Table 2.
Summary of all studies included in the systematic literature review.
| References | Study design | Study populations | Groups | Measurements | Baseline | After renal mass reduction | After anti-RAAS treatment | Adverse events (if any) |
|---|---|---|---|---|---|---|---|---|
| Animals | ||||||||
| Adamczak et al. [50] | Randomized | 58 Male -Sprague Dawley rats | •11 STN-X + ACEi •11 Sham |
BP, UAER |
In Sham Cr = 0.49 ± 0.006 mg/dl |
In STN-X Cr = 0.92 ± 0.008 mg/dl |
In STN-X + ACEi •BP = 116 mmHg •UAER = 4.85 ± 3.40 mg/24 h In Sham •BP = 127 mmHg •UAER = 0.47 ± 0.37 mg/24 h |
None |
| Kelly et al. [51] | Randomized | 80 Sprague-Dawley rats | •60 STN-X + ACEi •20 Sham |
SBP, Prot, CCr |
In Sham •SBP = 135 ± 10 mmHg •Prot = 1.3 ± 0.12 mg/d •CCr = 2.7 ± 0.14 ml/min |
In STN-X ↑SBP= (193 ± 11 mmHg) ↑Prot= (6.24 ± 0.94 mg/d) ↓CCr= (0.60 ± 0.11 ml/min) |
STN-X + ACEi for 12 weeks: ↓SBP=(131 ± 8 mmHg) ↓Prot=(2.5 ± 0.43 mg/d) ↑CCr=(1.23 ± 0.16 ml/min) |
None |
| Mishina et al. [52] | Randomized controlled | 6 Mongrel dogs | 7/8 renal ablation in all animals | Cr, CCr, SBP,DBP, RAAS components |
•Cr = 0.9 ± 0.2 mg/dl •CCr = 2.4 ± 0.5 ml/min/kg •SBP = 120.4 ± 10.3 mmHg •DBP = 71.3 ± 2.7 mmHg •PRA = 1.2 ± 0.9 ng/ml/h •ANGI = 474.4 ± 276.4 pg/ml •ANGII = 184.0 ± 143.2 pg/ml •ALD = 5.2 ± 6.5 ng/dl |
↑Cr = 2.8 ± 0.5 mg/dl (p < .05) ↓CCr = 1.0 ± 0.2 ml/min/kg (p < .05) ↑SBP = 152.5 ± 18.9 mmHg (p < .05) ↑DBP = 93.6 ± 11.7 mmHg (p < .05) ↑PRA = 6.0 ± 1.4 ng/ml/h ↑ANGI = 7312.8 ± 552.9 pg/ml ↑ANGII = 3612.4 ± 1067.3 pg/ml ↑ALD = 230.2 ± 84.5 ng/dl |
STN-X + ACEi for 2 weeks: ↓Cr = 2.5 ± 1.1 mg/dl ↑CCr = 1.46 ± 0.14 ml/min/Kg ↓SBP = 137.8 ± 12.4 mmHg ↓DBP = 82.9 ± 3.6 mmHg (p < .05) ↑PRA = 8.1 ± 1.3 ng/ml/h ↑ANGI = 7980.8 ± 2521.6 pg/ml ↓ANGII = 111.2 ± 106.2 pg/ml ↓ALD = 13.4 ± 10.8 ng/dl |
None |
| Singh et al. [53] | Randomized controlled | 10 pure- bred Australian merino female sheep | •5 fetal Uni-X + ARBs •5 Sham + ARB |
GFR, RBF, UNaV, FENa |
In Sham •GFR = 1.02 ± 0.1 ml/min/gkw •RBF = 10.1 ± 0.8 ml/min/gkw •UNaV = 2.0 ± 0.5 µmol/min/gkw •FENa %=1.4 ± 0.4 |
↓GFR=(0.62 ± 0.1 ml/min/gkw) [p < .001] ↓RBF = (5.3 ± 0.5 ml/min/gkw) [p < .001) ↓UNaV = (1.2 ± 0.2 µmol/min/gkw) ↓FENa% =(1.2 ± 0.4) |
ARB for 3 weeks in both groups: ↑GFR= most in Sham than Uni-X ↑RBF= most in Sham than Uni-X ↑UNaV= most in Sham than Uni-X ↑FENa=most in Sham than Uni-X |
None |
| Singh et al. [21] | Randomized controlled | 12 Australian merino male sheep | •6 fetal Uni-X + ARB •6 Sham + ARB |
GFR, RBF, UNaV, FENa |
In Sham •GFR = 1.0 ml/min/gkw •RBF = 6 ml/min/gkw •UNaV = 1.5 µmol/min/gkw •FENa=1.2% |
↓GFR= (0.8 ml/min/gkw) [p < .001] ↓RBF= (4.3 ml/min/gkw) [p < .001] ↓UNaV= (0.8 µmol/min/gkw) (p < .01) ↓FENa=0.8% |
ARB for 3 weeks in both groups ↑GFR=most in Sham than Uni-X ↑RBF= most in Sham than Uni-X ↑UNaV= most in Sham (p=.003) than Uni-X ↑FENa=most in Uni-X than Sham |
None |
| Humans | ||||||||
| Wühl et al. [54] | Multicentric randomized controlled trial | 385 children with CKD |
71 pts with hypo/dysplasia randomized to receiving ACEi | GFR, 24 h BP, Prot |
•GFR = 45.9 ml/min/1.73 m2 •24 h BP = 89.5 mmHg •Prot = 800 mg/m2/d |
•24 h BP=118.3 ± 14.3 mmHg •Prot= 0.82 g |
After 6 months of ACEi ↓24 h BP = 109.4 ± 14.4 mmHg ↓Prot= 0.36 g Progression in GFR reduction is delayed by use of ACEi. |
Hyperkalemia (18 pts) Hypotension (2 pts) |
| Basturk et al. [8] | Retrospective | 31 patients with SFK | 21 of them receiving ACEi | GFR, Prot | Prot= 470 ± 662 mg/d |
Pts without ACEi •Last GFR = 44.5 ± 33.4 ml/min •Last Prot = 0.95 ± 0.98 g/24 h |
Pts with ACEi •Last GFR = 55 ± 21.1 ml/min •Last Prot = 0.48 ± 0.79 g/24 h |
ESRD (2 pts) |
| Peco-Antìc et al. [55] | Prospective trial | 14 children with CRM | 5 children with CRM | Prot, GFR, 24 h BP | •Prot=0.93 ± 0.16 mg/mg •GFR=48.3 ± 13.4 ml/min/1.73 m2 •24 h BP = 85.4 ± 14.8 mmHg |
Before ACEi administration •Prot=0.92 ± 0.18 mg/mg •GFR=45.8 ± 10.1 ml/min/1.73 m2 •24 h BP=90.4 ± 14.3 mmHg |
After ACEi administration •Prot=0.23 ± 0.12 •GFR = 48.1 ± 1.8 ml/min/1.73 m2 •24 h BP = 80.5 ± 14.3 mmHg |
Not reported |
| Nyame et al. [56] | Observational | 900 patients underwent laparoscopic nephrectomy | 338 patients treated with ARBs 562 no ARBs |
GFR, Severe renal function, MACE |
Mean pre-operative GFR without RAAS blockade: 87.2 ml/min Mean pre-operative GFR with RAAS blockade: 81.5 ml/min |
Mean post-operative GFR without RAAS blockade (day 3): 77.2 ml/min Mean post-operative GFR with RAAS blockade (day 3): 69.3.5 ml/min |
•GFR in ARBs patients: 69.1 ml/min •GFR in untreated patients:75.9 ml/min •Rate of stage IV/V CKD in ARBs patients in postoperative follow-up: 3.6% •Rate of stage IV/V CKD in untreated patients in post-operative follow-up: 4.4% •Rate of MACE in continued ARBs patients: 13.7% •Rate of MACE in discharged patients: 17.7% |
Not reported |
| Hiremath et al. [57] | Systematic review of 21 randomized trials | 1549 patients | ARBs/ACEi groups Controls |
GFR, Prot | Mean GFR=61.6 ± 16.6 ml/min | Mean GFR=61.6 ± 16.6 ml/min |
GFR in ACEi/ARBs patients was lower than in controls (−5.7 ml/min; 95% CI −8.7 to −2.8, p < .001) In ACEi/ARBs patients was lower than in controls (−0.47 g/d; 95% CI −0.86 to 0.08, p = .16) |
Anemia and hyperkalemia (reported in 8 trials) |
STN-X: subtotal nephrectomy; UAER: urinary albumin excretion rate; Uni-X: unilateral-nephrectomy; Sham: Sham operated animals; ARB: angiotensin receptor blocker; ACEi: angiotensin converting enzyme; SBP: systolic blood pressure; DBP: diastolic blood pressure; Cr: creatinine; CCr: creatinine clearance; ESRD : end stage renal disease; PRA: plasma renin activity; ANG I: angiotensin I; ANG II: angiotensin II; ALD: aldosterone; GFR: glomerular filtration rate; RBF: renal blood flow; FF: filtration fraction; UNaV: urinary sodium excretion; FENa: fractional excretion of sodium; Pts: patients; CKD: chronic kidney disease; 24 h BP: 24 h blood pressure; N.P. : not performed; SFK : single functioning kidney; CRM: chronic renal malformation; MACE: major cardiovascular events; CI : confidence interval.