Why the study?
Optimizing blood pressure in CKD-associated hypertension is challenging, as tight control may worsen outcomes in elderly patients with advanced arteriosclerosis, and the mechanisms of protective therapies like SGLT2 inhibitors remain to be elucidated.
What are the optimal blood pressure targets and pharmacological strategies (including RAS inhibitors, calcium channel blockers, and SGLT2 inhibitors) to protect renal and cardiovascular outcomes in patients with CKD-associated hypertension?
What are the optimal blood pressure targets and pharmacological strategies (including RAS inhibitors, calcium channel blockers, and SGLT2 inhibitors) to protect renal and cardiovascular outcomes in patients with CKD-associated hypertension?
Answers are grounded in this paper and cite their sources.
This review outlines the rationale for the JSN CKD 2018 blood pressure targets in CKD-associated hypertension, emphasizing tailored moderate BP control, caution with RAS inhibitors in elderly atherosclerotic patients, and the emerging cardiorenal benefits of SGLT2 inhibitors.
When renal function declines, blood pressure rises, which in turn causes the kidneys to deteriorate. In order to stop this vicious cycle, it is necessary to lower the blood pressure to a "moderate" level in patients who have chronic kidney disease (CKD)-associated hypertension. Such optimization is problematic, since tight control of blood pressure might worsen the prognosis in elderly patients with CKD, especially those with advanced arteriosclerosis. Although renin-angiotensin system (RAS) inhibitors, angiotensinogen converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are first-line drugs for hypertensive patients with diabetes, they should be used with caution depending on the patients' conditions. Recently, there has been a focus on the preventive effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors, anti-diabetic drugs that have been shown to have an impact, on heart and kidney complications. SGLT2 inhibitors increase the amount of sodium chloride delivered to the macular densa of the distal tubules and correct glomerular hyperfiltration by contraction of afferent arterioles via the tubule-glomerular feedback system. It might be one of the reasons why SGLT2 inhibitors show the renal- and cardio-protective effects; however, the mechanism behind their function remains to be elucidated.
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Nagata et al. (2020) conducted a review in Chronic kidney disease (CKD)-associated hypertension. Antihypertensive therapy (RAS inhibitors, calcium channel blockers) and SGLT2 inhibitors vs. Different blood pressure targets and drug classes across major clinical guidelines was evaluated on Renal prognosis (progression to end-stage kidney disease, doubling of serum creatinine, eGFR decline) and cardiovascular events.
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