Tenofovir and Severe Symptomatic Hypophosphatemia

Area of Science:

• Nephrology
• Pharmacology
• Toxicology

Background:

• Tenofovir is a key antiretroviral medication for HIV treatment.
• Clinical use reveals a risk of renal damage (AKI/CKD), contrary to initial trial data.
• The mechanism involves Tenofovir accumulation in renal proximal tubule cells.

Observation:

• Tenofovir is transported into proximal tubule cells via organic anion transporters (hOAT1, OAT3).
• Excretion involves apical transporters (MRP4, MRP2).
• Mitochondrial injury in proximal tubule cells is implicated in Tenofovir nephrotoxicity.

Findings:

• Tenofovir-induced mitochondrial injury can cause Fanconi's syndrome.
• Manifestations include renal tubular acidosis, phosphaturia, aminoaciduria, glucosuria, and proteinuria.
• This case details severe hypophosphatemia necessitating hospitalization and IV phosphate therapy.

Implications:

• Understanding Tenofovir's renal transport and cellular effects is crucial.
• Monitoring for and managing Tenofovir-induced nephrotoxicity, including electrolyte disturbances, is essential.
• This case underscores the potential for severe metabolic complications requiring intensive treatment.