Two management approaches underpin the importance of hypertension in chronic kidney disease (CKD). High blood pressure raises the risk of heart disease, stroke, peripheral arterial disease (PAD), and kidney failure. The risk is increased if proteinuria is present. Hypertension is the second leading cause of End Stage Renal Disease (ESRD) after diabetes, but most diabetics and CKD patients also have hypertension. The decision to lower blood pressure in patient’s CKD is made to preserve target organ function. Properly treating hypertension in CKD patients reduces the risk of cardiovascular disease.
It is strongly recommended that sodium intake be kept to a maximum of 2,400mg per day. Frequent physical activity and limiting alcohol consumption to two drinks per day for men and one drink per day for women are advised to prevent kidney disease. The DASH diet (Dietary Approaches to Stop Hypertension) is also often suggested by medical professionals. Lowering salt intake can help reduce proteinuria and slow kidney function loss.
Suggestions for drug treatment
The first objective is to establish the blood pressure (BP) target. A blood pressure of 130/80mmHg or below is recommended for individuals with CKD by JNC-7 and the National Kidney Foundation. A blood pressure of 125/75mmHg is recommended for people with CKD who have more than 1g of proteinuria every 24 hours.
Mechanisms of pathogenesis
BP is controlled by four major interrelated systems. The majority of pharmacological treatments target one of these factors. Many of these processes are frequently addressed in the treatment of hypertension caused by CKD. Patients frequently take three or four medications, and in some cases even more, to reach BP goals. The JNC-6:25 risk stratification method is used to determine BP targets.
Blood pressure should be 140/90mmHg in low-risk patients, 130/80mmHg in diabetic patients, and 125/75mmHg in patients with significant proteinuria. Patients with discordant BPs (for example, 128/86mmHg in a higher-risk situation) may have controlled systolic BPs but uncontrolled diastolic BPs.
Retention of salt
In CKD patients, diuretic medication treats salt volume excess, which causes hypertension. When the glomerular filtration rate falls below 30cc/minute, hydrochlorothiazide loses its effectiveness as an antihypertensive, and metolazone is recommended instead. When taking generic loop diuretics like furosemide or bumetanide, dosing is usually done twice a day. This is because the duration of effect is limited to six or eight hours, and rebound salt reabsorption can reduce antihypertensive impact.
In advanced CKD, dose adjustments may be necessary, especially with loop diuretics. Diuretics can also help with other medications such angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and treatments that target nervous system components. If they aren’t used first, they are frequently administered as second-line agents.
System of renin–angiotensin
In non-diabetic CKD, the use of ARB therapy has gotten less attention. Losartan was first marketed in 1995, while captopril was first introduced in 1981, making it more recent than ACE inhibitors. In type 2 diabetic CKD, ARBs have been shown to be effective and beneficial. ARBs are considered to reduce blood pressure and maintain renal function in the same way that ACE inhibitors do, but with less hyperkalemia.
A review of nine ACE inhibitors versus ARB studies reveals a scarcity of significant comparisons in CKD and overall comparability in short-term end-points, such as proteinuria reduction and blood pressure control.
One ONTARGET study demonstrated no meaningful reduction in blood pressure with the combination of ACE inhibitors and ARBs in patients with CKD and hypertension. There was a minor but substantial decrease in glomerular filtration rate with combination therapy, as well as an increased incidence of hyperkalemia. Combination therapy lowers proteinuria in CKD patients but does not appear to slow the progression of the disease.
Nervous system sympathetic
Several studies have shown that beta-blocker therapy is effective in hypertensive patients with CKD. The increased risk of heart failure associated with the use of 1-adrenoreceptor blocking drugs has muted enthusiasm for their use as first or even second-line therapies, except for males with prostate enlargement symptoms.
In the African American Study of Kidney Disease (AASK) for CKD development, it was found that there were no significant differences in glomerular filtration rate slope change over time amongst the three medication groups (ramipril, metoprolol, and amlodipine). Given the sympathetic nervous system’s significant role in CKD progression and interim heart disease, a persuasive case may be made for its use in the management of hypertension in CKD patients.
However, a number of recent studies, such as the Losartan Intervention for Endpoint (LIFE), have found adverse cardiovascular outcomes and a higher incidence of stroke in high-risk hypertensive populations where atenolol was the beta-blocker of choice. The data on atenolol may not be applicable in this group because these patients did not have CKD.
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