The role of renin–angiotensin system in the chronic allograft nephropathy: an immunohistochemical study

Figures & data

Table 1. Clinical characteristics of patients with chronic allograft nephropathy (CAN).

Variables	CAN group
Patients (n) Recipient's gender (%)	58
Male	65.5
Recipient's age (yr, mean ± SD)
Native kidney disease (%)	31.79 ± 14.03
Glomerulonephritis	38.6%
Hypertension	12.3%
Indeterminate	29.8%
Others	19.3%
Donor type (%)
Living	75.9
HLA pretransplant mismatch (mean ± SD)	2.94 ± 1.28
Delayed graft function (%)	18.5
Acute rejection episodes (%)	43.1
SCr at the time of biopsy  (mg/dL, mean ± SD)	2.13 ± 0.90
SCr at 6 months (mg/dL, mean ± SD)	1.54 ± 0.57
SCr at 1 year (mg/dL, mean ± SD)	1.58 ± 0.60
SCr at the last visit (mg/dL, mean ± SD)	1.88 ± 0.89
Time of biopsy (mo, mean ± SD)	44.44 ± 23.74
Follow-up min–max (mo, mean ± SD)	8–251 m (113.02 ± 5310)

Abbreviation: SCr: serum creatinine.

Figure 1. Spearman's association between inflammatory infiltrate and interstitial fibrosis (Ci, Banff'score) (r = 0.719; p < 0.0001).

Figure 2. Intrarenal renin–angiotensin system and transforming growth factor β₁. Angiotensin-converting enzyme (ACE): Control group (A)—mild staining of proximal tubules brush border; CAN group (B)—intense staining of proximal tubules brush border. Angiotensin II (Angio II): Control group (C)—negative; CAN group (D)—positive staining in atrophic tubules and interstitial cells. Transforming growth factor β₁ (TGFβ₁): Control group (E)—mild focal staining of peritubular capillaries; CAN group (F)—intense staining of peritubular capillaries. IH-400×.

Table 2. Angiotensin converting-enzyme (ACE), angiotensin II (Angio II) and transforming growth factor β₁ (TGFβ₁) expression in groups of chronic allograft nephropathy (CAN; CAN grades I, II and III; CAN with and without arteriolar hyaline thickening; CAN with or without RAS blockade) and the control group.

Groups	ACE Median (min–max)	Angio II Median (min–max)	TGFβ1 Median (min–max)
CAN (n = 58)	5.0 (1.0–9.0)	2.0 (0.0–7.0)	9.0 (2.0–12)
Control (n = 20)	4.0 (3.0–8.0)	0.0 (0.0–0.0)	5.0 (1.0–7.0)
*p	0.37	<0.001	<0.001
CAN I (n = 22)	6.0 (3.0–8.0)^a	1.0 (0.0–6.0)	9.0 (2.0–12)
CAN II (n = 17)	5.0 (1.0–9.0)^b	2.0 (0.0–5.0)	9.0 (4.0–12)
CAN III (n = 19)	4.0 (1.0–7.0)^c	3.0 (0.0–7.0)	9.0 (4.0–12)
†p	0.002	0.19	0.46
CAN + positive ah (n = 45)	5.0 (1.0–9.0)	2.0 (0.0–7.0)	9.0 (2.0–12)
CAN + negative ah (n = 13)	7.0 (2.0–8.0)	2.0 (0.0–5.0)	9.0 (4.0–11)
*p	0.09	0.28	0.59
CAN (RAS blockade) (n = 20)	5.5 (1.0–9.0)	2.0 (0.0–6.0)	9.0 (2.0–12)
CAN (no blockade) (n = 33)	5.0 (1.0–8.0)	2.0 (0.0–7.0)	9.0 (4.0–12)
*p	0.77	0.73	0.27

Abbreviation: ah, arteriolar hyaline thickening.

*Mann–Whitney test.

†Kruskal–Wallis test complemented by Dunn method: a = b > c;

Figure 3. Allograft survival after the diagnosis of CAN according to ACE, Angio II, TGFβ₁ expression and RAS blockade.

Figure 4. Allograft survival after the diagnosis of CAN according to the inflammatory infiltrate intensity, grade of interstitial fibrosis (Banff Ci score), CAN Banff grades and hyaline arteriolar thickening (Banff ah score).