Acid Load and Phosphorus Homeostasis in CKD

Area of Science:

• Nephrology
• Endocrinology
• Acid-Base Physiology

Background:

• Kidneys maintain acid-base balance via ammonium and titratable acid excretion.
• Impaired kidney function in CKD can lead to metabolic acidosis.
• Metabolic acidosis may stimulate phosphaturic hormones, but this is not confirmed in humans.

Purpose of the Study:

• To investigate the association between acid load, acidosis, and phosphorus homeostasis in CKD patients.
• To determine if higher acid load and acidosis correlate with urinary phosphorus excretion, serum phosphorus, PTH, and FGF-23.
• To explore potential adaptations in acid-base and phosphorus regulation in CKD.

Main Methods:

• Cross-sectional study of 980 CKD participants from the CRIC Study.
• Measured 24-hour urine net acid excretion, estimated dietary potential renal acid load (PRAL), and serum bicarbonate.
• Assessed 24-hour urine phosphorus and calcium excretion, and serum phosphorus, FGF-23, and PTH concentrations.

Main Results:

• Higher net acid excretion, PRAL, and lower serum bicarbonate were associated with increased urinary phosphorus excretion (P<0.05).
• Higher net acid excretion and lower serum bicarbonate correlated with higher serum phosphorus concentrations (P=0.001).
• Neither net acid excretion nor PRAL consistently associated with FGF-23 or PTH; PTH was higher with lower bicarbonate (P<0.001).

Conclusions:

• In CKD, increased acid load and acidosis are independently linked to higher serum phosphorus and augmented phosphaturia.
• The study suggests an adaptive mechanism for acid-base homeostasis in CKD, increasing titratable acid excretion.
• Further interventional trials are needed to confirm if base administration can reduce phosphorus levels in CKD.