Pathogenesis (disease development)
In latent metabolic acidosis, the alkaline buffer reserves in the blood have already been nearly depleted, but a blood pH shift below 7.36 has not yet occurred. That is, in latent metabolic acidosis, homeostasis of pH is still present within its narrow limits between 7.38 and 7.42.
Etiology (causes)
Biographic causes
- Decrease in the functional reserve capacity of the kidney-beginning around age 40-for excretion of acid equivalents, meaning the kidney increasingly loses the ability to act regulatively by excreting acid equivalents in the event of acidosis and chronic renal insufficiency in old age:
- Decrease in creatinine clearance.
- Exhaustion of the renal enhancement capacity of ammonium production and excretion with persistent acid load.
- Renal plasma flow decreases by circa 10% per decade
- Increasing tubular acidosis due to decrease in regeneration of the major buffering substance bicarbonate (HCO3) in the upper tubule section (proximal tubule)
Behavioral causes
- Nutrition
- Diets (starvation diets; catabolism))
- Increased dietary intake of acid-forming foods (meat, fish, eggs, milk, white flour products, fast food, carbonated soft drinks, sugar, coffee, black tea and alcohol) or insufficient intake of base-donating foods (fruits, vegetables, herbs and still mineral water)
- Hyperalimentation
- Micronutrient deficiency (vital substances) – Latent micronutrient deficiency (vital substances), which can lead to a limitation of enzyme capacity and thus to an increase in cellular acids – see micronutrient therapy.
Disease-related causes
- Chronic renal failure
- Diabetes mellitus (diabetes)
- Liver disease (increase in hepatic acid production).
Laboratory diagnoses – laboratory parameters that are considered independent risk factors.
- Glomerular filtration rate (GFR) ↓
- Hyperuricemia (elevation of uric acid levels in the blood).