Epidemiology
Etiology
- Autoimmune diseases
- Chronic obstructive uropathy (e.g., congenital anomalies)
- Sickle cell nephropathy
- Drugs: ifosfamide, amphotericin B, lithium, NSAIDs (analgesic nephropathy)
Pathophysiology
The α-intercalated cells of the distal tubule are unable to secrete H+ (apical) → ↓ intracellular production of HCO3- → ↓ HCO3-/Cl- exchanger activity (basolateral) → decreased concentration of HCO3- in the blood → metabolic acidosis
Clinical features
- Nephrocalcinosis: calcium phosphate stones (due to an increase in urine pH
- Bone demineralization usually without overt rickets or osteomalacia (due to increased bone turnover)
- Impaired growth
Diagnostics
Treatment
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