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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