Regardless of high or normal blood pressure, creatinine is basically excreted through glomerular filtration, and renal injury caused by high blood pressure can reduce creatinine excretion through the glomerulus.
Creatinine in the human body is mainly produced by creatine formed by the metabolism of muscle tissue. Under normal circumstances, creatinine in the blood is mainly excreted through glomerular filtration, and basically does not pass through the reabsorption or secretion of the renal tubules.
Long-term sustained hypertension increases the pressure in the glomerular endocapsules, glomerular fibrosis and atrophy, and renal arteriosclerosis, leading to ischemia of the renal parenchyma and a continuous decrease in renal units, and a decrease in creatinine leakage from the glomeruli, which leads to an increase in blood creatinine. In malignant hypertension, proliferative endocarditis and fibrinoid necrosis occurs in the small incoming glomerular arteries and interlobular arteries, which can lead to elevated blood creatinine in a short period of time.
Hypertensive patients are recommended to consult regular hospitals in time, complete relevant examinations under the guidance of physicians, assess renal function, timely treatment, and delay the progression of renal disease.