History
Metabolic acidosis, per se, has no specific symptoms and signs, unless it is extremely severe or of acute onset; however, it can produce symptoms and signs from changes in pulmonary, cardiovascular, neurologic, and musculoskeletal function.
General
If the acidosis is marked and/or of acute onset, the patient may report headache, lack of energy, nausea, and vomiting.
Neurologic
Neurologic abnormalities such as mental confusion progressing to stupor, when observed, are not usually secondary to the acidosis but are the cause of the acidosis itself.
In general, neurologic abnormalities are less common in persons with metabolic acidosis than in persons with respiratory acidosis.
Pulmonary
An increase in minute ventilation of up to 4- to- 8-fold may occur in persons with respiratory compensation.
Persistent tachypnea or hyperpnea (affecting the depth more than the rate of ventilation) may be the only clinical clue to an underlying acidotic state. This type of tachypnea/hyperpnea characteristically persists in sleep or interferes with sleep.
Cardiovascular
Effects on the cardiovascular system include direct impairment of myocardial contraction (especially at a pH < 7.2), tachycardia, and increased risk of ventricular fibrillation or heart failure with pulmonary edema. Patients may report dyspnea upon exertion or, in severe cases, at rest.
In advanced stages, overt cardiovascular collapse may occur from impaired catecholamine release.
Musculoskeletal
Chronic acidemia, as is observed in RTA, can lead to a variety of skeletal problems. This is probably due in part to the release of calcium and phosphate during bone buffering of the excess protons. Decreased tubular absorption of calcium secondary to acidemia, especially in dRTA, leads to a negative calcium balance.
Clinical consequences include osteomalacia (leading to impaired growth in children), osteitis fibrosa (from secondary hyperparathyroidism), rickets (in children), and osteomalacia or osteopenia (in adults).
Genitourinary
Important complications of chronic renal tubular acidosis (mainly distal, type I) are nephrocalcinosis and urolithiasis. A number of pathophysiologic alterations contribute to stone formation:
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Buffering of the chronic acid load by the bone, causing bone dissolution and promoting hypercalciuria
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Diminution of renal tubular calcium reabsorption, further aggravating the hypercalciuria
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Hypocitraturia because of avid citrate reabsorption by the PCT
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High urinary pH, causing insolubility of calcium phosphate and promoting its precipitation
A study by Guimerà et al found that of 54 patients with calcium phosphate stones and a urinary pH of over 6.0, dRTA was present in 19 (35.2%). The report indicated that the occurrence of dRTA in these patients was associated with young age, bilateral stones, stone recurrence, hypercalciuria, hypocitraturia, and plasma hypokalemia. [14]
In contrast, stone disease is rare with type II RTA because of the difference in its pathogenesis. Since the fall in plasma HCO3- is nonprogressive, after the renal HCO3 threshold is reached (transport maximum not exceeded), there is complete absorption of luminal HCO3. At this point, the urine pH is acid, since urine is devoid of HCO3- and there is no defect in distal proton secretion. The daily acid load is thus excreted by the collecting duct, obviating the need for bone buffering. Also, citrate usually escapes proximal reabsorption (along with other solutes) and promotes calcium phosphate solubility.
Physical Examination
Pulmonary
An increase in minute ventilation of up to 4- to- 8-fold may occur in persons with respiratory compensation.
Tachypnea or hyperpnea (affecting the depth more than the rate of ventilation) may be the only clinical clue to an underlying acidotic state.
Musculoskeletal
Chronic acidemia, as is observed in RTA, can lead to a variety of skeletal problems. This is probably due in part to the release of calcium and phosphate during bone buffering of the excess protons. Decreased tubular absorption of calcium secondary to acidemia, especially in dRTA, leads to a negative calcium balance.
Clinical consequences include osteomalacia (leading to impaired growth in children), osteitis fibrosa (from secondary hyperparathyroidism), rickets (in children), and osteomalacia or osteopenia (in adults).
