p-Cresyl Sulfate is the major uremic toxin present in the blood of patients with chronic kidney disease and is derived from the metabolites of tyrosine and phenylalanine in the liver.

METHODS: H9C2 cardiomyocytes were treated with p-Cresyl Sulfate (3.125, 6.25, 12.5, 25.0 μg/mL) to study the changes in cell proliferation, cell size and mitochondrial parameters, including morphology, respiration, biogenesis and membrane potential.
RESULTS The lowest effective dose of p-Cresyl Sulfate (6.25 μg/mL) induced mitochondrial hypertransfusion, enhanced mitochondrial connectivity, increased mitochondrial oxygen consumption rate, mitochondrial mass, mitochondrial DNA copy number and cardiomyocyte volume; at the same time, p-Cresyl Sulfate increased the phosphorylation of energy-sensing adenosine monophosphate-activated protein kinase (AMPK), but did not induce cell apoptosis. [2]

METHODS: Mice with AKI induced by ischemia and reperfusion (IR) injury were treated with p-Cresyl Sulfate (20, 40, or 60 mg/L/day for 15 days) to evaluate the effects of p-Cresyl Sulfate administration on renal and cardiac function.
RESULTS p-Cresyl Sulfate at a dose of 20 mg/L resulted in decreased renal mass, increased cystatin C and kidney injury molecule 1 (KIM-1) gene expression, and decreased α-actin in the heart. [3]