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    Sumit Chaudhary
    Hypertension (HTN) and chronic kidney disease (CKD) have a bidirectional relationship where each can cause or worsen the other. HTN is the second leading cause of CKD in the US and is present in 80-95% of CKD patients, with prevalence increasing as kidney function declines. Uncontrolled HTN accelerates CKD progression and increases cardiovascular risks. CKD results in fewer functioning nephrons and impaired sodium excretion, blunting the normal blood pressure response to sodium intake and preventing effective pressure reduction through sodium and fluid excretion. This pathophysiology underlies the development of CKD-associated HTN.

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    First Page PDF

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    Hypertension (HTN) and chronic kidney disease (CKD) have a bidirectional relationship where each can cause or worsen the other. HTN is the second leading cause of CKD in the US and is present in 80-95% of CKD patients, with prevalence increasing as kidney function declines. Uncontrolled HTN accelerates CKD progression and increases cardiovascular risks. CKD results in fewer functioning nephrons and impaired sodium excretion, blunting the normal blood pressure response to sodium intake and preventing effective pressure reduction through sodium and fluid excretion. This pathophysiology underlies the development of CKD-associated HTN.

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    Hypertension (HTN) and chronic kidney disease (CKD) have a bidirectional relationship where each can cause or worsen the other. HTN is the second leading cause of CKD in the US and is present in 80-95% of CKD patients, with prevalence increasing as kidney function declines. Uncontrolled HTN accelerates CKD progression and increases cardiovascular risks. CKD results in fewer functioning nephrons and impaired sodium excretion, blunting the normal blood pressure response to sodium intake and preventing effective pressure reduction through sodium and fluid excretion. This pathophysiology underlies the development of CKD-associated HTN.

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    31 views1 page

    First Page PDF

    Uploaded by

    Sumit Chaudhary
    Hypertension (HTN) and chronic kidney disease (CKD) have a bidirectional relationship where each can cause or worsen the other. HTN is the second leading cause of CKD in the US and is present in 80-95% of CKD patients, with prevalence increasing as kidney function declines. Uncontrolled HTN accelerates CKD progression and increases cardiovascular risks. CKD results in fewer functioning nephrons and impaired sodium excretion, blunting the normal blood pressure response to sodium intake and preventing effective pressure reduction through sodium and fluid excretion. This pathophysiology underlies the development of CKD-associated HTN.

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    Disease-a-Month 61 (2015) 387–395

    Contents lists available at ScienceDirect

    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.

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