Disease-a-Month 61 (2015) 387–395

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Disease-a-Month

journal homepage: www.elsevier.com/locate/disamonth

Hypertension and chronic kidney disease

Richard Gargiulo, DO, Faten Suhail, MD, Edgar V. Lerma, MD

Epidemiology

Hypertension (HTN) and chronic kidney disease (CKD) have a unique relationship in that they
are both a cause and consequence of each other. Essential HTN is the second leading cause of
kidney disease in the United States behind only diabetes.1 CKD is currently estimated to affect
about 26 million people in the United States alone.2 African Americans and Hispanics have been
shown to be at greater risk for CKD and for faster development to end-stage renal disease
(ESRD).3 HTN is found in 80–85% of all CKD patients, with a higher prevalence being seen in
those with worse kidney function. The MDRD study showed HTN prevalence increasing from
65% to 95% as glomerular filtration rates (GFR) decreased from 85% to 15%.4 Multiple studies
have proven uncontrolled HTN to be a strong risk factor for progression of CKD to ESRD and
severe cardiovascular effects including heart disease and stroke.5 Resistant HTN and nocturnal
HTN are also found at higher rates in CKD patients and have been shown to result in a faster
renal decline and more cardiovascular complications.6,7 Treatment goals have recently been
changing due to new guidelines published by multiple medical societies, but overall, there has
been improvement in obtaining optimal blood pressure levels. The CRIC study, a cohort study of
3612 CKD patients in 2010, showed that 67% of patients reached their blood pressure goal of
o 140/90 mmHg and 46% reached their goal of o 130/90 mmHg. This is compared to HTN
control rates in the general population of 50% from 2007 to 2008.3,8

Pathophysiology

Abnormalities of sodium homeostasis are required for the development of HTN and play a
significant role in the development in CKD-associated HTN. Normal blood pressure levels are
usually tightly maintained through a process called “pressure natriuresis.” This occurs when the
renal vasculature notices an acute rise in systemic blood pressure leading to increased renal
sodium excretion and subsequent loss of extracellular fluid, thereby decreasing the overall blood
pressure. This mechanism also works in reverse, by retaining sodium and fluid when blood
pressure is low.9 The physiologic changes of CKD result in fewer nephrons and abnormal renal
tubular exchange leading to a decline in sodium excretion in a hypertensive environment.9,10
This causes a blunting of the normal diuretic response seen in pressure natriuresis and therefore
an inability to effectively decrease blood pressure elevations through sodium and fluid excretion.

http://dx.doi.org/10.1016/j.disamonth.2015.07.003
0011-5029/& 2015 Mosby, Inc. All rights reserved.