Metabolic acidosis occurs in CKD when failing kidneys can no longer excrete the 1 mEq/kg/day of acid generated by normal metabolism. Serum bicarbonate falls below 22 mEq/L. Untreated, acidosis accelerates muscle catabolism, worsens bone loss, and independently speeds eGFR decline. KDIGO 2024 recommends treatment with oral sodium bicarbonate to maintain bicarbonate at 23–29 mEq/L.
Every day, normal metabolism generates approximately 1 mEq/kg of acid from protein breakdown (sulphuric acid from sulphur-containing amino acids) and organic acids. Healthy kidneys excrete this acid through two mechanisms: (1) urinary ammonium (NH₄⁺) synthesis by renal tubular cells, and (2) titratable acid (H₂PO₄⁻) excretion. They simultaneously reclaim filtered bicarbonate to maintain blood pH at 7.35–7.45.
In CKD G3–G5, declining nephron mass reduces ammoniagenesis. As acid accumulates, serum bicarbonate — the primary blood buffer — is consumed, falling progressively below the normal 22–29 mEq/L range.
| Serum Bicarbonate | Interpretation | Action |
|---|---|---|
| > 22 mEq/L | Normal — no acidosis | Monitor per CKD stage schedule |
| 18–22 mEq/L | Mild metabolic acidosis | Initiate oral NaHCO₃; increase dietary alkali |
| < 18 mEq/L | Moderate-severe acidosis | Urgent bicarbonate supplementation; reassess diet and medications |
| Target: 23–29 mEq/L | KDIGO 2024 target range | Maintain with oral NaHCO₃ dose titration |
PRAL (Potential Renal Acid Load) is a formula that estimates the acid or alkali yield of foods after metabolism. Foods with negative PRAL are alkali-producing — they generate bicarbonate-equivalent metabolites and counteract CKD acidosis. Foods with positive PRAL are acid-producing and worsen acidosis.
| Food Category | PRAL Effect | Examples | CKD Benefit |
|---|---|---|---|
| Fruits | Strongly negative (alkali) | Apples, pears, berries, grapes | Raises serum bicarbonate; low potassium options available |
| Vegetables | Negative (alkali) | Broccoli, cauliflower, cabbage | Alkali load + KDIGO dietary recommendation |
| Legumes | Near-neutral | Lentils, white beans | Plant protein; low phosphorus bioavailability |
| Animal protein | Strongly positive (acid) | Beef, chicken, fish | High acid load; worsens acidosis and phosphorus |
| Hard cheese | Very positive (acid) | Parmesan, cheddar | High acid + high inorganic phosphorus |
| Processed foods | Positive (acid) + additives | Fast food, packaged meats | High acid load + STPP phosphate additives |
The BASE Pilot Trial (Goraya et al., CJASN 2013) showed that fruit and vegetable supplementation equivalent to ~2 alkali mEq/kg/day raised serum bicarbonate as effectively as sodium bicarbonate tablets in CKD G2–G3 patients — without the additional sodium load.
What causes metabolic acidosis in CKD?
CKD reduces ammoniagenesis — the kidney's ability to excrete acid as urinary ammonium. As eGFR falls below 30–40, acid accumulates in blood and bicarbonate falls below 22 mEq/L. Contributing factors: high dietary acid load (meat, processed foods) and declining tubular function.
What bicarbonate level indicates metabolic acidosis?
Serum bicarbonate below 22 mEq/L indicates metabolic acidosis in CKD. KDIGO 2024 target is 23–29 mEq/L. Below 18 mEq/L is severe and requires urgent treatment with oral sodium bicarbonate supplementation.
Does diet help with metabolic acidosis in CKD?
Yes — fruits and vegetables produce alkaline metabolites (negative PRAL), raising serum bicarbonate by 1–3 mEq/L. The BASE Pilot Trial showed this dietary alkali load works as effectively as bicarbonate tablets in early-stage CKD. Reduce meat and processed food intake to lower acid load.
How is metabolic acidosis treated in CKD?
KDIGO 2024 recommends oral sodium bicarbonate (0.5–1 mEq/kg/day in divided doses) and dietary modification (increase fruit and vegetables, reduce animal protein). Target serum bicarbonate 23–29 mEq/L. Monitor blood pressure as NaHCO₃ adds sodium load.