There are no official guidelines to assist in answering this question. I will search for relevant research papers instead.
The FDA Drug Labels for oseltamivir (PO) do not address this question.
From the Research
Tamiflu (Oseltamivir) and Acute Kidney Injury (AKI)
- There is evidence to suggest that oseltamivir can cause Acute Kidney Injury (AKI) in certain patients, particularly those with pre-existing renal impairment or those undergoing continuous venovenous hemodiafiltration (CVVHDF) 1.
- A study found that patients on CVVHDF due to acute kidney injury had 4-to 5-fold higher oseltamivir carboxylate concentrations, suggesting that the drug can accumulate in the plasma of patients with renal failure 1.
- Another study reported a case of granulomatous interstitial nephritis associated with influenza A: H1N1 infection, which was treated with oseltamivir phosphate (Tamiflu) 2.
- However, it is not clear if oseltamivir can cause AKI in patients with normal renal function after 4 days of treatment.
- A study on the pharmacokinetics and safety of oseltamivir in patients with end-stage renal disease treated with automated peritoneal dialysis found that oseltamivir was well tolerated, but the disposition of the drug was poorly understood in this patient population 3.
- The mechanisms of delayed onset type adverse reactions to oseltamivir, including renal disorders, are thought to be related to the inhibition of the host's endogenous neuraminidase 4.
Key Findings
- Oseltamivir can accumulate in the plasma of patients with renal failure, particularly those undergoing CVVHDF 1.
- Patients with pre-existing renal impairment or those undergoing CVVHDF may require dose reductions and monitoring of plasma levels of oseltamivir carboxylate 1.
- The disposition of oseltamivir is poorly understood in patients with end-stage renal disease, and further studies are needed to optimize dosing in this patient population 3.
- The mechanisms of adverse reactions to oseltamivir, including renal disorders, are thought to be related to the inhibition of the host's endogenous neuraminidase 4.