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Phosphate salivary secretion in hemodialysis patients: implications for the treatment of hyperphosphatemia
Vincenzo Savica1, Lorenzo A Calò, Renato Caldarera
1Department of Nephrology, University of Messina, Messina, Italy.
Insights
Patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD) have higher salivary phosphate levels. This suggests salivary phosphate binding could be a new therapeutic strategy for hyperphosphatemia in ESRD patients.
Area of Science:
- Nephrology
- Endocrinology
- Biochemistry
Background:
- Hyperphosphatemia is a significant risk factor for cardiac mortality in end-stage renal disease (ESRD) patients on hemodialysis (HD).
- Current phosphate binders achieve target serum phosphorus levels in only half of treated ESRD patients, necessitating novel therapeutic strategies.
- Salivary phosphate secretion in ESRD patients is not well-established, despite the potential contribution of saliva to overall phosphate balance.
Purpose of the Study:
- To investigate and compare salivary phosphate secretion levels in hemodialysis patients versus healthy controls.
- To explore the relationship between salivary phosphate, serum phosphate, and other relevant biochemical markers in ESRD patients.
Main Methods:
- Salivary phosphate and calcium levels were measured in 68 HD patients and 30 healthy subjects.
- Serum phosphate, calcium, and parathyroid hormone (PTH) levels were also assessed.
- Salivary function was confirmed as normal in both groups using Saxon's test.
Main Results:
- Hemodialysis patients exhibited significantly elevated salivary phosphorus concentrations compared to healthy controls (30.35 mg/dl vs. 12.1 mg/dl, p < 0.0001).
- Salivary phosphorus levels demonstrated a strong positive correlation with serum phosphorus levels (p < 0.0001).
- Serum phosphorus was identified as the sole significant predictor of salivary phosphorus levels via multiple regression analysis (p < 0.0001).
Conclusions:
- The increased salivary phosphate secretion in ESRD patients may represent a compensatory mechanism for renal failure.
- However, reabsorption of this elevated salivary phosphate could exacerbate hyperphosphatemia.
- Targeting salivary phosphate for binding presents a potential adjunctive therapeutic approach for managing hyperphosphatemia in ESRD.
Background/Aims:
Hyperphosphatemia is recognized as contributing to the increased risk of cardiac death in end-stage renal disease (ESRD) and hemodialysis (HD) patients. Currently available pharmacologic treatment for hyperphosphatemia is based on phosphate binders but, despite treatment, only half of the patients fall within the range for serum phosphorus of the K/DOQI guidelines. Therefore, there is a need to identify other therapeutic approaches in order to reduce serum phosphate. Salivary fluid contains phosphate which, if related to the daily salivary secretion (1,000-1,880 ml), may raise interest in order to identify further additive approaches to phosphorus removal in uremic patients, while data about salivary phosphate secretion in ESRD patients are controversial.
Methods:
This study evaluates salivary phosphate secretion in 68 HD patients compared with 30 healthy subjects. Saxon's test confirmed normal salivary function in patients and controls. Salivary calcium and serum phosphate, calcium and PTH were also measured.
Results:
HD patients had significantly higher salivary phosphorus levels compared with healthy controls: 30.35 (26.5-34.6) vs. 12.1 (10.58-14.73) mg/dl (p < 0.0001), and this significantly correlated (p < 0.0001) with serum phosphorus. Multiple regression analysis confirmed serum phosphorus as the only predictor (p < 0.0001) of salivary phosphorus.
Conclusions:
Given the functional secretive similarity between salivary glands and the kidneys, this increased salivary phosphate secretion might be interpreted as being compensatory in the presence of renal failure. Absorption of the increased salivary phosphate secretion, however, may worsen hyperphosphatemia; therefore, the binding of salivary phosphate might be considered as a further therapeutic approach to hyperphosphatemia in ESRD.
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Sodium dihydrogen phosphate does not fully dissociate in neutral or acidic solutions. When a strong base, such as sodium hydroxide (NaOH), is introduced into the solution, sodium dihydrogen phosphate...