Researchers studied 650 patients on kidney dialysis and found that a chemical called glycerol-3-phosphate (G-3-P) is much higher in their blood than in healthy people. This chemical appears to be connected to phosphate levels and a hormone called FGF23 that becomes dangerously high when kidneys fail. The study suggests that even damaged kidneys might still be making this chemical in response to phosphate buildup. Understanding this connection could help doctors better manage kidney disease and prevent serious complications.

The Quick Take

  • What they studied: Whether a chemical called glycerol-3-phosphate (G-3-P) is involved in controlling a hormone called FGF23 that gets too high in kidney failure patients
  • Who participated: 650 patients undergoing hemodialysis (kidney dialysis treatment) and 35 healthy people for comparison
  • Key finding: Dialysis patients had 2.2 times more G-3-P in their blood than healthy people. Higher phosphate levels were strongly linked to higher G-3-P, and G-3-P appeared to be an independent predictor of FGF23 levels
  • What it means for you: This finding may help doctors understand why kidney patients develop high FGF23 levels and could lead to better treatments. However, more research is needed before this changes how kidney disease is treated

The Research Details

This was an observational study where researchers measured blood levels of a chemical called glycerol-3-phosphate in two groups: 650 patients receiving hemodialysis (a treatment that filters waste from blood when kidneys don’t work) and 35 healthy people. They used a special laboratory technique called LC/MS to measure G-3-P levels accurately. The researchers then looked for patterns between G-3-P levels, phosphate levels, and a hormone called FGF23 using statistical analysis.

The researchers used two types of statistical analysis: simple comparisons and more complex analysis that controlled for other factors that might affect the results. This approach helps determine whether G-3-P is truly connected to FGF23 or if other factors are responsible for the connection.

Understanding what controls FGF23 levels is important because this hormone becomes dangerously high in kidney failure and can cause serious health problems like bone disease and heart problems. If G-3-P is truly involved in controlling FGF23, it could become a new target for treatment. This study is important because it’s one of the first to examine G-3-P in kidney failure patients.

This study has several strengths: it included a large number of dialysis patients (650), used precise laboratory measurements, and applied appropriate statistical methods. However, it’s observational, meaning researchers only measured what was already happening rather than testing a treatment. The study cannot prove that G-3-P causes high FGF23, only that they’re associated. The researchers acknowledge that more studies are needed to confirm their findings.

What the Results Show

Dialysis patients had significantly higher G-3-P levels (median 220 ng/mL) compared to healthy people (median 98 ng/mL)—more than double. This difference was consistent and remained even when researchers adjusted for other factors that might affect the results.

In dialysis patients, higher phosphate levels in the blood were strongly connected to higher G-3-P levels. This relationship held true even when researchers accounted for other factors like age, body weight, and time on dialysis. Importantly, this pattern was consistent even in patients who had been on dialysis for more than 10 years.

When researchers examined what predicted FGF23 levels, they found that G-3-P was an independent predictor—meaning it was connected to FGF23 levels even after accounting for other known factors like phosphate, calcium, and a hormone called PTH. This suggests G-3-P may play its own role in controlling FGF23.

The study found that several factors were associated with higher FGF23 levels: higher phosphate, higher calcium, higher PTH (another hormone), and use of active vitamin D. However, when all factors were analyzed together, G-3-P remained significantly associated with FGF23. Additional adjustments for markers of inflammation and iron metabolism didn’t change these findings.

Previous research in healthy people suggested that G-3-P might help control FGF23 when people eat high-phosphate foods. This study extends that finding to kidney failure patients, suggesting that even damaged kidneys might retain some ability to produce G-3-P in response to phosphate buildup. However, the researchers note that the source of G-3-P in kidney failure patients (whether from remaining kidney function or other tissues) remains unclear.

This study has important limitations: it’s observational, so it cannot prove cause-and-effect relationships. The study cannot determine whether G-3-P is actually produced by the kidneys or comes from other tissues. The researchers measured everything at one point in time, so they couldn’t track changes over time. Additionally, the study included only dialysis patients, so results may not apply to people with earlier stages of kidney disease. More research is needed to understand the exact mechanisms and to test whether targeting G-3-P could improve patient outcomes.

The Bottom Line

Current evidence suggests that monitoring phosphate levels remains important in dialysis patients, as it appears connected to G-3-P and FGF23 levels. However, there are no new treatment recommendations based on this single study. Patients should continue following their doctor’s advice about phosphate restriction and medications. Future research may lead to new treatments targeting G-3-P, but this is not yet available.

This research is most relevant to people with kidney failure on dialysis, their nephrologists (kidney doctors), and researchers studying kidney disease. People with early-stage kidney disease should be aware of this research direction but don’t need to change their current management. People with healthy kidneys don’t need to be concerned about these findings.

This is basic research aimed at understanding disease mechanisms, not a treatment study. It may take several years of additional research before any new treatments based on these findings become available. In the meantime, current kidney disease management remains the standard approach.

Want to Apply This Research?

  • For dialysis patients: Track serum phosphate levels at each dialysis session and record them weekly in the app. Create a simple graph to visualize trends over time and share with your nephrologist during appointments
  • Work with your dialysis team to optimize phosphate control through dietary choices (limiting high-phosphate foods like dairy, nuts, and processed meats) and medication adherence. Use the app to log phosphate-containing foods and set reminders for phosphate binder medications
  • Set up monthly check-ins to review phosphate trends and FGF23 levels when available. Track any symptoms of bone disease or heart problems. Share this data with your healthcare team to adjust treatment plans as needed

This research is preliminary and observational in nature. It does not establish cause-and-effect relationships and should not be used to change current kidney disease treatment without consulting your nephrologist. If you have kidney disease or are on dialysis, continue following your doctor’s recommendations regarding phosphate management, medications, and dietary restrictions. This article is for educational purposes only and is not a substitute for professional medical advice. Always discuss new research findings with your healthcare provider before making any changes to your treatment plan.