Limitations of RAS Blockade in IgA Nephropathy

Chapter
Recommendation statement
Grade
10.2
Antiproteinuric and antihypertensive therapy
 
10.2.1
We recommend long-term ACEI or ARB treatment when proteinuria is >1 g/day, with up-titration of the drug depending on blood pressure
1B
10.2.2
We suggest ACEI or ARB treatment if proteinuria is between 0.5 and 1 g/day (in children, between 0.5 and 1 g/day per 1.73 m2)
2D
10.3.3
We suggest the ACEI or ARB be titrated upward as far as tolerated to achieve proteinuria <1 g/day
2C
10.3.4
In IgAN, use blood pressure treatment goals of <130/80 mmHg in patients with proteinuria <1 g/day and <125/75 mmHg when initial proteinuria is >1 g/day
Not graded
10.3
Corticosteroids
 
10.3.1
We suggest that patients with persistent proteinuria ≥1 g/day, despite 3–6 months of optimized supportive care (including ACEI or ARBs and blood pressure control) and GFR >50 mL/min per 1.73 m2, receive a 6-month course of corticosteroid therapy
2C
(1) Strength of recommendation: grade 1–2
 Grade 1, “we recommend”
 – Implications for clinicians: Most patients should receive the recommended course of action
 – Implications for patients: Most people in your situation would want the recommended course of action and only a small proportion would not
 – Implications for policy: The recommendation can be evaluated as a candidate for developing a policy or a performance measure
 Grade 2, “we suggest”
 – Implications for clinicians: The majority of people in your situation would want the recommended course of action, but many would not
 – Implications for patients: Different choices will be appropriate for different patients. Each patient needs help to arrive at a management decision consistent with her or his values and preferences
 – Implications for policy: The recommendation is likely to require substantial debate and involvement of stakeholders before policy can be determined
(2) Quality of evidence: grade A–D
 Grade A, “high”
 – We are confident that the true effect lies close to that of the estimate of the effect
 Grade B, “moderate”
 – The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different
 Grade C, “low”
 – The true effect may be substantially different from the estimate of the effect
 Grade D, “very low”
 – The estimate of effect is very uncertain and often will be far from the truth
ACEI angiotensin-converting enzyme inhibitor, ARB angiotensin receptor blocker, GFR glomerular filtration rate, IgAN IgA nephropathy, KDIGO kidney disease: improving global outcomes, RAS renin-angiotensin system
Table 16.2
RAS blockade and use of corticosteroids in IgAN patients in Japanese Evidence-Based Clinical Practice Guideline for CKD 2013 [6, 56] and IgAN 2014
No
Clinical questions and statements
Grade
2
Are RAS inhibitors recommended for decreasing urinary protein and preserving renal function in patients with IgAN?
  
We recommend treatment with RAS inhibitors for patients with proteinuria ≥1 g/day and eGFR ≥30 mL/min/1.73 m2 (CKD G1 to G3b) because of their effect of preservation of renal function
A
We suggest treatment with RAS inhibitors if proteinuria is between 0.5 and 1.0 g/day because of their antiproteinuric effect
C1
3
Are corticosteroids recommended for decreasing urinary protein and preserving renal function in patients with IgAN?
  
We recommend that patients with proteinuria ≥1 g/day and eGFR ≥60 mL/min/1.73 m2 (CKD G1 to G2) receive a 6-month course of high-dose oral corticosteroids therapy (6-month regime of oral prednisone starting with 0.8–1 mg/kg/day for 2 months and then reduced gradually for the next 4 months)
B
We recommend that patients with proteinuria ≥1 g/day and eGFR ≥60 mL/min/1.73 m2 (CKD G1 to G2) receive high-dose pulse corticosteroids therapy (i.v. bolus injections of 1 g methylprednisolone for 3 days each at months 1, 3, and 5, followed by 0.5 mg/kg oral prednisone on alternate days for 6 months)
B
We tentatively suggest using corticosteroids for patients with proteinuria less than 1 g/day and eGFR ≥60 mL/min/1.73 m2 (CKD G1 to G2) because of their antiproteinuric effect
C1
Strength of recommendation: grade A–D
Grade A, strongly recommended because the scientific basis is strong
Grade B, recommended because there is some scientific basis
Grade C1, recommended despite having only a weak scientific basis
Grade C2, not recommended because there is only a weak scientific basis
Grade D, not recommended because scientific evidence shows the treatment to be ineffective or harmful
ACEI angiotensin-converting enzyme inhibitor, ARB angiotensin receptor blocker, IgAN IgA nephropathy, RAS renin-angiotensin system

16.2 RAS Blockade in IgA Nephropathy Patients in KDIGO Guideline and Japanese Guidelines

In KDIGO Clinical Practice Guideline for Glomerulonephritis, strength of recommendation of RAS blockade is different between IgAN patients with proteinuria >1 g/day and those with proteinuria <1 g/day. KDIGO guideline recommends RAS blockade in IgAN patients with proteinuria >1 g/day (statement 10.2.1, grade 1B), whereas it suggests RAS blockade in those with proteinuria between 0.5 and 1 g/day (statement 10.2.2, grade 2D) (Table 16.1). The rationales for the different strength of recommendation on RAS blockade are, first, that moderate-quality evidence identified proteinuria >1 g/day as a risk factor of accelerated decline in GFR [8] and, second, that the majority of randomized trials using ACEI or ARB recruited IgAN patients mainly with proteinuria >1 g/day (Tables 16.3a, 16.3b, 16.3c, 16.3d, 16.4a, 16.4b, 16.4c, 16.4d, 16.5a, 16.5b, 16.5c, and 16.5d). Interestingly, KDIGO guideline suggests IgAN patients with persistent proteinuria ≥1 g/day, despite 3–6 months of optimized supportive care (including ACEIs or ARBs and blood pressure control), and GFR >50 mL/min per 1.73 m2, receive a 6-month course of corticosteroid therapy (statement 10.3.1, grade 2C). As an initial therapy in IgAN patients with proteinuria ≥1 g/day, RAS blockade takes priority over corticosteroid therapy.
Table 16.3a
Study protocols of RCTs assessing efficacy of ACEI vs. no RAS blockade in IgAN patients
Author year
Interventions (dose)
Duration
Age
BP
Renal function
UP
Histology
Parallel group trials
Praga 2003 [9]
Enalapril (≤40 mg)
ND (76 months)
Adult
0–2 antihypertensive drugs
SCr ≤1.5 mg/dL
≥0.5 g/day
ND
No RAS blockade
No malignant hypertension
Li 2013 [10]
Ramipril (2.5 mg)
60 months
18–65 years
Normal blood pressure
SCr <120 μmol/L
<0.5 g/day
ND
No treatment
Coppo 2007 [11]
Benazepril (≤0.2 mg/kg)
36 months
3–35 years
BP <140/90 mmHg (adults)
eGFR >50 mL/min/1.73 m2
1.0–3.4 g/day
ND
Placebo
BP <95 % (children)
Kanno 2005 [12]
ACEI (≤2 mg)a
≥3 years
ND
No previous ACEI
ND
ND
ND
Amlodipine (5 mg)
Ruggenenti 2000 [13]
Ramipril (≤5 mg)
63 months
18–70 year
BP <220/115 mmHg
Ccr 20–70 mL/min/1.73 m2
≥1.0 g/day
ND
Placebob
Bannister 1995 [14]
Enalapril (ND)
12 months
ND
Hypertension
GFR 30–90 mL/min
ND
ND
Nifedipine (ND)
Nakamura 2000 [15]
Trandolapril (2 mg)
3 months
ND
Normal blood pressure
Ccr >80 mL/min/1.73 m2
≤3.0 g/day
ND
Candesartan (8 mg)
(BP <140/90 mmHg)
Verapamil (120 mg)
Placebo
Crossover trials
Maschio 1994 [16]
Fosinopril (20 mg)
4 months
ND
Normal blood pressure
SCr <1.4 mg/dL
≥1.0 g/day
ND
Placebo
(BP <140/90 mmHg)
Ccr >90 mL/min/1.73 m2
Ikeda 1989 [17] (sub)
Captopril (ND)
ND
ND
ND
ND
ND
ND
Nicardipine (ND)
ACEI angiotensin-converting enzyme inhibitor, BP blood pressure, Ccr creatinine clearance, CKD chronic kidney disease, eGFR estimated GFR, GFR glomerular filtration rate, IgAN IgA nephropathy, RAS renin-angiotensin system, SCr serum creatinine, UP urinary protein
aTemocapril (≤2 mg) or trandolapril (≤2 mg)
bThe patients’ code was opened at 27th month of randomization
Table 16.3b
Baseline characteristics of IgAN patients included in RCTs assessing efficacy of ACEI vs. no RAS blockade
Author year
Interventions
N
Age
SBP/DBP or MAP
SCr
GFR
UP
Histology
(Year)
(mmHg)
(mg/dL)
(mL/min)
Parallel group trials
Praga 2003 [9]
Enalapril
23
27.8 ± 12
102 ± 11
1 ± 0.2
Ccr
102 ± 25
2 ± 1.3 g/day
ND
No RAS blockade
21
29.9 ± 12.3
98 ± 12
0.9 ± 0.2
  
99 ± 22
1.7 ± 0.8
  
Li 2013 [10]
Ramipril
30
42.2 ± 11.0
115.5 ± 13.0/69.6 ± 10.3
0.88 ± 0.19c
eGFR
106.8 ± 20.9 per1.73 m2
0.10 ± 0.13 g/gCr
Haas’ [57] and
No treatment
30
41.0 ± 7.5
114.2 ± 16.3/70.1 ± 9.3
0.85 ± 0.14c
 
102.9 ± 15.2
0.12 ± 0.13 g/gCr
To’s [58]
Coppo 2007 [11]
Benazepril
32
21.8 ± 6.3
122.59 ± 9.0/77.81 ± 8.0
ND
Ccr
113.2 ± 23.5 per 1.73 m2
1.61 ± 0.70 g/day per 1.73 m2
ND
Placebo
34
19.3 ± 6.1
117.06 ± 11.0/72.09 ± 9.0
    
114.1 ± 19.0
1.87 ± 0.74
  
Kanno 2005 [12]
ACEIa
26
35 ± 10b
143 ± 15b/87 ± 10b
1.07 ± 0.66b
Ccr
92.8 ± 31.6b
1.09 ± 0.82b g/day
TIF index
Amlodipine
23
35 ± 14b
140 ± 14b/83 ± 10b
1.02 ± 0.38b
 
90.8 ± 34.1b
1.10 ± 0.72b
 
Ruggenenti 2000 [13]
Ramipril
39
42.3 ± 12.9
142.8 ± 16.3/91.8 ± 9.9
1.96 ± 0.73
Cio
48.1 ± 20.3 per 1.73 m2
3.05 ± 2.17 g/day
ND
Placebo
36
45.9 ± 11.2
137.6 ± 12.8/89.3 ± 8.0
2.12 ± 0.94
  
44.2 ± 16.7
3.19 ± 1.93
  
Bannister 1995 [14]
Enalapril
13
49 [34–74]
116 ± 9.0b
ND
CDTPA
74.6 ± 24.9b
ND
ND
Nifedipine
10
53 [32–69]
114 ± 7.5b
   
62.5 ± 13.8b
   
Nakamura [15] 2000
Trandolapril
8
32.6 [18–54]
118 ± 14/80 ± 6
0.8 ± 0.2
Ccr
108 ± 16 per 1.73 m2
1.9 ± 0.7 g/day
ND
Candesartan
8
  
118 ± 16/78 ± 6
0.7 ± 0.2
  
112 ± 14
1.8 ± 0.8
  
Verapamil
8
  
116 ± 12/82 ± 8
0.9 ± 0.2
  
110 ± 12
1.8 ± 0.6
  
Placebo
8
  
120 ± 12/80 ± 8
0.8 ± 0.2
  
112 ± 12
1.6 ± 0.6
  
Crossover trials
Maschio [16] 1994
Fosinopril
39
33.2 ± 11.4 [18–58]
92.8 ± 9.1
1.0 ± 0.2
Ccr
103 ± 23 per 1.73 m2
1.74 ± 0.84 g/day
ND
Placebo
Ikeda [17] 1989(sub)
Captopril
4
40.5 ± 12.6
167.5 ± 21.4/110.0 ± 14.0
ND
Ccr
78.0 ± 20.5
2.9 ± 0.6 g/day
ND
Nicardipine
Mean ± SD, median [range]
ACEI angiotensin-converting enzyme inhibitor, Ccr creatinine clearance, C DTPA 99mTc-diethylenetriaminepentaacetic acid clearance, Cio iohexol clearance, Cr creatinine, eGFR estimated GFR, GFR glomerular filtration rate, IgAN IgA nephropathy, MAP mean arterial pressure, RAS renin-angiotensin system, RCT randomized controlled trial, SBP/DBP systolic and diastolic blood pressure, SCr serum creatinine, TIF tubulointerstitial fibrosis, UP urinary protein
aTemocapril or trandolapril
bSE was multiplied by √N to calculate SD
cAn original unit, μmol/L, was divided by 88.4 for conversion to mg/dL
Table 16.3c
Outcomes of renal function in RCTs assessing efficacy of ACEI vs. no RAS blockade in IgAN patients
Author year
Interventions
N
Follow-up
ESKD
ΔSCr ≥100 %
ΔSCr ≥50 %
SCr at last visit
GFR at last visit
ΔGFR
(N)
(N)
(N)
(mg/dL)
(mL/min)
(mL/min per 1.73 m2)
Parallel group trials
Praga 2003 [9]
Enalapril
23
78 ± 37 [36–120] months
ND
ND
3
1.2 ± 0.5
Ccr
95 ± 30
ND
No RAS blockade
21
74 ± 36 [29–108]
12*
1.9 ± 1.9
64 ± 31*
Li 2013 [10]
Ramipril
30
60 month
ND
ND
ND
ND
eGFR
108.1 ± 29.0 per 1.73 m2
0.39 ± 2.57 per year
No treatment
30
105.7 ± 17.7
0.59 ± 1.63
Coppo 2007 [11]
Benazepril
32
35b [0–58] mo
0
ND
ND
ND
Ccr
124.0 ± 31 per 1.73 m2
ND
Placebo
34
38b [3–53] mo
0
109.3 ± 29.8*
Kanno 2005 [12]
ACEIa
26
≥36 months
ND
ND
ND
1.18 ± 1.33d
Ccr
85.5 ± 28.0d
ND
Amlodipine
23
1.23 ± 2.01d
85.5 ± 35.5d
Ruggenenti 2000 [13]
Ramipril
39
30.0b (16.4–47.5) moc
7
ND
ND
ND
Cio
ND
0.36 ± 0.56d per month
Placebob
36
9
0.55 ± 0.78d
Bannister 1995 [14]
Enalapril
13
12 months
ND
ND
ND
ND
  
ND
ND
Nifedipine
10
Nakamura 2000 [15]
Trandolapril
8
3 months
ND
ND
ND
0.8 ± 0.3
Ccr
110 ± 14 per 1.73 m2
ND
Candesartan
8
0.8 ± 0.2
110 ± 16
Verapamil
8
0.8 ± 0.2
106 ± 14
Placebo
8
0.8 ± 0.3
110 ± 12
Crossover trials
Maschio 1994 [16]
Fosinopril
39
3 months
ND
ND
ND
ND
Ccr
105 ± 23 per 1.73 m2
ND
Placebo
107 ± 25
Ikeda 1989 [17] (sub)
Captopril
4
ND
ND
ND
ND
ND
Ccr
71.9 ± 25.3
ND
Nicardipine
77.5 ± 20.4
Mean ± SD, [range], (25–75 %)
ACEI angiotensin-converting enzyme inhibitor, Ccr creatinine clearance, C DTPA 99mTc-diethylenetriaminepentaacetic acid clearance, Cio iohexol clearance, Cr creatinine, eGFR estimated GFR, ESKD end-stage kidney disease, GFR glomerular filtration rate, IgAN IgA nephropathy, RAS renin-angiotensin system, RCT randomized controlled trial, TIF tubulointerstitial fibrosis, ΔGFR a decrease in GFR from the baseline value, ΔSCr an increase in serum creatinine from the baseline value
*P < 0.05 (vs. ACEI intervention)
aTemocapril or trandolapril
bMedian
cFollow-up period of the whole cohort including IgAN patients (N = 75) and other CKD patients (N = 277)
dSE was multiplied by √N to calculate SD
Table 16.3d
Outcomes of urinary protein in RCTs assessing efficacy of ACEI vs. no RAS blockade in IgAN patients
Author year
Interventions
N
Follow-up
At last visit
At 12th month
At 3rd month
Histology
UP (g/day)
ΔUP (%)
UP (g/day)
ΔUP (%)
UP (g/day)
ΔUP (%)
Parallel group trials
Praga 2003 [9]
Enalapril
23
78 ± 37 [36–120] months
0.9 ± 1
ND
1.2 ± 1.1
36 ± 40.1
ND
ND
ND
No RAS blockade
21
74 ± 36 [29–108]
2 ± 1.8*
1.8 ± 1.5
−23 ± 79*
Li 2013 [10]
Ramipril
30
60 months
ND
ND
ND
ND
ND
ND
ND
No treatment
30
Coppo 2007 [11]
Benazepril
32
35b [0–58] mo
0.94 ± 0.98 per 1.73m2
ND
0.96 ± 0.68 per 1.73 m2
ND
ND
ND
ND
Placebo
34
38b [3–53] mo
1.80 ± 1.34*
ND
Kanno 2005 [12]
ACEIa
26
≥36 months
0.79 ± 1.84d
ND
ND
ND
ND
ND
ND
Amlodipine
23
1.33 ± 2.91d
Ruggenenti 2000 [13]
Ramipril
39
30.0b (16.4–47.5) moc
ND
ND
ND
ND
ND
ND
ND
Placebob
36
Bannister 1995 [14]
Enalapril
13
12 months
ND
ND
ND
ND
ND
ND
ND
Nifedipine
10
Nakamura 2000 [15]
Trandolapril
8
3 months
1.2 ± 0.5
36.8 ± 15.2
ND
ND
1.2 ± 0.5
36.8 ± 15.2
ND
Candesartan
8
1.1 ± 0.6
38.9 ± 16.6
1.1 ± 0.6
38.9 ± 16.6
Verapamil
8
1.4 ± 0.5
22.2 ± 8.4*
1.4 ± 0.5
22.2 ± 8.4*
Placebo
8
1.7 ± 0.7
ND
1.7 ± 0.7
ND
Crossover trials
Maschio 1994 [16]
Fosinopril
39
3 months
1.37 ± 0.98
ND
ND
ND
1.37 ± 0.98
ND
ND
Placebo
1.79 ± 1.20*
1.79 ± 1.20
Ikeda 1989 [17]
Captopril
4
ND
1.4 ± 0.6
ND
ND
ND
ND
ND
ND
Nicardipine
2.5 ± 0.7
Mean ± SD, [range], (25–75 %)
ACEI angiotensin-converting enzyme inhibitor, IgAN IgA nephropathy, RAS renin-angiotensin system, RCT randomized controlled trial, UP urinary protein, ΔUP decrease in UP from the baseline value
*P < 0.05 (vs. ACEI intervention)
aTemocapril or trandolapril
bMedian
cFollow-up period of the whole cohort including IgAN patients (N = 75) and other CKD patients (N = 277)
dSD was calculated multiplying SE by √N
Table 16.4a
Study protocols of RCTs assessing efficacy of ARB vs. no RAS blockade in IgAN patients
Author year
Interventions (dose)
Duration
Age(yr)
BP
Renal function
UP (g/day)
Histology
Parallel group trials
Li 2006 [18]
Valsartan (≤160 mg)
104 weeks
≥18
No malignant hypertension
SCr <2.8 mg/dL and UP ≥1.0 g/d
ND
  
Placebo
or SCr 1.4–2.8 mg/dL
Horita 2007 [19]
Losartan (12.5 mg) + PSL (≤30 mg)
24 months
ND
Normal blood pressure
eCcr >50 mL/min/1.73 m2
1.0–2.6
Katafuchi’s scale [54] 4–7
PSL (≤30 mg)
(BP <140/90 mmHg)
Shimizu 2008 [20]
Losartan (≤25 mg)
12 months
ND
Normal blood pressure
eGFR >50 mL/min/1.73 m2
≥0.4
ND
Antiplatelet
(BP <140/90 mmHg)
Xie 2011 [21]
Losartan (100 mg) + MZR (≤250 mg)
12 months
14–70
ND
SCr <4.0 mg/dLa
0.5–3.5
ND
Losartan (100 mg)
MZR (≤250 mg)
Nakamura 2000 [15]
Trandolapril (2 mg)
3 months
ND
Normal blood pressure
Ccr >80 mL/min/1.73 m2
≤3.0
ND
Candesartan (8 mg)
(BP <140/90 mmHg)
Verapamil (120 mg)
Placebo
Park 2003 [22]
Losartan (50 mg)
12 weeks
ND
Hypertension
SCr <3.0 mg/dL
≥1.0
ND
Amlodipine (5 mg)
Systolic BP ≤210 mmHg
BP blood pressure, Ccr creatinine clearance, CKD chronic kidney disease, eCcr estimated Ccr, eGFR estimated glomerular filtration rate, MZR mizoribine, PSL prednisolone, SCr serum creatinine, UP urinary protein
aAn original unit, μmol/L, was divided by 88.4 for conversion to mg/dL
Table 16.4b
Baseline characteristics of IgAN patients included in RCTs assessing efficacy of ARB vs. no RAS blockade
Author year
Interventions
N
Age
SBP/DBP or MAP
SCr
GFR
UP
Histology
(Year)
(mmHg)
(mg/dL)
(mL/min)
(g/day)
Parallel group trial
Li 2006 [18]
Valsartan
54
40 ± 10
136 ± 20/81 ± 11
1.11 ± 0.48
eGFR
87 ± 36 per 1.73m2
1.8 ± 1.2
ND
Placebo
55
41 ± 9
137 ± 17/83 ± 14
1.29 ± 0.54
78 ± 38
2.3 ± 1.7
Horita 2007 [19]
Losartan + PSL
20
34 ± 12
120 ± 8/73 ± 6
0.8 ± 0.2
Ccr
104 ± 36 per 1.73 m2
1.6 ± 0.6
Katafuchi’s [59]
PSL
18
32 ± 10
121 ± 7/75 ± 7
0.7 ± 0.1
103 ± 28
1.6 ± 0.4
Shimizu 2008 [20]
Losartan
18
36.0 ± 8.5
119.3 ± 10.8/74.8 ± 7.5
1.0 ± 0.2
eGFR
72.0 ± 15.9
0.81 ± 0.52
Taneda’s [60]
Antiplatelet
18
35.7 ± 8.1
122.1 ± 9.6/73.4 ± 12.1
0.9 ± 0.2
75.4 ± 18.1
0.73 ± 0.36
Xie 2011 [21]
Losartan + MZR
34
33.68 ± 10.29
101.15 ± 9.94
0.96 ± 0.37a
eGFR
91.50 ± 29.83 per 1.73 m2
1.21 ± 0.56
ND
MZR
35
33.63 ± 11.71
97.61 ± 8.54
0.90 ± 0.25a
95.63 ± 28.31
1.35 ± 0.74
Losartan
30
33.67 ± 11.62
101.13 ± 9.88
0.88 ± 0.26a
97.85 ± 32.87
1.12 ± 0.54
Nakamura 2000 [15]
Trandolapril
8
32.6 [18–54]
118 ± 14/80 ± 6
0.8 ± 0.2
Ccr
108 ± 16 per 1.73 m2
1.9 ± 0.7
ND
Candesartan
8
118 ± 16/78 ± 6
0.7 ± 0.2
112 ± 14
1.8 ± 0.8
Verapamil
8
116 ± 12/82 ± 8
0.9 ± 0.2
110 ± 12
1.8 ± 0.6
Placebo
8
120 ± 12/80 ± 8
0.8 ± 0.2
112 ± 12
1.6 ± 0.6
Park 2003 [22]
Losartan
20
39.3 ± 8.7
131 ± 16/89 ± 9
ND
Ccr
63 ± 22 per 1.73 m2
2.3 ± 1.5
ND
Amlodipine
16
44.3 ± 13.4
131 ± 12/86 ± 11
63 ± 24
2.1 ± 0.7
Mean ± SD, [range]
ARB angiotensin II receptor blocker, Ccr creatinine clearance, DBP diastolic blood pressure, eGFR estimated GFR, GFR glomerular filtration rate, IgAN IgA nephropathy, MAP mean arterial pressure, MZR mizoribine, PSL prednisolone, RAS renin-angiotensin system, RCT randomized controlled trial, SBP systolic blood pressure, SCr serum creatinine, UP urinary protein
aAn original unit, μmol/L, was divided by 88.4 for conversion to mg/dL
Table 16.4c
Outcomes of renal function in RCTs assessing efficacy of ARB vs. no RAS blockade in IgAN patients
Author year
Interventions
N
Follow-up
ESKD
ΔSCr ≥100 %
ΔSCr ≥50 %
SCr at last visit
GFR at last visit
ΔGFR
(N)
(N)
(N)
(mg/dL)
(mL/min)
(mL/min)
Parallel group trial
Li 2006 [18]
Valsartan
54
104 weeks
ND
1
ND
ND
eGFR
72.36 ± 34.20 per 1.73 m2
5.62 ± 6.79 per year
Placebo
55
4
63.39 ± 34.79
6.98 ± 6.17
Horita 2007 [19]
Losartan + PSL
20
24 months
ND
ND
0
0.8 ± 0.2
Ccr
100 ± 38 per 1.73 m2
ND
PSL
18
4*
0.9 ± 0.2
84 ± 34
Shimizu 2008 [20]
Losartan
18
12 months
ND
ND
ND
0.9 ± 0.3
eGFR

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Jul 4, 2016 | Posted by in NEPHROLOGY | Comments Off on Limitations of RAS Blockade in IgA Nephropathy

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