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Treatment of Resistant

CONTINUING EDUCATION

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16harry.scher@va.gov . Michelle L. Drew, DNP, MPH, CNM, FNP-C, is an XX in the Department of XX. Damon B. Cottrell, DNP, FNP-C, ACNS-BC, CCNS, is an XX in the Department of XX. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a con fl ict of interest. T reatment of resistant hypertension (RHTN) (CKD) presents nurse practitioners (NPs) signi fi cant threat, because long-standing high levels of blood pressure along with concomitant debilitating entities, such as CKD, create a prominent high- cardiovascular-risk milieu. Effective individualized treatment for RHTN requires NPs to recognize that RHTN and CKD are entangled in a complex and vicious interaction. The purpose of this study is to in a patient with chronic kidney disease with unique challenges as they attempt to effectively treat RHTN while preserving kidney function. Notwithstanding appropriate treatment, the “ un- controllable ” part of hypertension, RHTN, is a This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their understanding of the importance of treating resistant high blood pressure (HBP) in patients with chronic kidney disease (CKD). At the conclusion of this activity, the participant will be able to: A. Identify the evidence-based medical treatments for resistant HBP B. Describe the lifestyle modi fi cations effective in managing resistant HBP in patents with CKD C. Explain diagnostic studies for several causes of secondary HBP The authors, reviewers, editors, and nurse planners all report no fi nancial relationships that would pose a con fl ict of interest. The authors do not present any off-label or non-FDA-approved recommendations for treatment. This activity has been awarded 1.0 contact hours for nurses of which 1.0 credit is in the area of pharmacology. The activity is valid for CE credit until July 1, 2017. Readers may receive the 1.0 CE credit free by reading the article and answering each question online at www.npjournal.org , or they may mail the test answers and Q7 evaluation, along with a processing fee check for $10 made out to Elsevier, to PO Box 1461, American Fork, UT 84003. Required minimum passing score is 70%. This educational activity is provided by Nurse Practitioner Alternatives . NPA is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center ’ s Commission on Accreditation. Accreditation does not imply endorsement by the provider, Elsevier, or ANCC of recommendations or any commercial products displayed or discussed in conjunction with the educational activity. www.npjournal.org The Journal for Nurse Practitioners - JNP 1 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-0-104" src="pdf-obj-0-104.jpg">

Hypertension in the Patient With

Chronic Kidney Disease

Q8 Harry E. Scher, MS, APRN, Michelle L. Drew, DNP, FNP, and

Damon B. Cottrell, DNP, FNP ABSTRACT
Damon B. Cottrell, DNP, FNP
ABSTRACT

The burden of risk and the impact of disease associated with poorly controlled hypertension in the United

States population presents signicant challenges to primary care providers, including nurse practitioners. The

lack of blood pressure control leads to a staggering number of premature deaths annually. To reduce risk for

major cardiovascular events, aggressive approaches to treatment of resistant hypertension must be considered.

Hypertension plays a key role in the progression of chronic kidney disease. The goal of treating resistant

hypertension must be directed at reducing cardiovascular risk while preserving renal function.

Keywords: chronic kidney disease, clinical inertia, hypertension, resistant hypertension

Published by Elsevier, Inc.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16harry.scher@va.gov . Michelle L. Drew, DNP, MPH, CNM, FNP-C, is an XX in the Department of XX. Damon B. Cottrell, DNP, FNP-C, ACNS-BC, CCNS, is an XX in the Department of XX. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a con fl ict of interest. T reatment of resistant hypertension (RHTN) (CKD) presents nurse practitioners (NPs) signi fi cant threat, because long-standing high levels of blood pressure along with concomitant debilitating entities, such as CKD, create a prominent high- cardiovascular-risk milieu. Effective individualized treatment for RHTN requires NPs to recognize that RHTN and CKD are entangled in a complex and vicious interaction. The purpose of this study is to in a patient with chronic kidney disease with unique challenges as they attempt to effectively treat RHTN while preserving kidney function. Notwithstanding appropriate treatment, the “ un- controllable ” part of hypertension, RHTN, is a This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their understanding of the importance of treating resistant high blood pressure (HBP) in patients with chronic kidney disease (CKD). At the conclusion of this activity, the participant will be able to: A. Identify the evidence-based medical treatments for resistant HBP B. Describe the lifestyle modi fi cations effective in managing resistant HBP in patents with CKD C. Explain diagnostic studies for several causes of secondary HBP The authors, reviewers, editors, and nurse planners all report no fi nancial relationships that would pose a con fl ict of interest. The authors do not present any off-label or non-FDA-approved recommendations for treatment. This activity has been awarded 1.0 contact hours for nurses of which 1.0 credit is in the area of pharmacology. The activity is valid for CE credit until July 1, 2017. Readers may receive the 1.0 CE credit free by reading the article and answering each question online at www.npjournal.org , or they may mail the test answers and Q7 evaluation, along with a processing fee check for $10 made out to Elsevier, to PO Box 1461, American Fork, UT 84003. Required minimum passing score is 70%. This educational activity is provided by Nurse Practitioner Alternatives . NPA is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center ’ s Commission on Accreditation. Accreditation does not imply endorsement by the provider, Elsevier, or ANCC of recommendations or any commercial products displayed or discussed in conjunction with the educational activity. www.npjournal.org The Journal for Nurse Practitioners - JNP 1 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-0-140" src="pdf-obj-0-140.jpg">

All authors are afliated with Texas Womans University in Dallas. Harry E. Scher, MS, APRN, BC, is an XX in the Department of XX. He can be reached at harry.scher@va.gov. Michelle L. Drew, DNP, MPH, CNM, FNP-C, is an XX in the Department of XX. Damon B. Cottrell, DNP, FNP-C, ACNS-BC, CCNS, is an XX in the Department of XX. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conict of interest.

T reatment of resistant hypertension (RHTN)

(CKD) presents nurse practitioners (NPs)

signicant threat, because long-standing high levels of blood pressure along with concomitant debilitating entities, such as CKD, create a prominent high- cardiovascular-risk milieu. Effective individualized treatment for RHTN requires NPs to recognize that RHTN and CKD are entangled in a complex and vicious interaction. The purpose of this study is to

in a patient with chronic kidney disease

with unique challenges as they attempt to effectively

treat RHTN while preserving kidney function.

Notwithstanding appropriate treatment, the un-

controllablepart of hypertension, RHTN, is a

This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their understanding of the importance of treating resistant high blood pressure (HBP) in patients with chronic kidney disease (CKD).

At the conclusion of this activity, the participant will be able to:

  • A. Identify the evidence-based medical treatments for resistant HBP

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16harry.scher@va.gov . Michelle L. Drew, DNP, MPH, CNM, FNP-C, is an XX in the Department of XX. Damon B. Cottrell, DNP, FNP-C, ACNS-BC, CCNS, is an XX in the Department of XX. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a con fl ict of interest. T reatment of resistant hypertension (RHTN) (CKD) presents nurse practitioners (NPs) signi fi cant threat, because long-standing high levels of blood pressure along with concomitant debilitating entities, such as CKD, create a prominent high- cardiovascular-risk milieu. Effective individualized treatment for RHTN requires NPs to recognize that RHTN and CKD are entangled in a complex and vicious interaction. The purpose of this study is to in a patient with chronic kidney disease with unique challenges as they attempt to effectively treat RHTN while preserving kidney function. Notwithstanding appropriate treatment, the “ un- controllable ” part of hypertension, RHTN, is a This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their understanding of the importance of treating resistant high blood pressure (HBP) in patients with chronic kidney disease (CKD). At the conclusion of this activity, the participant will be able to: A. Identify the evidence-based medical treatments for resistant HBP B. Describe the lifestyle modi fi cations effective in managing resistant HBP in patents with CKD C. Explain diagnostic studies for several causes of secondary HBP The authors, reviewers, editors, and nurse planners all report no fi nancial relationships that would pose a con fl ict of interest. The authors do not present any off-label or non-FDA-approved recommendations for treatment. This activity has been awarded 1.0 contact hours for nurses of which 1.0 credit is in the area of pharmacology. The activity is valid for CE credit until July 1, 2017. Readers may receive the 1.0 CE credit free by reading the article and answering each question online at www.npjournal.org , or they may mail the test answers and Q7 evaluation, along with a processing fee check for $10 made out to Elsevier, to PO Box 1461, American Fork, UT 84003. Required minimum passing score is 70%. This educational activity is provided by Nurse Practitioner Alternatives . NPA is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center ’ s Commission on Accreditation. Accreditation does not imply endorsement by the provider, Elsevier, or ANCC of recommendations or any commercial products displayed or discussed in conjunction with the educational activity. www.npjournal.org The Journal for Nurse Practitioners - JNP 1 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-0-181" src="pdf-obj-0-181.jpg">
  • B. Describe the lifestyle modications effective in managing resistant HBP in patents with CKD

  • C. Explain diagnostic studies for several causes of secondary HBP

The authors, reviewers, editors, and nurse planners all report

no nancial relationships that would pose a conict of interest.

The authors do not present any off-label or non-FDA-approved recommendations for treatment. This activity has been awarded 1.0 contact hours for nurses of which 1.0 credit is in the area of pharmacology. The activity is valid for CE credit until July 1, 2017. Readers may receive the 1.0 CE credit free by reading the article and answering each question online at www.npjournal.org, or they may mail the test answers and

Q7

evaluation, along with a processing fee check for $10 made out to Elsevier, to PO Box 1461, American Fork, UT 84003. Required minimum passing score is 70%.

This educational activity is provided by Nurse Practitioner Alternatives .

NPA is accredited as a provider of continuing nursing education by the American Nurses Credentialing Centers Commission on Accreditation.

Accreditation does not imply endorsement by the provider, Elsevier, or ANCC of recommendations or any commercial products displayed or discussed in conjunction with the educational activity.

The Journal for Nurse Practitioners - JNP

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99 enhance and expand NPs ’ understanding of RHTN 100 101 102 103 104 105 106
  • 99 enhance and expand NPsunderstanding of RHTN

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with CKD through discussion of evidence-based best

practice. The discussion includes a review of patho-

physiologic mechanisms related to RHTN associated

with CKD as well as both pharmacologic and non-

pharmacologic treatment. A real-life case study is pre-

sented to demonstrate the use of treatment principles.

PROBLEM IDENTIFICATION

Essential hypertension (HTN) is the most prevalent

controllable disease in developed countries, affecting

> 25% of the adult population. The global disease

burden is immense, with 62% of strokes, 49% of heart

disease, and 7.5 million deaths per year attributed

to HTN, which is a major modiable risk factor

affecting nearly 1 in 3 adults in the United States.

Thus, HTN, as the foremost risk factor for coronary

artery disease and stroke, is responsible for the ma-

jority of cardiovascular morbidity and mortality in

providers can lead to prevention of renal disease and decrease risk of cardiovascular disease. Numerous risk factors contribute to the devel- opment of hypertension. Figure 1 includes a summary of the social determinants as well as the main behavioral and metabolic risk factors that may contribute to the development of HTN and complications.

99 enhance and expand NPs ’ understanding of RHTN 100 101 102 103 104 105 106

OVERVIEW OF RESISTANT HTN IN CKD

RHTN is both a cause and a consequence of CKD. Failure to effectively treat RHTN increases the risk of important adverse outcomes, including kidney failure, early development and accelerated progres- sion of cardiovascular disease, and premature death. 5 To achieve effective treatment, the NP utilizes an understanding of pathophysiology and the impor- tance of blood pressure control in patients with RHTN and CKD.

99 enhance and expand NPs ’ understanding of RHTN 100 101 102 103 104 105 106

the US. Furthermore, HTN is also the leading cause

of congestive heart failure, either directly causing

Pathophysiology

hypertensive heart disease or indirectly contributing

RHTN plays a key role in progression of CKD. 5 A strong association exists between the 2 conditions, with a complex reciprocal interaction. 1 Renal dysfunction causes increased sodium and water retention. Patients with water retention may develop uid overload, which in turn makes blood pressure control difcult. Persistently elevated blood pressure causes nephrosclerosis, leading to further kidney damage and perpetuation of the cycle. Adequate blood pressure control slows the progression of glomerular ltration rate (GFR) decline in patients with proteinuria and serves to preserve current renal function. 5 The sympathetic nervous system is known to be a major contributor to the pathophysiology of RHTN. Increased renal sympathetic activity leads to a cascade of actions including: (a) decreased renal blood ow and decreased glomerular ltration rate by renal vasoconstriction; and (b), through stimulation of the release of renin by the juxtaglomerular cells, angio- tensin II is produced. The cascade of action is further amplied by direct activation of renin resulting from kidney injury secondary to poorly controlled RHTN. Increases in renal sympathetic nerve activity also directly increase renal tubular sodium reabsorp- tion. 6 The complex cycle that includes activation of

to ischemic cardiomyopathy. 1 Lack of blood pressure

control presents as RHTN, a common clinic problem

encountered by NPs, primary care clinicians, and

specialists. Although the exact prevalence of RHTN

is unknown, clinical trials suggested that it is not rare

and involves perhaps 20%-30% of patients with HTN. 2

RHTN has been dened as blood pressure that

remains above goal despite concurrent use of 3

antihypertensive agents of different classes, ideally

including a diuretic, and all at optimal doses. 1 An

increased interest in the independent role of RHTN

has evolved from the common observation that

many patients with essential HTN fail to meet their

treatment goal despite polytherapy.

Recent studies have struggled to approximate the

prevalence of RHTN, which may occur in up to

30% of all patients with HTN. 3 Other studies focused

on documenting the strength of an association with

chronic diseases such as CKD. In some cases, CKD

99 enhance and expand NPs ’ understanding of RHTN 100 101 102 103 104 105 106

was found to be almost 4 times more common in

patients with RHTN. 1 It is of paramount importance

that NPs recognize that the increased prevalence of

kidney failure associated with high costs and poor

outcomes of treatment constitute a worldwide public health threat. 4 Aggressive treatment of RHTN by

  • 2 The Journal for Nurse Practitioners - JNP

Volume -, Issue -, -/- 2015

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Figure 1. Main factors that contribute to the development of high blood pressure and its complications. Reproduced

with the permission of the publisher, from Global Brief on Hypertension, Geneva, World Health Organization, 2013 (Fig. 9, Page 18 http://apps.who.int/iris/bitstream/10665/79059/1/WHO_DCO_WHD_2013.2_eng.pdf? ua¼l. Accessed 17 November 2014).

191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206http://apps.who.int/iris/bitstream/10665/79059/1/WHO_DCO_WHD_2013.2_eng.pdf? ua ¼ l . Accessed 17 November 2014). Secondary Causes of HTN renin, renal vasoconstriction, and tubular sodium reabsorption results in a worsening of CKD- related RHTN. Importance of Blood Pressure Control Blood pressure control is critical in the treatment of patients with CKD. Multiple landmark studies have demonstrated unequivocally that lowering blood pressure in individuals of any age with moderate to severe hypertension reduces risk of stroke, CKD, and cardiovascular events. With a focus on preserving current renal function in patients with CKD, clinical practice may be directed by strong evidence that a lower blood pressure target has been well documented in the general population to reduce cardiovascular risk and, in CKD patients, to reduce the rate of CKD progression. National data suggest that < 45% of persons with CKD meet target blood pressure goals, and adequate control often requires 3 or 4 medications. Despite widespread dissemination of the clinical guidelines established by the Eighth Joint National Committee, achieving blood pressure targets among patients with CKD remains challenging. Secondary HTN is elevated blood pressure that re- sults from an underlying, identi fi able, often correct- able cause. Although only about 5%-10% of HTN cases are thought to result from secondary causes, HTN is so common that secondary HTN will likely be encountered more frequently by the NP. Pseudoresistance. The importance of identi- fying the presence of pseudoresistance cannot be overstated. Pseudoresistance HTN must be excluded during the initial evaluation phase of treatment. Pseudoresistance is identi fi ed in those patients who: (a) lack blood pressure control secondary to an inac- curate suboptimal treatment regimen; (b) have poor adherence to antihypertensive therapy; (c) have life- style and diet issues; and (d) use anti-in fl ammatory agents or have “ white-coat ” hypertension. In most patients, home blood pressure monitoring can assist the NP in identifying white-coat hypertension. Ambu- latory blood pressure monitoring can also be useful in identifying RHTN and hypotensive episodes. The identi fi cation of pseudoresistance in patients with CKD is of paramount importance, as white-coat HTN is not associated with increased cardiorenal risk. www.npjournal.org The Journal for Nurse Practitioners - JNP 3 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279 280 281 282 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-2-103" src="pdf-obj-2-103.jpg">
191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206http://apps.who.int/iris/bitstream/10665/79059/1/WHO_DCO_WHD_2013.2_eng.pdf? ua ¼ l . Accessed 17 November 2014). Secondary Causes of HTN renin, renal vasoconstriction, and tubular sodium reabsorption results in a worsening of CKD- related RHTN. Importance of Blood Pressure Control Blood pressure control is critical in the treatment of patients with CKD. Multiple landmark studies have demonstrated unequivocally that lowering blood pressure in individuals of any age with moderate to severe hypertension reduces risk of stroke, CKD, and cardiovascular events. With a focus on preserving current renal function in patients with CKD, clinical practice may be directed by strong evidence that a lower blood pressure target has been well documented in the general population to reduce cardiovascular risk and, in CKD patients, to reduce the rate of CKD progression. National data suggest that < 45% of persons with CKD meet target blood pressure goals, and adequate control often requires 3 or 4 medications. Despite widespread dissemination of the clinical guidelines established by the Eighth Joint National Committee, achieving blood pressure targets among patients with CKD remains challenging. Secondary HTN is elevated blood pressure that re- sults from an underlying, identi fi able, often correct- able cause. Although only about 5%-10% of HTN cases are thought to result from secondary causes, HTN is so common that secondary HTN will likely be encountered more frequently by the NP. Pseudoresistance. The importance of identi- fying the presence of pseudoresistance cannot be overstated. Pseudoresistance HTN must be excluded during the initial evaluation phase of treatment. Pseudoresistance is identi fi ed in those patients who: (a) lack blood pressure control secondary to an inac- curate suboptimal treatment regimen; (b) have poor adherence to antihypertensive therapy; (c) have life- style and diet issues; and (d) use anti-in fl ammatory agents or have “ white-coat ” hypertension. In most patients, home blood pressure monitoring can assist the NP in identifying white-coat hypertension. Ambu- latory blood pressure monitoring can also be useful in identifying RHTN and hypotensive episodes. The identi fi cation of pseudoresistance in patients with CKD is of paramount importance, as white-coat HTN is not associated with increased cardiorenal risk. www.npjournal.org The Journal for Nurse Practitioners - JNP 3 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279 280 281 282 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-2-105" src="pdf-obj-2-105.jpg">

Secondary Causes of HTN

renin, renal vasoconstriction, and tubular sodium

reabsorption results in a worsening of CKD-

related RHTN.

Importance of Blood Pressure Control

Blood pressure control is critical in the treatment of

patients with CKD. Multiple landmark studies have

demonstrated unequivocally that lowering blood

pressure in individuals of any age with moderate to

severe hypertension reduces risk of stroke, CKD, and

cardiovascular events. 7 With a focus on preserving

current renal function in patients with CKD, clinical

practice may be directed by strong evidence that a

lower blood pressure target has been well

documented in the general population to reduce

cardiovascular risk and, in CKD patients, to reduce

the rate of CKD progression. 5 National data suggest

that < 45% of persons with CKD meet target blood

191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206http://apps.who.int/iris/bitstream/10665/79059/1/WHO_DCO_WHD_2013.2_eng.pdf? ua ¼ l . Accessed 17 November 2014). Secondary Causes of HTN renin, renal vasoconstriction, and tubular sodium reabsorption results in a worsening of CKD- related RHTN. Importance of Blood Pressure Control Blood pressure control is critical in the treatment of patients with CKD. Multiple landmark studies have demonstrated unequivocally that lowering blood pressure in individuals of any age with moderate to severe hypertension reduces risk of stroke, CKD, and cardiovascular events. With a focus on preserving current renal function in patients with CKD, clinical practice may be directed by strong evidence that a lower blood pressure target has been well documented in the general population to reduce cardiovascular risk and, in CKD patients, to reduce the rate of CKD progression. National data suggest that < 45% of persons with CKD meet target blood pressure goals, and adequate control often requires 3 or 4 medications. Despite widespread dissemination of the clinical guidelines established by the Eighth Joint National Committee, achieving blood pressure targets among patients with CKD remains challenging. Secondary HTN is elevated blood pressure that re- sults from an underlying, identi fi able, often correct- able cause. Although only about 5%-10% of HTN cases are thought to result from secondary causes, HTN is so common that secondary HTN will likely be encountered more frequently by the NP. Pseudoresistance. The importance of identi- fying the presence of pseudoresistance cannot be overstated. Pseudoresistance HTN must be excluded during the initial evaluation phase of treatment. Pseudoresistance is identi fi ed in those patients who: (a) lack blood pressure control secondary to an inac- curate suboptimal treatment regimen; (b) have poor adherence to antihypertensive therapy; (c) have life- style and diet issues; and (d) use anti-in fl ammatory agents or have “ white-coat ” hypertension. In most patients, home blood pressure monitoring can assist the NP in identifying white-coat hypertension. Ambu- latory blood pressure monitoring can also be useful in identifying RHTN and hypotensive episodes. The identi fi cation of pseudoresistance in patients with CKD is of paramount importance, as white-coat HTN is not associated with increased cardiorenal risk. www.npjournal.org The Journal for Nurse Practitioners - JNP 3 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279 280 281 282 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-2-149" src="pdf-obj-2-149.jpg">

pressure goals, and adequate control often requires 3

or 4 medications. 8 Despite widespread dissemination

of the clinical guidelines established by the Eighth

Joint National Committee, achieving blood pressure

targets among patients with CKD remains challenging. 9

Secondary HTN is elevated blood pressure that re- sults from an underlying, identiable, often correct- able cause. Although only about 5%-10% of HTN cases are thought to result from secondary causes, HTN is so common that secondary HTN will likely be encountered more frequently by the NP. 10 Pseudoresistance. The importance of identi- fying the presence of pseudoresistance cannot be overstated. Pseudoresistance HTN must be excluded during the initial evaluation phase of treatment. Pseudoresistance is identied in those patients who:

(a) lack blood pressure control secondary to an inac- curate suboptimal treatment regimen; (b) have poor adherence to antihypertensive therapy; (c) have life- style and diet issues; and (d) use anti-inammatory agents or have white-coathypertension. 3,11 In most patients, home blood pressure monitoring can assist the NP in identifying white-coat hypertension. Ambu- latory blood pressure monitoring can also be useful in identifying RHTN and hypotensive episodes. 5 The identication of pseudoresistance in patients with CKD is of paramount importance, as white-coat HTN is not associated with increased cardiorenal risk. 11

The Journal for Nurse Practitioners - JNP

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The challenging yet common form of pseudore-

sistance, medication nonadherence, continues to be a

serious threat to the overall physical, mental, and

economic health of the US population. 12 Some large,

randomized, controlled trials indicated nonadherence

is a major problem related to the treatment of HTN,

and was found to be the most common cause of

pseudoresistance, seen in 12% of the population

treated with prescribed medication. 13 The correlation

between medication adherence and health literacy is

well documented. 14 Once medication nonadherence

is identied, all providers should offer patients

personalized education focused on improving health

literacy and promoting a better understanding of risks

related to poorly controlled HTN.

Another signicant issue leading to pseudoresist-

ance involves errors in measurement of blood pres-

sure. One of the most common causes of blood

pressure assessment occurs when using a blood pres-

secondary cause of HTN. The secondary causes may include such common disorders as obstructive sleep apnea or chronic renal disease. Examples of rare secondary causes include coarctation of the aorta and pheochromocytoma. Table 1 identies the disorders that may cause secondary hypertension and includes diagnostic studies useful in making a diagnosis.

283 284 285 286 287 288 289 290 291 292 293 294 295 296 297 298

MANAGEMENT OF RESISTANT HTN IN PATIENTS WITH CKD

Effective treatment of RHTN in patients with CKD can prevent worsening of renal function and may also slow progression, reduce complications of decreased GFR, reduce risk of cardiovascular disease, and improve survival and quality of life. 4 The NPs greatest challenge is implementing an individualized treatment plan leading to successful blood pressure control and cardiovascular risk reduction.

Lifestyle
Lifestyle

sure cuff that is either too small or too large for the

patients arm. These types of errors, or what may be

Lifestyle modications in patients with RHTN are effective in lowering blood pressure. Numerous outcomes studies support the importance and effec- tiveness of lifestyle changes encompassing:

considered a poor blood monitoring technique, can

lead to undertreatment of HTN.

Other Causes of Secondary HTN

Dietary sodium restriction. Alcohol intake restriction. Weight loss.

After aggressively treating HTN with 3 or more

medications, NPs should consider a possible

Table 1. Secondary Hypertension Disorders and Associated Diagnostic Studies

Disorder Suspected

Diagnostic Studies

Obstructive sleep apnea

Hypothyroidism

Hyperthyroidism

Hyperparathyroidism Pheochromocytoma

Cushings syndrome

Aldosteronism

Sleep study Thyroid-stimulating hormone level Thyroid-stimulating hormone level Serum calcium, parathyroid hormone level Urinary catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrines) Dexamethasone-suppression test

Ratio of plasma aldosterone to plasma renin activity, computed tomography scan of adrenal glands

283 284 285 286 287 288 289 290 291 292 293 294 295 296 297 298

Renal parenchymal disease Renovascular disease

Coarctation of aorta

Acromegaly Erythropoietin side effect

Creatinine clearance, renal ultrasonography Magnetic resonance angiography, renal arteriography Doppler or computed tomography imaging of aorta Growth hormone level Off drug trial

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High-ber, low-fat diet.

Physical activity. 15

Incorporation of lifestyle changes in concert with

medication management enhances the opportunity

for effective treatment of HTN. Dietary sodium re-

striction improves blood pressure control in patients

with normal renal function and RHTN. The non-

pharmacologic intervention of dietary sodium re-

striction is pivotal in CKD, because the condition is

characterized by high sodium sensitivity of blood

pressure. 11 Numerous trials in the general population

have provided evidence that restricting salt intake

clearly lowers blood pressure. Alcohol consumption

has been shown to produce both acute and chronic

increases in blood pressure, suggesting that restricting

alcohol intake would lower blood pressure. In

patients with RHTN, the importance of achieving or

maintaining a healthy weight, having a high-ber,

low-fat diet, and increasing physical activity are key

edema, and commonly have a salt-sensitive form of hypertension. 17 For patients in CKD stages 1-3 (GFR > 30 mL/min per 1.73 m 2 ), a thiazide diuretic given once daily should be considered. Loop diuretics given once or twice daily are recommended in patients with GFR < 30 mL/min per 1.73 m . ACEIs and ARBs can be used safely in most pa- tients with CKD. 5 These drugs are frequently administered to patients with CKD and usually given for the treatment of HTN, due to their cardiorenal protective effects. 17 The most consistent HTN treatment benet is noted with use of ACEIs and ARBs, usually in association with diuretic drugs, in patients with HTN and high concentrations of albuminuria. 4 Proteinuria is a major risk factor for cardiovascular disease and CKD progression. In CKD patients with proteinuria, many randomized, controlled trials have shown that the use of ARBs or ACEIs can decrease hard outcomes, such as the doubling of serum creatinine level, kidney failure, or death. 5 The recently updated Kidney Disease Improving Global Outcomes clinic practice guideline on CKD and blood pressure recommends treatment with ACEI and ARB as rst-line therapy in patients with concomitant HTN and proteinuria, to slow progression of CKD. 18 One recent study showed that, in nondialysis-dependent patients with CKD, ACEI/ARB administration was associated with increased survival. 19 Although b-blockers are not considered a rst- line medication for the treatment RHTN, they are commonly used in patients with CKD, either for the treatment of HTN or for their cardioprotective ef- fects. The renoprotective effects of b-blockers in the CKD population have been established in several trials where they have been used as adjunctive ther- apy. 17 Commonly prescribed b-blockers known to be extensively metabolized in the liver, such as metoprolol and carvedilol, may be utilized safely to manage HTN in patients with CKD. 17 Central a-agonists can be useful in treating CKD patients with RHTN. As sympathetic activation plays an important and distinct role in HTN and target organ damage associated with CKD, clonidine can provide added treatment value when prescribed to patients who have not responded well to other classes of medication. Patients may experience rebound

2 5

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tools in the management of RHTN. 5

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Medication Management

Medication management for the patient with RHTN

and CKD is complex. Recommendations for treat-

ment of RHTN vary; some investigators have pro-

posed a therapeutic approach of a step-by-step

addition of HTN drug classes in patients with

RHTN. Others suggest what is known as triple ther-

apy, where combining an angiotensin-converting

enzyme inhibitor (ACEI) or angiotensin receptor

blocker (ARB) along with a diuretic and a calcium-

channel blocker (CCB) is a reasonable approach to

initial therapy. 16 Prescription practice for CKD-

related RHTN should be mindful of the need for

multiple drugs with a minimum of 1 drug being a

properly dosed diuretic. Diuretics remain a mainstay

of therapy for RHTN and for volume overload in

the presence of CKD. Diuretic agents include loop

diuretics, such as furosemide and torsemide, and

thiazide diuretics, such as hydrochlorothiazide and

chlorothalidone. By reducing extracellular uid vol-

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ume, diuretics lower blood pressure and thus are

capable of potentiating the effects of other drugs such

as ACEIs, ARBs, and other antihypertensive agents,

including CCBs. NPs should understand that CKD

patients have a 10%-30% increase in extracellular uid and blood volume, even in the absence of overt

The Journal for Nurse Practitioners - JNP

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HTN with missed clonidine dosing and when dis-

continuing the medication. 17

Mineralocorticoid receptor antagonists (MRAs)

may be prescribed in patients found to have sec-

ondary HTN related to primary aldosteronism. In

address unmet blood pressure goals. 22 Table 2 lists factors that may contribute to clinical inertia in the clinical setting. In the next section, a real-life case study is presented to demonstrate application of the treatment principles previously presented.

patients with RHTN, MRAs provide signicant

benet when added to existing multidrug regimens. 2

Despite the fact that MRAs are associated with a

signicant risk of hyperkalemia, they are

recommended to treat RHTN as they have been

found to reduce proteinuria and blood pressure

among patients in all stages of CKD. Data are still

lacking in relation to how MRAs affect progression

to end-stage renal disease and overall mortality. 20

Potent vasodilators, such as hydralazine, are

effective when added to a medication treatment

regimen. However, hydralazine usually requires

concomitant therapy with a diuretic and b-blocker.

Minoxidil is not commonly prescribed to treat

CASE STUDY

467 468 469 470 471 472 473 474 475 476 477 478 479 480 481 482

Mr. Jones is in your ofce for an initial evaluation for HTN, CKD, and renovascular and hyperparathyroid disease. He is a 67-yeareold, Caucasian male with a history of encapsulated renal cell carcinoma that resulted in a right nephrectomy in 2001. His current medications include amlodipine 5 mg, furosemide 40 mg/day, with carvedilol 50 mg twice daily, and hy- dralazine 100 mg and clonidine 0.1 mg 3 times daily for treatment of RHTN. He has been referred to an NP-managed HTN shared medical visit clinic for evaluation and treatment, which includes a multi- disciplinary treatment approach incorporating moti- vational interviewing, medication management, and dietary education. His blood pressure is 181/81 mm Hg with a pulse rate of 64 beats/min. A recent lab report revealed creatinine of 3.1 mg/dL, estimated GFR of 20 mL/min, potassium of 4.1, and para- thyroid hormone of 93. Mr. Jones reports that the recent addition of an ACEI resulted in severe hyperkalemia and hospitalization. He reports to you that he feels the lack of care coordination among previous providers contributed to an acute illness leading to hospitalization. After consulting with Dr. M, the patients nephrologist, you learn that Mr. Jones has a diagnosis of renovascular disease, which can often cause hyperkalemia when ACEIs or ARBs

467 468 469 470 471 472 473 474 475 476 477 478 479 480 481 482

RHTN, as it often causes problematic volume

retention that negates the antihypertensive effects of

other currently prescribed drugs. 21

Clinical Inertia

A major contributor to poor blood pressure control is

clinical inertia. 22 Clinical inertia is dened as the

failure of medical providers to initiate or intensify

therapy when treatment goals are unmet. NPs are

often managing a large panel of patients, many of

whom have poorly controlled blood pressure.

Progress notes in a patients record may often refer to

issues such as white-coat hypertension or non-

adherence. However, studies have shown that ther-

apeutic inertia occurs in 75% of consultations for

HTN where treatment change is actually indicated. 23

Other studies have indicated that clinical inertia

Table 2. Factors That May Contribute to Clinical Inertia

arises from a combination of medical provider, pa-

tient, and ofce system factors. Addressing these

Lack of provider education Lack of standardized treatment protocols Uncertainty regarding which medication change to recommend Poor recognition of elevated blood pressure Measurement of blood pressure using variable ofce techniques Focus on nonhypertension-related concerns during ofce visits Inability to provide patient outreach when blood pressure remains elevated

factors simultaneously is the most effective way to

overcome the problem. Clinical inertia may be pre-

sent in as many as two thirds of HTN clinic visits.

467 468 469 470 471 472 473 474 475 476 477 478 479 480 481 482

Recent reviews have identied clinical inertia as a

key intervention target for improving blood pres-

sure control. 22

Future success in treating patients with RHTN

and CKD may require increased use of clinical practice guidelines and sustained patient outreach to

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  • 6 The Journal for Nurse Practitioners - JNP

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  • 559 are prescribed to treat HTN. During the conversation

  • 560 with Dr. M, you discover that causes of secondary

  • 561 HTN have been eliminated except for pheochro-

  • 562 mocytoma. You immediately recognize that Mr.

  • 563 Joness CCB has not been optimized, so his dose of

  • 564 amlodipine is increased to 10 mg/day. After veri-

  • 565 cation is made that Mr. Jones has not been taking

  • 566 calcitriol daily as prescribed, a rell order is placed. A

  • 567 renal sonogram and 24-hour urine for metanephrines

  • 568 is ordered.

  • 569 Recognizing that patients with stage 4 CKD have

  • 570 improved outcomes when evaluated and treated by a

  • 571 nephrologist, the patient is encouraged to continue

  • 572 seeking care through his nephrologist. Mr. Jones is

  • 573 educated regarding the importance of not exceeding

  • 574 2,000 mg/day of dietary sodium chloride. During the

  • 575 initial visit with the patient, a comprehensive social

  • 576 and medical history reveals a current use of cannabis.

  • 577 Mr. Jones is then informed of the striking relationship

and medication adherence. Lifestyle changes reported by Mr. Jones conrm a decrease in dietary sodium reduction and an increase in daily exercise. He also proudly reports having not used cannabis products in at least 3 weeks. A review of Mr. Joness case study reveals successful treatment of RHTN as well as improvement in renal function. He will continue to receive care from his nephrologist and his primary care provider. In the event Mr. Jones experiences uncontrolled RHTN, he may return to the shared medical visit clinic for ongoing treatment.

559 are prescribed to treat HTN. During the conversation 560 with Dr. M, you discover thatwww.npjournal.org The Journal for Nurse Practitioners - JNP 7 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-6-71" src="pdf-obj-6-71.jpg">

CONCLUSION

We have presented an overview and treatment summary related to the management of RHTN in the patient with CKD. Solutions were discussed with regard to the unique challenges often experienced by NPs. Approaches to effectively treat RHTN while preserving kidney function were emphasized. HTN is the most common condition seen in primary care and can lead to RHTN, myocardial infarction, stroke, renal failure, and death if not detected early and treated appropriately. HTN and RHTN play a key role in the progression of CKD. In addition to controlled blood pressure, antihyperten- sive therapy affects other key modiable factors related to kidney disease progression, including pro- teinuria, vascular stiffness, and increased activity of the renin-angiotensin system. 5 When treating RHTN to lower risk for cardiovascular events, aggressive pharmacologic therapy is needed to lower both systolic and diastolic blood pressure. NPs should strive to avoid clinical inertia when treating patients with RHTN and CKD. Lack of response to antihypertensive medication should prompt an evaluation for nonadherence and sec- ondary causes of HTN. Finally, NPs should understand that blood pres- sure control is critical in the treatment of patients with CKD. Goals of therapy, education, and encouraging medication adherence must be directed toward reducing cardiovascular risk and slowing progression of kidney disease.

559 are prescribed to treat HTN. During the conversation 560 with Dr. M, you discover thatwww.npjournal.org The Journal for Nurse Practitioners - JNP 7 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-6-83" src="pdf-obj-6-83.jpg">
559 are prescribed to treat HTN. During the conversation 560 with Dr. M, you discover thatwww.npjournal.org The Journal for Nurse Practitioners - JNP 7 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-6-85" src="pdf-obj-6-85.jpg">
  • 578 between cardiovascular complications related to

  • 579 cannabis use, especially in the patient at risk related to

  • 580 chronic disease. 24 During the evaluation of RHTN,

Q2

  • 581 pseudoresistance and white-coat hypertension

  • 582 were excluded.

  • 583 Mr. Jones returns to the clinic 3 weeks after his

  • 584 initial visit. His ambulatory blood pressure log reveals

  • 585 an average systolic blood pressure of 171.2 mm Hg.

  • 586 The lab report indicates a potassium level of 4.4

  • 587 mEq/L, creatinine of 2.1 mg/dL, and urinary meta-

  • 588 nephrines level of 151 . The renal sonogram test in-

Q3

  • 589 dicates no hydronephroAn ovsis or masses. The

Q4

  • 590 blood pressure reading in the ofce is 198/91 mm

  • 591 Hg, which suggests white-coat HTN. Mr. Jones has

  • 592 been seen by the nephrologist since his previous visit

  • 593 who recommended an increase in dosage of the loop

  • 594 diuretic, furosemide, to 40 mg twice daily. Mr. Jones

  • 595 is noted to have 1 þ bilateral pedal edema on phys-

  • 596 ical exam.

  • 597 Six weeks after his initial visit, Mr. Jones returns

  • 598 for a third shared medical visit. His average ambula-

  • 599 tory systolic blood pressure is 152.9 mm Hg. The lab

559 are prescribed to treat HTN. During the conversation 560 with Dr. M, you discover thatwww.npjournal.org The Journal for Nurse Practitioners - JNP 7 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-6-165" src="pdf-obj-6-165.jpg">
  • 600 report indicates a PTH of 44, creatinine of 1.8 mg/dL,

  • 601 and estimated GFR of 38. He is noted to have

Q5

  • 602 bilateral trace pedal edema on physical exam. He

  • 603 denies any problems related to medical treatment of

  • 604 HTN and CKD. A signicant improvement is noted in blood pressure, pedal edema, and renal function

References

  • 1. Acharya T, Tringali S, Singh M, Huang J. Resistant hypertension and associated comorbidities in a veterans affairs population. J Clin Hypertens. 2014;16(10):741-745.

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651 652 653 654 655 656 657 658 659 660 661 662 663 664 665 666http://dx.doi.org/10.1016/j.nurpra.2015.03.018 740 741 742 743 744 745 746 747 748 749 750 751 752 753 754 755 756 757 758 Published by Elsevier, Inc. 759 760 761 762 763 764 765 766 767 768 769 770 771 772 773 774 775 776 777 778 779 780 781 782 783 784 785 786 787 788 789 790 791 792 793 794 795 796 797 798 799 800 801 802 803 804 805 806 8 The Journal for Nurse Practitioners - JNP Volume - , Issue - , - / - 2015 FLA 5.2.0 DTD TJNP2331_proof 21 April 2015 5:19 pm ce " id="pdf-obj-7-158" src="pdf-obj-7-158.jpg">

Q6

  • 2. Calhoun DA, Jones D, Textor S, et al. Resistant hypertension: diagnosis, evaluation, and treatment: a scientic statement from the American Heart

    • 15. Kumar N, Calhoun DA, Dudenbostel T. Management of patients with resistant

729

hypertension: current treatment options. Integr Blood Press Contr.

730

Association Professional Education Committee of the Council for High Blood

2013;6:139-151.

731

Pressure Research. Hypertension. 2008;51(6):1403-1419.

  • 3. Hajizadeh N, Assadi F. Resistant hypertension: current status, future

    • 16. Doumas M, Tsious C, Faselis C, Lazaridis A, Grassos H, Papademetriou V.

732

Non-interventional management of resistant hypertension. World J Cardiol.

733

challenges. Int J Prev Med. 2014;5(Suppl 1):S21-S24.

2014;6(10):1080-1090.

734

  • 4. Levey AS, Coresh J. Chronic kidney disease. Lancet. 2012;379(9811):165-180.

  • 5. Hypertension and antihypertensive agents in chronic kidney disease (CKD).

    • 17. Sica DA. Pharmacologic issues in treating hypertension in CKD. Adv Chron

735

Kidney Dis. 2011;18(1):42-47.

736

Ind J Nephrol. 2014;24(7, Suppl):S6.

  • 6. Vink EE, Blankenstijn PJ. Evidence and consequences of the centrol role of the

    • 18. Damman K, Lambers-Heerspink HJ. Are renineangiotensinealdosterone

737

system inhibitors lifesaving in chronic kidney disease? J Am Coll Cardiol.

738

kidneys in the pathophysiology of sympathetic hyperactivity. Front Physiol.

2014;63(7):659-660.

739

2012;3(29):1-6.

  • 7. Lewis JB. Blood pressure control in chronic kidney disease: is less really more? J Am Soc Nephrol. 2010;21(7):1086-1092.

  • 8. Peralta CA, Norris KC, Li S, et al. Blood pressure components and end-stage renal disease in persons with chronic kidney disease: the kidney early evaluation program (KEEP). Arch Intern Med. 2012;172(1):41-47.

  • 9. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507-520.

  • 10. Onusko E. Diagnosing secondary hypertension. Am Fam Phys. 2003;67(1):67-74.

  • 11. De Nicola L, Gabbai FB, Agarwal R, et al. Prevalence and prognostic role of resistant hypertension in chronic kidney disease patients. J Am Coll Cardiol. 2013;61(24):2461-2467.

  • 12. Chisholm-Burns MA, Spivey CA. The costof medication nonadherence: consequences we cannot afford to accept. J Am Pharm Assoc. 2012;52:823-826.

  • 13. Daugherty SL, Powers JD, Magid DJ, et al. Incidence and prognosis of resistant hypertension in hypertensive patients. Circulation. 2012;125(13):1635-1642.

  • 19. Molnar MZ, Kalantar-Zadeh K, Lott EH, et al. Angiotensin-converting enzyme inhibitor, angiotensin receptor blocker use, and mortality in patients with chronic kidney disease. J Am Coll Cardiol. 2014;63(7):650-658.

2012;3(29):1-6. 7. Lewis JB. Blood pressure control in chronic kidney disease: is less really more? Jhttp://dx.doi.org/10.1016/j.nurpra.2015.03.018 " id="pdf-obj-7-308" src="pdf-obj-7-308.jpg">
  • 20. Hirsch JS, Drexler Y, Bomback AS. Aldosterone blockade in chronic kidney disease. Semin Nephrol. 2014;34(3):307-322.

  • 21. Mann SJ. Drug therapy for resistant hypertension: a simplied, mechanistic approach. J Clin Hypertens. 2011;12(2):120-130.

  • 22. Huebschmann AG, Mizrahi T, Soenksen A, Beaty BL, Denberg TD. Reducing clinical inertia in hypertension treatment: a pragmatic randomized controlled trial. J Clin Hypertens. 2012;14(5):322-329.

  • 23. Redon J, Coca A, Lazaro P, et al. Factors associated with therapeutic inertia in hypertension: validation of a predictive model. J Hypertens. 2010;28(8):1770-1777.

  • 24. Jouanjus E, Lapeyre-Mestre M, Micallef J. The French Association of the Regional Abuse and Dependence Monitoring Centres (CEIP-A) Working Group on Cannabis Complications. Cannabis use: signal of increasing risk of serious cardiovascular disorders. JAMA. 2014;3(2).

1555-4155/15/$ see front matter

  • 14. Jones JH, Treiber LA, Jones MC. Intervening at the intersection of medication

2012;3(29):1-6. 7. Lewis JB. Blood pressure control in chronic kidney disease: is less really more? Jhttp://dx.doi.org/10.1016/j.nurpra.2015.03.018 " id="pdf-obj-7-336" src="pdf-obj-7-336.jpg">

adherence and health literacy. J Nurse Pract. 2014;10(8):527-534.

2012;3(29):1-6. 7. Lewis JB. Blood pressure control in chronic kidney disease: is less really more? Jhttp://dx.doi.org/10.1016/j.nurpra.2015.03.018 " id="pdf-obj-7-344" src="pdf-obj-7-344.jpg">

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