| Theme |
Abnormal Blood Pressure in Dialysis Patients |
| Title |
Mechanisms of high blood pressure in CKD patients |
| Author |
Hiroo Kumagai |
Department of Nephrology, National Defense Medical College |
| Author |
Naoki Oshima |
Department of Nephrology, National Defense Medical College |
| Author |
Kojiro Yamamoto |
Department of Nephrology, National Defense Medical College |
| Author |
Atsushi Watanabe |
Department of Nephrology, National Defense Medical College |
| Author |
Takahiro Uchida |
Department of Nephrology, National Defense Medical College |
| [ Summary ] |
In patients with chronic kidney diseases (CKD) and hemodialysis, various pathophysiological factors elevate blood pressure (BP). Since the slope of the pressure natriuresis curve is gradual, elevation of systemic BP is needed to help CKD patients secrete increased sodium loads. This is a mechanism underlying high salt sensitivity in hypertensive patients with CKD. Non-dipper type BP variability contributes high blood pressure. Plasma renin activity and sympathetic nerve activities should be suppressed when sodium loads are increased. However, plasma renin activity and sympathetic activities are not suppressed in CKD patients, which contributes to hypertension. In CKD model rats, activity in the kidneys, such as renal injury, ischemia, and changes in angiotensin II levels, stimulates afferent renal sensory nerves. Information from stimulated afferent renal nerves is transmitted to the hypothalamus. Potentiated activities of the hypothalamus and rostral ventrolateral medulla neurons stimulate efferent sympathetic activities to the heart, arterioles and kidneys, elevating BP. |