ROGÉRIO BAUMGRATZ DE PAULA

PROFESSOR TITULAR - NEFROLOGIA

UNIVERSIDADE FEDERAL DE JUIZ DE FORA - MG

REDUZIR A PRESSÃO ARTERIAL PARA VALORES ABAIXO DE 130 x 80 É BENÉFICO NO PACIENTE HIPERTENSO COM NEFROPATIA DIABÉTICA OU

NÃO ASSOCIADA?

Meta Análise: Menor PAM retarda progressão da DRC

em diabéticos e não-diabéticos

95 98 101 104 107 110 113 116 119

r = 0.69; P < 0.05

MAP (mmHg)

GFR

(m

L/m

in/y

ear

)

130/85 140/90

UntreatedHTN

0

-2

-4

-6

-8

-10

-12

-14

Bakris GL, et al. Am J Kidney Dis. 2000;36(3):646-661. 2

Meta pressórica de 130 x 80 mmHg é apropriada para o paciente com DRC ?

1- NEFROPROTEÇÃO EM DIABÉTICOS

2- NEFROPROTEÇÃO EM NÃO DIABÉTICOS

3- PROTEINÚRIA COMO MARCADOR

4- QUAL A META?

-

4

11 diabéticos tipo 1

Hidralazina, Metoprolole Furosemida

PA inicial: 143 x 96 mmHg

PA final: 130 x 84 mmHg

Parving HH and colsAm J Kidney Dis, 1993;22(1): 188-95

Lewis EJ et al. N Engl J Med 1993;329:1456-1462.

Progressão

para Morte,

Diálise ou

Transplante

(%)

Captopril

T. Convencional

Anos

0 1 2 3 4

0

10

20

30

40

*

* p = 0.006 vs placebo.

Nx DM 1 - IECA e nefroproteção

409 pacientesCr> 1,5 mg/dLProt > 2,7 g/24 horas

6

MENSAGEM 1

Controle pressórico se associa a nefroproteção, em especial por meio do uso de IECAs

Meta-análise IECA reduz progressão DRC, não Mortes

Giatras, I et al, 1997

United Kingdom Prospective Diabetes Study

Controle da PA salva vidas

24%

37%

21%

32%

44%

p = 0,005

p = 0,009

p = 0,130

p = 0,017

p = 0,013

Qualquer evento final relacionado ao DM

Eventos microvasculares finais

Infarto do miocárdio

Mortes relacionadas ao diabetes

Acidente vascular cerebral

Controle intensivo (n=1.148): 144 / 85 vs 154 / 74 mmHg

BMJ, 1998

Heart Outcomes Prevention Evaluation:

Ramipril reduziu eventos C-V e progressão DRC

-35

-30

-25

-20

-15

-10

-5

0

Nefropatia IAM AVC Morte CV

%

N=3.677

Lancet 2000;355:253-259

2xCr / IRCT / Morte

IRCT

Morte

IRCT ou morte

+50 0 -50

Porcentagem de Redução de Risco(95% CI)

favorece Losartana favorece Placebo

RENAAL: Resumo de Desfechos de Composto Primário e Clínicos

de Zeeuw et al. 2004

IDNT: PAS BAIXA REDUZIU EVENTOS RENAIS EM DIABETICOS

IDNT – JASN 2005;16;3027-37

Conclusion: In patients with diabetes, protection from stroke increases with the magnitude of BP reduction. We were unable to detect such a relation for MI.

Effects of intensive blood pressure reduction on myocardial infarction and stroke in diabetes: a meta-analysis in 73 913 patients

Journal of Hypertension 2011, 29:1253–1269

McBrien and cols

Arch Intern Med. 2012;172(17):1296-1303.

NEJM, 2010

TRATAMENTO INTENSIVO NÃO REDUZIU EVENTOS C-V

NEJM, 2010

MENSAGEM 2

Controle pressórico retarda progressão da DRC mas NÃO reduz eventos cardiovasculares de modo

consistente

Meta pressórica de 130 x 80 mmHg é apropriada para o paciente com DRC ?

1- NEFROPROTEÇÃO EM DIABÉTICOS

2- NEFROPROTEÇÃO EM NÃO DIABÉTICOS

3- PROTEINÚRIA COMO MARCADOR

4- QUAL A META?

-

APENAS 3 ESTUDOS EM NEFROLOGIA

MDRD between BP interventions and

baselineproteinuria, and therewasare-

duction in proteinuria in patients who

were randomly assigned to a MAP of

92mmHgin both study A and study B;

however, a major confounding factor

was the more frequent use of renin-an-

giotensin inhibitors, known modifiersof

renal progression, in thelow-BPgroup.33

Theprimary result of theBPstudy in the

MDRD wasnegative: Therewasno ben-

efit in slowing therateof declineof renal

function. Only a secondary analysis in

the subgroup with proteinuria supports

the low BP goal and is confounded by

imbalance in theuseof therenin-angio-

tensin inhibitors.

The MDRD results and the results of

theobservational studiesnoted formed the

basis for the Kidney Disease Outcomes

Quality Initiative (KDOQI) guideline of

130/80 mmHg for patients with CKD

and proteinuria 1 g/24 h.34 Guideline

committees tend to use available evi-

denceto makebest practical recommen-

dations, but a careful review of the data

confirms that real uncertainty remains

on appropriateBPgoalsfor patientswith

CKD. Another quirk of the KDOQI

guidelines isthat they were largely based

on the MDRD study, in which the

low-BP group wasrandomly assigned to

a MAP of 92 mmHg. A MAP goal al-

lowsawiderangeof SBPand DBPcom-

binations. Although never published, the

actual mean follow-up systolic and dia-

stolic BP in the usual group were 132.7

( 1.0 to 14.9)/80.2 ( 1.0 to 7.5) mmHg

and in the low-BP group were 125.6

( 1.0 to 13.8)/76.7 ( 1.0 to 6.8) mmHg

(Tom Greene, PhD, personal communi-

cation, October 2009). The low-MAP

group had awiderangeof SBP, approxi-

mately 98 to 154 mmHg. Achieving SBP

in thisrange isavery different interven-

tion than targeting all patients’ SBP to

130 mmHg (Figure3).

Other evidence hasbecome available

since the appearance of these KDOQI

guidelines. At the completion of the

MDRD study, thepatientswerereturned

to the care of their usual physician, and

there was no longer any BP separation

between the two randomly assigned

groups. After 7 years in routine care,

fewer of those patients who were origi-

nally randomly assigned to a MAP 92

versus 107mmHgreached ESRD or the

compositeend point of ESRD or death.35

The second large study, the AASK,

was completed by randomly assigning

1094 black patients with hypertension

and a urine protein-creatinine ratio of

2.5 to aMAPof 92 versus102 to 107

mmHg. Therewasno significant benefit

of being randomly assigned to the

low-BP group for the full cohort.36 In

De

clin

e in

glo

me

rula

r filtra

tio

n r

ate

(ml/m

m)

Month after randomization

Low blood pressure group

B315

12

9

6

3

0

F4 F12 F20 F28 F36

Usual blood pressure group

Figure 1. Estimated mean SE decline in the GFR from baseline (B) to selected

follow-up times (F) in MDRD. The patients who were assigned to the usual-BP group

(dashed line) are compared with those assigned to the low-BP group (solid line). Adapted

from Klahr et al.,32 with permission.

<1 1–<3 3

Base-line urinary protein (g/day)

Me

an

ra

te o

f G

FR

de

clin

e(m

l/m

in/y

r)

<1 1–<3 3

n = 420 n = 104 n = 54 n = 136 n = 63 n = 3212

8

4

0

12

8

4

0

Figure 2. Decline in the GFR according to baseline urinary protein excretion and BP

group in MDRD. The mean SE rate of decline per year in the GFR from baseline to 3

years, for study A and study B categorized by baseline urine protein, is projected.

F , patients with usual BP; E, patients with low BP. The number at the bottom of each

panel indicates the total number of patients with follow-up GFRmeasurements in the two

BP groups combined. Adapted from Klahr et al.,32 with permission.

100

Pa

tien

ts (

%)

110 120 130 140

Guideline BP MDRD lowMAP group

Figure 3. The solid line is the hypothetical representation of the average mean SBP and

1 SD on either side of that mean found in the MDRD study low-MAP group. Dashed line

is the hypothetical representation of distribution of average SBP if guidelines target all

SBP at 130 mmHg.

SPECIAL ARTICLE www.jasn.org

1088 Journal of the American Society of Nephrology J Am Soc Nephrol 21: 1086–1092, 2010

MDRD– SEM DIFERENÇA DESFECHOS

Lazarus J et al. Hypertension 1997;29:641-650

(n=840)

MDRD between BP interventions and

baselineproteinuria, and therewasare-

duction in proteinuria in patients who

were randomly assigned to a MAP of

92mmHgin both study A and study B;

however, a major confounding factor

was the more frequent use of renin-an-

giotensin inhibitors, known modifiersof

renal progression, in thelow-BPgroup.33

Theprimary result of theBPstudy in the

MDRD wasnegative: Therewasno ben-

efit in slowing therateof declineof renal

function. Only a secondary analysis in

the subgroup with proteinuria supports

the low BP goal and is confounded by

imbalance in theuseof therenin-angio-

tensin inhibitors.

The MDRD results and the results of

theobservational studiesnoted formed the

basis for the Kidney Disease Outcomes

Quality Initiative (KDOQI) guideline of

130/80 mmHg for patients with CKD

and proteinuria 1 g/24 h.34 Guideline

committees tend to use available evi-

denceto makebest practical recommen-

dations, but a careful review of the data

confirms that real uncertainty remains

on appropriateBPgoalsfor patientswith

CKD. Another quirk of the KDOQI

guidelines isthat they werelargely based

on the MDRD study, in which the

low-BP group wasrandomly assigned to

a MAP of 92 mmHg. A MAP goal al-

lowsawiderangeof SBPand DBPcom-

binations. Although never published, the

actual mean follow-up systolic and dia-

stolic BP in the usual group were 132.7

( 1.0 to 14.9)/80.2 ( 1.0 to 7.5) mmHg

and in the low-BP group were 125.6

( 1.0 to 13.8)/76.7 ( 1.0 to 6.8) mmHg

(Tom Greene, PhD, personal communi-

cation, October 2009). The low-MAP

group had awiderangeof SBP, approxi-

mately 98 to 154 mmHg. Achieving SBP

in thisrange isavery different interven-

tion than targeting all patients’ SBP to

130 mmHg (Figure3).

Other evidence has become available

since the appearance of these KDOQI

guidelines. At the completion of the

MDRD study, thepatientswerereturned

to the care of their usual physician, and

there was no longer any BP separation

between the two randomly assigned

groups. After 7 years in routine care,

fewer of those patients who were origi-

nally randomly assigned to a MAP 92

versus 107mmHgreached ESRD or the

compositeend point of ESRD or death.35

The second large study, the AASK,

was completed by randomly assigning

1094 black patients with hypertension

and a urine protein-creatinine ratio of

2.5 to aMAPof 92 versus102 to 107

mmHg. Therewasno significant benefit

of being randomly assigned to the

low-BP group for the full cohort.36 In

De

clin

e in

glo

me

rula

r filtra

tio

n r

ate

(ml/m

m)

Month after randomization

Low blood pressure group

B315

12

9

6

3

0

F4 F12 F20 F28 F36

Usual blood pressure group

Figure 1. Estimated mean SE decline in the GFR from baseline (B) to selected

follow-up times (F) in MDRD. The patients who were assigned to the usual-BP group

(dashed line) are compared with those assigned to the low-BP group (solid line). Adapted

from Klahr et al.,32 with permission.

<1 1–<3 3

Base-line urinary protein (g/day)

Me

an

ra

te o

f G

FR

de

clin

e(m

l/m

in/y

r)

<1 1–<3 3

n = 420 n = 104 n = 54 n = 136 n = 63 n = 3212

8

4

0

12

8

4

0

Figure 2. Decline in the GFR according to baseline urinary protein excretion and BP

group in MDRD. The mean SE rate of decline per year in the GFR from baseline to 3

years, for study A and study B categorized by baseline urine protein, is projected.

F , patients with usual BP; E, patients with low BP. The number at the bottom of each

panel indicates the total number of patients with follow-up GFRmeasurements in the two

BP groups combined. Adapted from Klahr et al.,32 with permission.

100

Pa

tie

nts

(%

)

110 120 130 140

Guideline BP MDRD lowMAP group

Figure 3. The solid line is the hypothetical representation of the average mean SBP and

1 SD on either side of that mean found in the MDRD study low-MAP group. Dashed line

is the hypothetical representation of distribution of average SBP if guidelines target all

SBP at 130 mmHg.

SPECIAL ARTICLE www.jasn.org

1088 Journal of the American Society of Nephrology J Am Soc Nephrol 21: 1086–1092, 2010

Study A - GFR 25-55 ml/min Study B – GFR 13-24 ml/min

MDRD - SUBANÁLISE

REIN Study: ACE Inhibition in Proteinuric Non-Diabetic Nephropathy

Baseline

SBP∆ SBP

Baseline

DBP∆ DBP

Ramipril 149.8 -5.8 mmHg 92.4 -4.2 mmHg

Placebo 148.0 -3.4 mmHg 91.3 -3.4 mmHg

0 6 12 18 24 30 36

100

80

60

40

20

0

Ramipril

Placebo

P=0.02

The GISEN Group. Lancet. 1997;349:1857–1863.

% o

f p

atie

nts

wit

ho

ut

com

bin

ed e

nd

po

int*

*Combined endpoint = doubling of baseline serum creatinine concentration or end stage renal failure

American African Study of Kidney Diseases and Hypertension (AASK)

JAMA 2002

1094 hipertensos negros com lesão renal e, não diabéticos

Clearence entre 20 – 65 ml/min (3 a 6,4 anos)

3 fármacos: Ramipril, Anlodipino e Metoprolol

2 níveis de PAM: < 92 mmHg e 102-107 mmHg

Desfechos: Redução do RFG > 50% ou 25 ml/min - TRS

AASK STUDYAASK – Arch Int Med, 2002

141 x 85 mmHg

128 x 78 mmHg

Intensive Blood-Pressure Control in Hypertensive Chronic

Kidney Disease

Lawrence J. Appel, M.D., M.P.H., Jackson T. Wright Jr., M.D., Ph.D., Tom Greene, Ph.D.,

Lawrence Y. Agodoa, M.D., Brad C. Astor, M.P.H., Ph.D., George L. Bakris, M.D., William H.

Cleveland, M.D., Jeanne Charleston, R.N., Gabriel Contreras, M.D., M.P.H., Marquetta L.

Faulkner, M.D., Francis B. Gabbai, M.D., Jennifer J. Gassman, Ph.D., Lee A. Hebert, M.D.,

Kenneth A. Jamerson, M.D., Joel D. Kopple, M.D., M.P.H., John W. Kusek, Ph.D., James P.

Lash, M.D., Janice P. Lea, M.D., Julia B. Lewis, M.D., Michael S. Lipkowitz, M.D., Shaul G.

Massry, M.D., Edgar R. Miller, Ph.D., M.D., Keith Norris, M.D., Robert A. Phillips, M.D.,

Ph.D., Velvie A. Pogue, M.D., Otelio S. Randall, M.D., Stephen G. Rostand, M.D., Miroslaw J.

Smogorzewski, M.D., Robert D. Toto, M.D., and Xuelei Wang, M.S.* for the AASK

Collaborative Research Group

Abstract

BACKGROUND—In observational studies, the relationship between blood pressure and end-

stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic

kidney disease and ESRD is especially high among black patients. Yet few trials have tested

whether intensive blood-pressure control retards the progression of chronic kidney disease among

black patients.

METHODS—We randomly assigned 1094 black patients with hypertensive chronic kidney

disease to receive either intensive or standard blood-pressure control. After completing the trial

phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less

than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of

chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis

of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years.

RESULTS—During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-

control group and 141/86 mm Hg in the standard-control group. During the cohort phase,

corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases,

there was no significant between-group difference in the risk of the primary outcome (hazard ratio

in the intensive-control group, 0.91; P = 0.27). However, the effects differed according to the

baseline level of proteinuria (P = 0.02 for interaction), with a potential benefit in patients with a

protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P = 0.01).

CONCLUSIONS—In overall analyses, intensive blood-pressure control had no effect on kidney

disease progression. However, there may be differential effects of intensive blood-pressure control

in patients with and those without baseline proteinuria. (Funded by the National Institute of

Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health

Disparities, and others.)

Copyright © 2010 Massachusetts Medical Society.

Address reprint requests to Dr. Appel at Johns Hopkins University, 2024 E. Monument St., Suite 2-618, Baltimore, MD 21205-2223,or at lappel@jhmi.edu.*Members of the African-American Study of Kidney Disease and Hypertension (AASK) Collaborative Research Group are listed inthe Appendix.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

NIH Public AccessAuthor ManuscriptN Engl J Med. Author manuscript; available in PMC 2013 May 24.

Published in final edited form as:

N Engl J Med. 2010 September 2; 363(10): 918–929. doi:10.1056/NEJMoa0910975.

NIH

-PA

Author M

anuscriptN

IH-P

A A

uthor Manuscript

NIH

-PA

Author M

anuscript

AASK – NEJM 2010

CONTROLE PRESSÓRICO RIGOROSO NÃO MELHORA DESFECHOS RENAIS

ANÁLISE DE SUBGRUPOS COM PROTEINÚRIA SIGNIFICATIVA SUGEREM BENEFICIOS COM REDUÇÃO INTENSIVA DA PA

MENSAGEM 3

Meta pressórica de 130 x 80 mmHg é apropriada para o paciente com DRC ?

1- NEFROPROTEÇÃO EM DIABÉTICOS

2- NEFROPROTEÇÃO EM NÃO DIABÉTICOS

3- PROTEINÚRIA COMO MARCADOR

4- QUAL A META?

-

1.0

0.9

0.8

0.7

0.6

0.5

0 1 2 3 4 5 6

Years

Surv

ival

(al

l- c

ause

mo

rtal

ity)

Normoalbuminuria(n=191)

Microalbuminuria(n=86)

Macroalbuminuria(n=51)

P<0.01 Normo vs micro

P<0.001 Normo vs macro

P<0.05 Micro vs macro

Proteinuria as a Risk Factor for Mortality in Type 2 Diabetes

Gall MA, et al. Diabetes. 1995;44:1303-09

ReductionEnd PointsNoninsulinDM Angiotensin Antagonist Losartan

Proteinuria Basal Prediz Eventos Renais

de Zeeuw et al, 2004

Intensive Blood-Pressure Control in Hypertensive Chronic

Kidney Disease

Lawrence J. Appel, M.D., M.P.H., Jackson T. Wright Jr., M.D., Ph.D., Tom Greene, Ph.D.,

Lawrence Y. Agodoa, M.D., Brad C. Astor, M.P.H., Ph.D., George L. Bakris, M.D., William H.

Cleveland, M.D., Jeanne Charleston, R.N., Gabriel Contreras, M.D., M.P.H., Marquetta L.

Faulkner, M.D., Francis B. Gabbai, M.D., Jennifer J. Gassman, Ph.D., Lee A. Hebert, M.D.,

Kenneth A. Jamerson, M.D., Joel D. Kopple, M.D., M.P.H., John W. Kusek, Ph.D., James P.

Lash, M.D., Janice P. Lea, M.D., Julia B. Lewis, M.D., Michael S. Lipkowitz, M.D., Shaul G.

Massry, M.D., Edgar R. Miller, Ph.D., M.D., Keith Norris, M.D., Robert A. Phillips, M.D.,

Ph.D., Velvie A. Pogue, M.D., Otelio S. Randall, M.D., Stephen G. Rostand, M.D., Miroslaw J.

Smogorzewski, M.D., Robert D. Toto, M.D., and Xuelei Wang, M.S.* for the AASK

Collaborative Research Group

Abstract

BACKGROUND—In observational studies, the relationship between blood pressure and end-

stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic

kidney disease and ESRD is especially high among black patients. Yet few trials have tested

whether intensive blood-pressure control retards the progression of chronic kidney disease among

black patients.

METHODS—We randomly assigned 1094 black patients with hypertensive chronic kidney

disease to receive either intensive or standard blood-pressure control. After completing the trial

phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less

than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of

chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis

of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years.

RESULTS—During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-

control group and 141/86 mm Hg in the standard-control group. During the cohort phase,

corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases,

there was no significant between-group difference in the risk of the primary outcome (hazard ratio

in the intensive-control group, 0.91; P = 0.27). However, the effects differed according to the

baseline level of proteinuria (P = 0.02 for interaction), with a potential benefit in patients with a

protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P = 0.01).

CONCLUSIONS—In overall analyses, intensive blood-pressure control had no effect on kidney

disease progression. However, there may be differential effects of intensive blood-pressure control

in patients with and those without baseline proteinuria. (Funded by the National Institute of

Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health

Disparities, and others.)

Copyright © 2010 Massachusetts Medical Society.

Address reprint requests to Dr. Appel at Johns Hopkins University, 2024 E. Monument St., Suite 2-618, Baltimore, MD 21205-2223,or at lappel@jhmi.edu.*Members of the African-American Study of Kidney Disease and Hypertension (AASK) Collaborative Research Group are listed inthe Appendix.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

NIH Public AccessAuthor ManuscriptN Engl J Med. Author manuscript; available in PMC 2013 May 24.

Published in final edited form as:

N Engl J Med. 2010 September 2; 363(10): 918–929. doi:10.1056/NEJMoa0910975.

NIH

-PA

Author M

anuscriptN

IH-P

A A

uthor Manuscript

NIH

-PA

Author M

anuscript

AASK – NEJM 2010

MDRD between BP interventions and

baselineproteinuria, and therewasare-

duction in proteinuria in patients who

were randomly assigned to a MAP of

92mmHgin both study A and study B;

however, a major confounding factor

was the more frequent use of renin-an-

giotensin inhibitors, known modifiersof

renal progression, in thelow-BPgroup.33

Theprimary result of theBPstudy in the

MDRD wasnegative: Therewasno ben-

efit in slowing therateof declineof renal

function. Only a secondary analysis in

the subgroup with proteinuria supports

the low BP goal and is confounded by

imbalance in theuseof therenin-angio-

tensin inhibitors.

The MDRD results and the results of

theobservational studiesnoted formed the

basis for the Kidney Disease Outcomes

Quality Initiative (KDOQI) guideline of

130/80 mmHg for patients with CKD

and proteinuria 1 g/24 h.34 Guideline

committees tend to use available evi-

denceto makebest practical recommen-

dations, but a careful review of the data

confirms that real uncertainty remains

on appropriateBPgoalsfor patientswith

CKD. Another quirk of the KDOQI

guidelines isthat they werelargely based

on the MDRD study, in which the

low-BP group wasrandomly assigned to

a MAP of 92 mmHg. A MAP goal al-

lowsawiderangeof SBPand DBPcom-

binations. Although never published, the

actual mean follow-up systolic and dia-

stolic BP in the usual group were 132.7

( 1.0 to 14.9)/80.2 ( 1.0 to 7.5) mmHg

and in the low-BP group were 125.6

( 1.0 to 13.8)/76.7 ( 1.0 to 6.8) mmHg

(Tom Greene, PhD, personal communi-

cation, October 2009). The low-MAP

group had awiderangeof SBP, approxi-

mately 98 to 154 mmHg. Achieving SBP

in thisrange isavery different interven-

tion than targeting all patients’ SBP to

130 mmHg (Figure3).

Other evidence has become available

since the appearance of these KDOQI

guidelines. At the completion of the

MDRD study, thepatientswerereturned

to the care of their usual physician, and

there was no longer any BP separation

between the two randomly assigned

groups. After 7 years in routine care,

fewer of those patients who were origi-

nally randomly assigned to a MAP 92

versus 107mmHgreached ESRD or the

compositeend point of ESRD or death.35

The second large study, the AASK,

was completed by randomly assigning

1094 black patients with hypertension

and a urine protein-creatinine ratio of

2.5 to aMAPof 92 versus102 to 107

mmHg. Therewasno significant benefit

of being randomly assigned to the

low-BP group for the full cohort.36 In

De

clin

e in

glo

me

rula

r filtra

tio

n r

ate

(ml/m

m)

Month after randomization

Low blood pressure group

B315

12

9

6

3

0

F4 F12 F20 F28 F36

Usual blood pressure group

Figure 1. Estimated mean SE decline in the GFR from baseline (B) to selected

follow-up times (F) in MDRD. The patients who were assigned to the usual-BP group

(dashed line) are compared with those assigned to the low-BP group (solid line). Adapted

from Klahr et al.,32 with permission.

<1 1–<3 3

Base-line urinary protein (g/day)

Me

an

ra

te o

f G

FR

de

clin

e(m

l/m

in/y

r)

<1 1–<3 3

n = 420 n = 104 n = 54 n = 136 n = 63 n = 3212

8

4

0

12

8

4

0

Figure 2. Decline in the GFR according to baseline urinary protein excretion and BP

group in MDRD. The mean SE rate of decline per year in the GFR from baseline to 3

years, for study A and study B categorized by baseline urine protein, is projected.

F , patients with usual BP; E, patients with low BP. The number at the bottom of each

panel indicates the total number of patients with follow-up GFRmeasurements in the two

BP groups combined. Adapted from Klahr et al.,32 with permission.

100

Pa

tie

nts

(%

)

110 120 130 140

Guideline BP MDRD lowMAP group

Figure 3. The solid line is the hypothetical representation of the average mean SBP and

1 SD on either side of that mean found in the MDRD study low-MAP group. Dashed line

is the hypothetical representation of distribution of average SBP if guidelines target all

SBP at 130 mmHg.

SPECIAL ARTICLE www.jasn.org

1088 Journal of the American Society of Nephrology J Am Soc Nephrol 21: 1086–1092, 2010

Study A - GFR 25-55 ml/min Study B – GFR 13-24 ml/min

MDRD - SUBANÁLISE

Jafar TH and colsAnn Intern Med 2003;139:244

Jicheng Lv et al. CMAJ 2013;185:949-957

N=9.287

11 estudos

Meta pressórica de 130 x 80 mmHg é apropriada para o paciente com DRC ?

1- NEFROPROTEÇÃO EM DIABÉTICOS

2- NEFROPROTEÇÃO EM NÃO DIABÉTICOS

3- PROTEINÚRIA COMO MARCADOR

4- QUAL A META?

-

Thomopoulosa C et al

Journal of Hypertension 2016, 34:613–622

CUIDADO COM POPULAÇÕES DE RISCO

INDIVIDUALIZE !

MENSAGEM 4

RENAL FUNCTION TRAJECTORY IN

CHRONIC KIDNEY DISEASE PATIENTS:

RESULTS OF A REAL-LIFE STUDY

E. A. de Paula, C. P. Vanelli, M. S. Caminhas, B. C. Soares, F. A.

Bassoli, D. M. da Costa, C. M. Lanna, A. G. Galil, F. A. Colugnati,

M. B. Costa, M. G. Bastos, R. B. de Paula

ERA-EDTA, 2014

SBP SBP DBP DBPbasal final basal final

BP Control CHM-JF – Real Life

De Paula EA and cols - NDT 29 Suppl 3, 2014

De Paula EA and cols - NDT 29 Suppl 3, 2014

MENSAGEM FINAL

META INFERIOR A 130 X 80 mmHg PARECE EFICAZ, EM ESPECIAL NA PRESENÇA DE ALBUMINURIA

QUAL O PONTO DE CORTE INFERIOR???

-

ACCORD

Cushman WC. NEJM 2010;362: 1575-1585