Bicarbonate and Acid Balance in Kidney Failure
Bicarbonate does not turn to acid in kidney failure; rather, the kidneys fail to excrete acid and regenerate bicarbonate, leading to acid accumulation and decreased serum bicarbonate levels. 1, 2
Pathophysiology of Acid-Base Imbalance in Kidney Failure
The kidneys play a critical role in acid-base homeostasis through three main mechanisms:
- Reabsorption of filtered bicarbonate
- Excretion of titratable acids
- Production and excretion of ammonium
In chronic kidney disease (CKD), these processes become impaired:
- Reduced Acid Excretion: As kidney function declines, the ability to excrete acid in the form of ammonium decreases 3
- Bicarbonate Handling: Contrary to the question's premise, bicarbonate is not converted to acid; instead, the kidneys fail to regenerate enough bicarbonate to buffer the daily acid load 2
- Acid Retention: This leads to accumulation of acids in the body, resulting in metabolic acidosis 1
Clinical Manifestations
Metabolic acidosis typically develops when glomerular filtration rate (GFR) falls below 20-25% of normal 4, 2. Key characteristics include:
- Serum bicarbonate concentrations typically range from 12-22 mEq/L (mmol/L) 4
- Both high anion gap and normal anion gap (hyperchloremic) acidosis can occur 1, 2
- Severity of acidosis generally correlates with the degree of renal impairment 4
Diagnostic Considerations
- Laboratory evaluation should include arterial blood gases, serum electrolytes with calculated anion gap, and renal function tests 1
- The urine anion gap (UAG) is a valuable tool for evaluating hyperchloremic metabolic acidosis and assessing renal ammonium excretion 1
- UAG calculation: (Na⁺ + K⁺) - Cl⁻ 1
- Positive UAG indicates impaired renal acid excretion
- Negative UAG suggests adequate renal ammonium excretion
Clinical Implications and Complications
Metabolic acidosis in kidney failure is associated with several adverse consequences:
- Muscle wasting and protein catabolism
- Bone disease and impaired growth
- Progression of kidney disease
- Increased mortality
- Abnormalities in hormone secretion
- Impaired insulin sensitivity 4, 2
Treatment Approach
Treatment is recommended when serum bicarbonate falls below 22 mmol/L 2, 3:
- Focus on correcting the underlying cause when possible
- Administer base supplementation (sodium bicarbonate or citrate)
- Target serum bicarbonate levels carefully - evidence suggests maintaining levels between 22-24 mEq/L 2, 3
- Avoid excessive correction (>26 mEq/L) due to potential cardiovascular risks 3
Special Considerations
- Diabetic patients with advanced kidney failure tend to have less severe metabolic acidosis compared to non-diabetic patients with similar kidney function 5
- Extrarenal buffering may help maintain near-normal acid-base status even with marked reduction in GFR 6
- Monitoring for complications of bicarbonate therapy is essential, including volume overload, hypertension, and potential vascular calcifications 4
Clinical Pearls
- Acidosis is rarely seen until GFR decreases to less than 20-25% of normal 4, 2
- The acidosis of kidney failure is primarily due to reduced functional renal mass rather than bicarbonate wastage 6
- Per-nephron bicarbonate reabsorption and ammonium production are actually enhanced in the remaining functional nephrons 6
- The decision to initiate dialysis may be influenced by uncontrollable acidosis 6