Fibroblast Growth Factor 23, Plasma

Bone

Report in 192Hrs

At Home

No Fasting Required

Details

Hormone regulating phosphate.

₹10,730₹15,329

30% OFF

Fibroblast Growth Factor 23 Plasma - Comprehensive Medical Test Guide

Section 1: Why is it done?
- Test Overview: This test measures the level of Fibroblast Growth Factor 23 (FGF23), a hormone produced primarily by bone cells (osteocytes) that plays a crucial role in regulating phosphate and vitamin D metabolism. FGF23 acts on the kidneys to increase phosphate excretion and suppress active vitamin D production.
- Primary Indications for Testing: Evaluation of chronic kidney disease (CKD) progression, assessment of phosphate metabolism disorders, investigation of hypophosphatemia (low phosphate levels), diagnosis of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and X-linked hypophosphatemia (XLH), monitoring of mineral metabolism abnormalities in dialysis patients, and evaluation of unexplained bone disease or growth abnormalities in children.
- Clinical Circumstances: Testing is typically performed in patients with stages 3-5 CKD, those with unexplained hyperphosphatemia despite kidney disease, patients with suspected fibroblast growth factor-related disorders, and individuals with family history of hereditary phosphate-wasting disorders. May also be ordered when monitoring patients on FGF23-targeted therapies or novel mineral metabolism treatments.
Section 2: Normal Range
- Reference Range Values: Normal plasma FGF23 levels typically range from 12-60 pg/mL (picograms per milliliter), though this may vary slightly depending on the laboratory assay used (intact FGF23 vs C-terminal FGF23). Some laboratories may report ranges as 20-200 RU/mL (relative units) for older assays. It is important to consult the specific reference range provided by the testing laboratory.
- Interpretation of Results: Low/Normal FGF23 (12-60 pg/mL): Indicates appropriate phosphate regulation and normal mineral metabolism in kidney disease stages 1-2 or in healthy individuals. Elevated FGF23 (>60 pg/mL): Suggests impaired renal phosphate excretion, early-stage mineral metabolism abnormalities in CKD, or phosphate-wasting disorders. Progressive elevation correlates with CKD stage advancement and secondary hyperparathyroidism risk. Markedly Elevated FGF23 (>1000 pg/mL): Indicates severe phosphate-wasting disorders (XLH, HHRH, or other genetic conditions) or advanced CKD with significant secondary hyperparathyroidism.
- Clinical Significance: Normal FGF23 levels indicate that the kidneys are adequately regulating phosphate balance and vitamin D metabolism. Abnormal values suggest dysregulation of mineral homeostasis and increased risk of bone disease, cardiovascular complications, and progressive renal dysfunction.
Section 3: Interpretation
- Detailed Result Interpretation: FGF23 functions as an early biomarker of mineral metabolism disturbance in CKD. As glomerular filtration rate (GFR) declines, FGF23 progressively rises in a compensatory mechanism to maintain serum phosphate balance. Early elevation (2-3 fold above normal) may occur before significant changes in serum phosphate, calcium, or parathyroid hormone (PTH), making it a sensitive early indicator of secondary hyperparathyroidism development.
- Clinical Patterns and Their Significance: Mild Elevation in CKD Stage 3: May indicate early mineral metabolism changes requiring monitoring of dietary phosphate intake and vitamin D status. Marked Elevation in CKD Stage 4-5: Associated with secondary hyperparathyroidism, increased cardiovascular mortality risk, bone disease acceleration, and potential need for therapeutic intervention. Disproportionate Elevation with Low Phosphate: Highly suggestive of hereditary phosphate-wasting disorders (XLH, HHRH, autosomal dominant hypophosphatemic rickets). Persistently Normal FGF23 in CKD: Rare but may indicate FGF receptor resistance or specific genetic variants affecting FGF23 physiology.
- Factors Affecting FGF23 Levels: Renal function (GFR decline increases FGF23), serum phosphate levels, dietary phosphate intake, vitamin D status, intact PTH levels, age (higher in elderly), ethnicity variations, medications (phosphate binders, vitamin D analogs), parathyroid gland function, bone turnover state, and presence of genetic mutations affecting phosphate metabolism.
- Prognostic Value: Elevated FGF23 independently predicts progression of CKD, increased cardiovascular events, higher mortality rates in dialysis patients, and increased risk of vascular calcification. Serial FGF23 measurements can assess response to mineral-targeted therapies and predict long-term complications.
Section 4: Associated Organs
- Primary Organ Systems Involved: Kidneys (primary target organ for FGF23 action, site of phosphate reabsorption regulation and vitamin D metabolism), Bone (primary source of FGF23 production), Parathyroid Glands (secondary regulation through mineral metabolism effects), and Cardiovascular System (affected by mineral metabolism dysregulation).
- Primary Conditions Associated with Abnormal FGF23: Chronic Kidney Disease (all stages, most common cause of elevated FGF23), X-linked Hypophosphatemia (XLH - genetic disorder causing severe phosphate wasting), Autosomal Dominant Hypophosphatemic Rickets (ADHR), Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH), Tumor-Induced Osteomalacia (caused by phosphate-regulating hormone-related peptide secretion), McCune-Albright Syndrome, Fibrous Dysplasia, Secondary Hyperparathyroidism, and End-Stage Renal Disease.
- Complications Associated with Abnormal FGF23 Levels: Bone Complications: Osteomalacia, rickets in children, accelerated bone loss, increased fracture risk, impaired skeletal growth in pediatric patients. Renal Complications: Progressive glomerular filtration rate decline, increased risk of kidney disease progression, acceleration toward end-stage renal disease. Cardiovascular Complications: Vascular calcification, increased arterial stiffness, left ventricular hypertrophy, increased myocardial infarction risk, higher cardiovascular mortality. Systemic Complications: Secondary hyperparathyroidism, impaired growth and development in children, increased infection susceptibility in CKD patients, mineral metabolism dysregulation affecting multiple organ systems.
- Impact on Organ Function: Elevated FGF23 suppresses vitamin D activation in kidneys, reduces intestinal calcium and phosphate absorption, promotes renal phosphate wasting, and alters bone remodeling patterns. These effects collectively impair overall mineral homeostasis and contribute to development of secondary hyperparathyroidism and chronic kidney disease-mineral bone disorder (CKD-MBD).
Section 5: Follow-up Tests
- Recommended Follow-up Tests Based on FGF23 Results: Serum Phosphate (assess phosphate balance), Serum Calcium (evaluate calcium homeostasis), 25-Hydroxyvitamin D (assess vitamin D stores), 1,25-Dihydroxyvitamin D (assess active vitamin D status), Intact Parathyroid Hormone (PTH - evaluate secondary hyperparathyroidism), Alkaline Phosphatase (assess bone metabolism), Serum Creatinine and Estimated GFR (assess renal function), 24-hour Urinary Phosphate (evaluate renal phosphate excretion), Bone-Specific Alkaline Phosphatase (assess bone formation).
- Additional Investigations for Abnormal Results: Bone Mineral Density (DEXA scan - assess fracture risk), Skeletal Survey or X-rays (evaluate rickets or bone disease), Bone Biopsy (assess bone histology and turnover in select cases), Genetic Testing (for suspected hereditary phosphate-wasting disorders such as FGF23, PHEX, DMP1, ENPP1 mutations), Parathyroid Imaging (ultrasound or sestamibi scan if secondary hyperparathyroidism suspected), Vascular Calcification Assessment (coronary artery calcification scoring, arterial stiffness measures).
- Monitoring Frequency: CKD Stage 3a: Annual or every 12 months. CKD Stage 3b: Every 6-12 months. CKD Stage 4: Every 3-6 months. CKD Stage 5 (on dialysis): Every 1-3 months. Hereditary Disorders: Baseline and then as clinically indicated, typically every 6-12 months to assess treatment response.
- Complementary Tests Providing Related Information: Phosphate-Regulating Genes with Homologies to Endopeptidases on the X Chromosome (PHEX) gene testing, Dentin Matrix Protein 1 (DMP1) genetic analysis, Ectonucleotide Pyrophosphatase/Phosphodiesterase 1 (ENPP1) mutations, C-terminal FGF23 vs Intact FGF23 (different assays provide complementary information about FGF23 fragments), Alpha-Klotho levels (co-receptor for FGF23 signaling), FGF Receptor 1 (FGFR1) assessment.
- Timing of Follow-up Testing: After initiation of FGF23-targeting therapy (burosumab for hereditary disorders or standard CKD-MBD treatments), repeat testing should be performed 4-8 weeks after therapy initiation to assess response, then at regular intervals based on clinical stability. When significant changes in renal function occur, repeat FGF23 testing within 2-4 weeks to reassess mineral metabolism status.
Section 6: Fasting Required?
- Fasting Requirement: No - Fasting is NOT required for FGF23 plasma testing. The test can be performed at any time during the day, regardless of food intake status.
- Specimen Collection Requirements: Blood sample collection via venipuncture into appropriate collection tube (typically EDTA or heparin plasma tube depending on laboratory specifications). The sample should be collected in the morning when possible for consistency, though timing is not strictly required.
- Medications to Avoid: No specific medications need to be withheld prior to FGF23 testing. However, inform your healthcare provider about all medications you are taking, including: Vitamin D supplements and analogs (calcitriol, ergocalciferol, paricalcitol), Phosphate binders (calcium acetate, sevelamer, lanthanum carbonate), Calcimimetics (cinacalcet), Active vitamin D analogs, Phosphate supplements, Corticosteroids, and any FGF23-targeted therapies (burosumab). These medications may affect FGF23 levels and should be documented but do not require discontinuation prior to testing.
- Patient Preparation Instructions: No special fasting preparation needed - eat and drink normally before testing. Come well-hydrated for blood draw. Wear comfortable clothing with easily accessible arms for venipuncture. Inform phlebotomist of any bleeding disorders, anticoagulation therapy, or difficulty with blood draws. Arrive 10-15 minutes early to allow time for check-in. Remain calm and relaxed during specimen collection as stress may affect blood pressure and vessel access.
- Dietary Considerations: No specific dietary restrictions required before testing. However, for CKD patients and those with mineral metabolism disorders, dietary phosphate and calcium intake may be relevant to clinical interpretation, so inform your healthcare provider about your typical dietary intake.
- Sample Handling and Processing: Samples should be processed promptly according to laboratory protocol. Plasma should be separated from whole blood immediately and either analyzed fresh or frozen at -20°C or lower for later testing. Samples are stable for 24 hours at room temperature or longer when properly frozen. Ensure proper chain of custody documentation and patient identification to avoid specimen mix-up.

How our test process works!