who lost her ability to walk and was bedridden for two years. First, the initial diagnostic laboratory work-up did not include serum phosphorus measurements, second, the suspicion of adverse effects of pioglitazone as an underlying cause delayed correct diagnosis for at least two years. After biochemical discovery of hyperphosphaturic hypophosphatemia at a tertiary referral centre, a FGF23-producing tumor of the mandible was discovered on physical examination, and then surgically removed. Postoperatively, severe hypophosphatemia and muscle weakness prolonged the need for ventilation support, intensive care and phosphate supplementation. After two years of rehabilitation, the patient was able to walk short distances. The tumor has not recurred, and serum phosphate concentration has remained within normal limits during 3.5 years of follow-up.ConclusionsThe case report illustrates knowledge gaps in the diagnostic work-up of rare causes of low bone mass and fragility fractures. Compared to other low phosphate conditions, surgical recovery from TIO-induced hypophosphatemia warrants special attention. Increased alkaline phosphatase concentration may indicate impaired postsurgical recovery due to prolonged hypophosphatemia, underlining the need for proactive perioperative correction of hypophosphatemia.

Radiation oncology and functional imaging

2005 ◽  
Vol 44 (S 01) ◽  
pp. S38-S40
Author(s):  
Th. Herrmann
Keyword(s):  
Functional Imaging ◽  
Radiation Oncology ◽  
Bronchogenic Carcinoma ◽  
Brain Tumours ◽  
Tumour Volume ◽  
Target Volume ◽  
Head And Neck Tumours ◽  
Pet Ct ◽  
Surrounding Healthy Tissue ◽  
Prostate Carcinomas

Summary:PET/CT imaging is most likely to be of use in radiation oncology with patients who have poorly defined target volume areas, e.g. brain tumours, bronchogenic carcinoma, and cases of miscellaneous geographical miss. Other tumours that call for dose escalated radiotherapy, such as head and neck tumours, bronchogenic carcinoma, and prostate carcinomas may further benefit from an accurate delineation of the metabolically active tumour volume and its differentiation from surrounding healthy tissue, or tumour atelectasis.

Novel Nanolipoidal Systems for the Management of Skin Cancer

2020 ◽  
Vol 14 (2) ◽  
pp. 108-125
Author(s):  
Apoorva Singh ◽  
Nimisha
Keyword(s):  
Skin Cancer ◽  
Survival Rates ◽  
Cancer Therapeutics ◽  
The Body ◽  
Surgical Removal ◽  
The Novel ◽  
Skin Cancers ◽  
Recent Developments ◽  
Abnormal Cells ◽  
The Stability

: Skin cancer, among the various kinds of cancers, is a type that emerges from skin due to the growth of abnormal cells. These cells are capable of spreading and invading the other parts of the body. The occurrence of non-melanoma and melanoma, which are the major types of skin cancers, has increased over the past decades. Exposure to ultraviolet radiations (UV) is the main associative cause of skin cancer. UV exposure can inactivate tumor suppressor genes while activating various oncogenes. The conventional techniques like surgical removal, chemotherapy and radiation therapy lack the potential for targeting cancer cells and harm the normal cells. However, the novel therapeutics show promising improvements in the effectiveness of treatment, survival rates and better quality of life for patients. Different methodologies are involved in the skin cancer therapeutics for delivering the active ingredients to the target sites. Nano carriers are very efficient as they have the ability to improve the stability of drugs and further enhance their penetration into the tumor cells. The recent developments and research in nanotechnology have entitled several targeting and therapeutic agents to be incorporated into nanoparticles for an enhancive treatment of skin cancer. To protect the research works in the field of nanolipoidal systems various patents have been introduced. Some of the patents acknowledge responsive liposomes for specific targeting, nanocarriers for the delivery or co-delivery of chemotherapeutics, nucleic acids as well as photosensitizers. Further recent patents on the novel delivery systems have also been included here.

scholarly journals Tumor Heterogenity in Gastro-Entero-Pancreatic Neuroendocrine Neoplasia

Endocrines ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 28-36
Author(s):  
Ludovica Magi ◽  
Maria Rinzivillo ◽  
Francesco Panzuto
Keyword(s):  
Functional Imaging ◽  
Clinical Heterogeneity ◽  
Therapeutic Approaches ◽  
Prognostic Role ◽  
Neuroendocrine Neoplasia ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Owing to the rarity and the biological and clinical heterogeneity of gastroenteropancreatic neuroendocrine neoplasia (GEP NEN), the management of these patients may be challenging for physicians. This review highlights the specific features of GEP NEN with particular attention on the role of Ki67 heterogeneity, the potential prognostic role of novel radiological techniques, and the clinical usefulness of functional imaging, including 68Ga-DOTA-SST PET/CT and 18F-FDG PET/CT. Understanding these specific features may help to plan proper and tailored follow-up programs and therapeutic approaches.

scholarly journals FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

Medicina ◽  
2020 ◽  
Vol 57 (1) ◽  
pp. 15
Author(s):  
Altynay Balmukhanova ◽  
Kairat Kabulbayev ◽  
Harika Alpay ◽  
Assiya Kanatbayeva ◽  
Aigul Balmukhanova
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Ckd Stage ◽  
Advanced Stages ◽  
Fgf 23 ◽  
Stage 1

Background and objectives: Chronic kidney disease (CKD) in children is a complex medical and social issue around the world. One of the serious complications is mineral-bone disorder (CKD-MBD) which might determine the prognosis of patients and their quality of life. Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone which is involved in the pathogenesis of CKD-MBD. The purpose of the study was to determine what comes first in children with CKD: FGF-23 or phosphate. Materials and Methods: This cross-sectional study included 73 children aged 2–18 years with CKD stages 1–5. We measured FGF-23 and other bone markers in blood samples and studied their associations. Results: Early elevations of FGF-23 were identified in children with CKD stage 2 compared with stage 1 (1.6 (1.5–1.8) pmol/L versus 0.65 (0.22–1.08), p = 0.029). There were significant differences between the advanced stages of the disease. FGF-23 correlated with PTH (r = 0.807, p = 0.000) and phosphate (r = 0.473, p = 0.000). Our study revealed that the elevated level of FGF-23 went ahead hyperphosphatemia and elevated PTH. Thus, more than 50% of children with CKD stage 2 had the elevating level of serum FGF-23, and that index became increasing with the disease progression and it achieved 100% at the dialysis stage. The serum phosphate increased more slowly and only 70.6% of children with CKD stage 5 had the increased values. The PTH increase was more dynamic. Conclusions: FGF-23 is an essential biomarker, elevates long before other markers of bone metabolism (phosphate), and might represent a clinical course of disease.

scholarly journals Increased Levels of sRAGE in Diabetic CKD-G5D Patients: A Potential Protective Mechanism against AGE-Related Upregulation of Fibroblast Growth Factor 23 and Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Elena Dozio ◽  
Valentina Corradi ◽  
Elena Vianello ◽  
Elisa Scalzotto ◽  
Massimo de Cal ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cardiac Remodeling ◽  
Glycated Albumin ◽  
Fibroblast Growth Factor 23 ◽  
Protective Mechanism ◽  
Fibroblast Growth ◽  
Increased Risk ◽  
Fgf 23

Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.

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