Description
Many processes influence the management of chronic kidney disease (CKD) and lead to the development of hypertension in the disease. Increased sympathetic tone in patients with chronic kidney disease (CKD) is a result of afferent signals produced by functionally failing kidneys. The great majority of CKD patients suffer from hypertension, which can both cause and result from the disease. In people with CKD, controlling hypertension is crucial since it lowers the risk of CVD and slows the disease's course. There is no agreement on the ideal blood pressure (BP) targets provided by current guidelines. Consequently, when deciding how to care specific patients.
Summary Listen
- Hypertension, often starting in the kidneys due to RAS system imbalances, is a major modifiable cardiovascular risk factor. Resistant hypertension is defined as uncontrolled BP despite using three or more antihypertensive medications, while controlled resistant hypertension requires four or more medications. A significant portion of the Indian population has hypertension, with a large majority of cases being uncontrolled.
- Pseudo-resistant hypertension needs to be differentiated from true hypertension by excluding white coat hypertension through home or ambulatory BP monitoring. Poor medication adherence, often due to a lack of perceived symptoms, can also mimic resistance and can be addressed through combination or long-acting medications. Proper BP measurement techniques in the clinic are crucial, including patient relaxation, empty bladder, proper cuff size and placement, and arm support.
- Hypertensive nephrosclerosis, the damage to kidney tissue due to hypertension, has risk factors including black race, low birth weight, and certain genes. Pathologically, vascular changes like intimal thickening, glomerular sclerosis, and tubulointerstitial fibrosis are observed. While hypertension alone doesn't rapidly worsen kidney function, it accelerates decline in individuals with pre-existing conditions or severe hypertension.
- Recommended BP targets vary: less than 130/80 mmHg for diabetics and CKD patients (according to ADA and KDIGO guidelines), and less than 140/90 mmHg for elderly or frail patients. Masked hypertension, where BP is elevated outside of clinical settings, is common in CKD and associates with poor outcomes. Pathophysiological factors contributing to hypertension in CKD include increased sympathetic tone, RAS upregulation, salt sensitivity, endothelial dysfunction, and arterial stiffness.
- Treatment strategies involve lifestyle modifications, starting with thiazide diuretics or calcium channel blockers in combination with ACE inhibitors or ARBs. The ACE inhibitor or ARB with thiazide is a strong combination and additional therapies can be added based on patient response. The importance of close potassium and creatinine monitoring when initiating ACE inhibitors or ARBs cannot be overstated.
- Future directions include the use of SGLT2 inhibitors, synthetic MRAs like finerenone, and GLP-1 analogs, particularly in diabetic CKD patients. Ruling out secondary causes of hypertension, such as OSA, hyperaldosteronism, and renal artery stenosis, is also crucial. A stepwise approach to medication management is recommended, starting with optimizing first-line agents and escalating to alpha blockers, beta blockers, loop diuretics, or central alpha-2 agonists.
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