Praliciguat alone or with enalapril as background therapy in a mouse model of primary FSGS and a rat model of secondary FSGS showed that praliciguat alone offered no benefit.
Clinically approved drugs induced ChAT expression and acetylcholine production in podocytes in vivo, suggesting the pathway could be pharmacologically targeted.
Bodily pain, vitality, and general health perceptions showed stronger associations with quality of life at lower proteinuria thresholds.
Across all patients, higher urinary CD93 was strongly associated with a faster time to a 40% decline in eGFR and a faster time to kidney failure.
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