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Posted By: Ben Taylor, PA-C, PhD, DFAAPA
February 15, 2019
Hypertension (HTN) is present in approximately 80% to 85% of patients with chronic kidney disease (CKD). Uncontrolled HTN is the second leading cause of kidney failure in the US behind diabetes. The prevalence of HTN is elevated in patients with kidney damage and a normal glomerular filtration rate (GFR) and increases further as the GFR falls.
HTN treatment is the mainstay of slowing progression of CKD. The blood pressure (BP) goal should be below 140/90 mm Hg in CKD without proteinuria and if proteinuria is present, the BP should be lower than 130/80 mm Hg. Overall, the best evidence supports more intensive BP lowering, which reduces the risk of end-stage renal disease (ESRD) in patients with proteinuric CKD but not in patients with nonproteinuric CKD. It is also thought that more intensive BP lowering may reduce mortality in patients with CKD (whether they have proteinuria or not), even though there is no benefit on renal endpoints among patients without proteinuria. The mortality benefit from aggressive BP lowering is most evident when patients are followed over the long-term.
Multiple guidelines discuss the importance of lowering BP to slow the progression of renal disease and reduce cardiovascular morbidity and mortality. However, in order to achieve and maintain adequate BP control, most patients with CKD require combinations of antihypertensive agents; often up to three or four medication classes may need to be utilized.
Angiotensin-converting-enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) are the first-line drugs of therapy unless contraindicated. These agents target the renin-angiotensin system to prevent kidney decline more so than other agents, even when achieving similar BP goals. These results were found primarily in patients with proteinuria, whereas the benefit was less substantial for those without proteinuria. You will most likely see a modest increase of serum creatinine levels up to 30% from baseline, which may be tolerated and should not be an indication for cessation. Sodium restriction is essential and improves end point results for both HTN and CKD. Diuretics are effective in the edematous CKD patient. Non-dihydropyridine calcium blockers are second-line therapy in hypertensive CKD patients. Mineralocorticoid antagonists decrease both BP and proteinuria, but the risk of hyperkalemia in high doses and in combination with ACEIs and ARBs should be kept in mind. Lastly, bedtime antihypertensive medication may be helpful in CKD patients with HTN who demonstrate non-dipper patterns.
- Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis.2004;43:S1.
- Ku E, Gassman J, Appel LJ, et al. BP control and long-term risk of ESRD and mortality. J Am Soc Nephrol. 2017;28:671.
- Lv J, Ehteshami P, Sarnak MJ, et al. Effects of intensive blood pressure lowering on the progression of chronic kidney disease: a systematic review and meta-analysis. CMAJ. 2013;185:949-957.
- Malhotra R, Nguyen HA, Benavente O, et al. Association between more intensive vs less intensive blood pressure lowering and risk of mortality in chronic kidney disease stages 3 to 5: a systematic review and meta-analysis. JAMA Intern Med. 2017;177:1498.
- National Institute of Health. United States renal data system. www.usrds.org/adr.aspx. Accessed February 11, 2019.
- Tsai WC, Wu HY, Peng YS, et al. Association of intensive blood pressure control and kidney disease progression in nondiabetic patients with chronic kidney disease: a systematic review and meta-analysis. JAMA Intern Med. 2017;177:792.
- Upadhyay A, Earley A, Haynes SM, Uhlig K. Systematic review: blood pressure target in chronic kidney disease and proteinuria as an effect modifier. Ann Intern Med. 2011;154:541.
Filed under: Urology