Victoza® is not indicated for weight loss.
Studies in adults with type 2 diabetes
There is limited experience with Victoza® in patients with end stage renal disease.
Victoza® has not been found to be directly nephrotoxic in animal studies or clinical trials. There have been postmarketing reports of acute renal failure and worsening of chronic renal failure, which may sometimes require hemodialysis in Victoza®-treated patients. Some of these events were reported in patients without known underlying renal disease. A majority of the reported events occurred in patients who had experienced nausea, vomiting, diarrhea, or dehydration. Use caution when initiating or escalating doses of Victoza® in patients with renal impairment.
Victoza® is not filtered by the kidneys5
In the LIRA-RENAL study, Victoza® showed no significant difference in renal function vs placebo as measured by eGFR, as a safety endpoint.6
Study-related adverse events
Adverse reactions reported in ≥5% of patients and occurring more frequently with Victoza® compared with placebo included nausea (21.4% vs 4.4%), vomiting (12.1% vs 2.2%), diarrhea (7.1% vs 2.9%), constipation (5.7% vs 1.5%), increased lipase (15.0% vs 8.8%), GFR rate decreased (6.4% vs 5.1%), and headache (5.0% vs 2.9%).
A 26-week, double-blind, placebo-controlled, parallel-group, randomized study in adult patients with type 2 diabetes and moderate renal impairment (eGFR 30-59 mL/min/1.73 m2). Patients were randomized to receive Victoza® 1.8 mg (n=140) or placebo (n=139) in addition to existing oral antidiabetics and/or insulin therapy. The primary endpoint was change in A1C. The insulin dose was reduced by 20% at randomization for patients with baseline A1C ≤8% and fixed until liraglutide dose escalation was complete. Dose reduction of insulin and SU was allowed in case of hypoglycemia; up titration of insulin was allowed but not beyond the pre-trial dose.
Victoza® was superior in reducing A1C from baseline versus placebo at 26 weeks4
Overall, the type, and severity of adverse reactions in adolescents and children aged 10 years and above were comparable to that observed in the adult population.
In pediatric patients 10 years of age and older, the risk of hypoglycemia was higher with Victoza® regardless of insulin and/or metformin use.
The change from baseline to end-of-treatment visit in A1C was analyzed using a pattern mixture model with multiple imputation. Missing observations (10.6% in the Victoza®, 14.5% in the placebo) were imputed from the placebo arm based on multiple (x10,000) imputations. The data for week 26 was then analyzed with an ANCOVA model containing treatment, sex, and age group as fixed effects and baseline value as covariate.
A 26-week, randomized, parallel-group, placebo-controlled trial with a 26-week double-blind period followed by a 26-week open-label extension. Eligible patients (N=135) between the ages 10-17 had A1C levels between 7%-11% if they were being treated with diet and exercise alone or between 6.5%-11% if they were being treated with metformin (with or without insulin) and had a body-mass index (BMI) greater than the 85th percentile. Patients were randomized (1:1) to receive once-daily Victoza® (n=66) or placebo (n=68) for 26 weeks in combination with metformin with or without basal insulin on a background of diet and exercise regimen.
The treatment (Victoza® or placebo) was unblinded after the 26-week visit, and the trial was continued for an additional 26-week open-label extension. The basal insulin dose was decreased by 20% at randomization and Victoza® was initiated at 0.6 mg/day and was titrated to 1.2 mg and 1.8 mg over the course of 2-3 weeks based on tolerability and an average fasting plasma glucose goal of ≤110 mg/dL. The primary endpoint was change in A1C from baseline at 26 weeks.
CKD=chronic kidney disease; DPP-4=dipeptidyl peptidase-4; eGFR=estimated glomerular filtration rate; GLP-1 RA=glucagon-like peptide-1 receptor agonist; OAD=oral antidiabetic drug.