Maribavir and Renal Tubular Acidosis
Maribavir does not cause renal tubular acidosis in transplant recipients being treated for refractory cytomegalovirus infection. This agent has a distinctly favorable renal safety profile compared to traditional CMV antivirals.
Key Safety Profile
Maribavir demonstrates no nephrotoxicity, which represents a major advantage over foscarnet and cidofovir 1. In the pivotal phase III trial, maribavir was associated with significantly less acute kidney injury compared to foscarnet (8.5% vs 21.3%) 1. This absence of renal toxicity extends to all forms of kidney injury, including tubular dysfunction.
Comparative Renal Safety
The renal safety advantage of maribavir is particularly striking when compared to alternative agents:
- Foscarnet: Requires monitoring for nephrotoxicity and electrolyte abnormalities, including renal tubular acidosis 2, 3
- Cidofovir: Known for significant nephrotoxicity limiting its use 1
- Maribavir: No dose adjustment required for renal function and no observed nephrotoxicity 4
Actual Adverse Effects of Maribavir
The most common treatment-related adverse events with maribavir are:
- Dysgeusia (taste disturbance): Most frequent side effect, occurring in 65% of patients, though rarely leading to discontinuation 5
- Minimal myelosuppression: Neutropenia occurred in only 9.4% versus 33.9% with valganciclovir/ganciclovir 1
- No electrolyte disturbances: Unlike foscarnet, which causes renal tubular acidosis and electrolyte abnormalities 2
Clinical Implications
When treating refractory or resistant CMV infections in transplant recipients:
- Maribavir is preferred for patients with renal dysfunction precisely because it lacks nephrotoxicity 6
- No monitoring for renal tubular acidosis is required with maribavir, unlike foscarnet 2, 4
- The 56% clearance rate in refractory CMV comes without the renal complications seen with foscarnet (21.3% acute kidney injury) 1, 3
Important Caveat
The primary concern with maribavir is treatment-emergent resistance, not renal toxicity. Resistance mutations can develop in 66.7% of non-responders, particularly in patients with high baseline viral loads 7, 6. Close monitoring for CMV viral load rebound is essential, with consideration for repeat resistance testing if treatment fails 7.