Creatinine does not necessarily go down when uric acid goes down with medication.
The mechanisms leading to high uric acid are mainly increased uric acid production and decreased uric acid excretion. Current uric acid-lowering drugs target the pathogenesis, including uric acid-excreting drugs, drugs that inhibit uric acid production, and alkalizing drugs.
Creatinine is the metabolic end product of creatine in muscle tissue. Creatinine does not bind to protein in the blood and can pass freely through the glomerulus, and is currently the most commonly used indicator to indirectly reflect glomerular filtration function. When the renal parenchyma is damaged, the blood creatinine concentration rises significantly.
Uric acid decreases after taking medication, mainly through increasing uric acid excretion, inhibiting uric acid production, alkalizing the urine and other pathways, making uric acid decrease. Uric acid-lowering drugs, usually no repair of renal function, increase glomerular filtration rate, creatinine generally does not fall.
A small number of patients with high uric acid kidney damage, after active uric acid lowering treatment, uric acid decline, renal function can be partially restored, creatinine may appear to decline.
When patients have abnormal uric acid and creatinine, it is recommended to go to regular hospitals in time, improve the examination to clarify the cause of the disease, and then give targeted treatment or therapy under the guidance of the doctor.