Upload
danglien
View
214
Download
0
Embed Size (px)
Citation preview
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 [email protected].*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 [email protected].*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