Interpretation of Hypertensive Nephropathy

Hypertensive nephropathy and ventilatory nephropathy caused by essential hypertension in benign small arteries of renal sclerosis (also known as hypertensive renal arteriosclerosis) and malignant arterial nephrosclerosis, accompanied by the corresponding clinical manifestations of the disease. The following Tong Shantang experts on the history of hypertension nephropathy symptoms, physical examination and auxiliary examination and other three aspects to resolve.

Interpretation of Hypertensive Nephropathy

History and symptoms

Age more than 40 to 50 years of age, high blood pressure history of 5 to 10 years. Early only nocturia increased, followed by proteinuria, inpidual cases can be due to sudden rupture of capillaries and hematuria, but not with significant low back pain. Often associated with arteriosclerotic retinopathy, left ventricular hypertrophy, coronary heart disease, heart failure, cerebral arteriosclerosis and / or cerebrovascular accident history. Slow progress in the course of a small part of the gradual development of renal failure, the majority of renal dysfunction and severe conventional urine abnormalities. Malignant hypertension, diastolic blood pressure should be more than 16kpa (120mmhg), accompanied by significant heart and brain complications and rapid development, a large number of proteinuria, often accompanied by hematuria, renal dysfunction.

Physical examination found

General blood pressure continued to increase (20,0 / 13kpa, 150 / 100mmhg above); some eyelids and / or lower extremity edema, heart sector expansion; most arteriosclerotic retinopathy, when the eye has a stripe, flame bleeding and cotton Like soft exudation, to support the diagnosis of malignant renal arteriosclerosis. Accompanied by hypertensive encephalopathy may have the corresponding signs of the nervous system.

Auxiliary check

(Red blood cells, white blood cells, transparent tube type) less, may have hematuria; early increase in serum uric acid, urine nag enzyme, β2-2g, Mg increased, urine concentration - dilution dysfunction; ccr more slowly decreased, blood urea nitrogen, creatinine increased. Renal tubular damage more than glomerular damage.

Imaging examination of the kidney more than no change, the development of renal failure can occur in varying degrees of renal reduction; radionuclide early detection of renal damage; ECG often prompted left ventricular high voltage; chest x-ray or echocardiography often suggest aortic Hardening, left ventricular hypertrophy or enlargement.