Table 1. Open in new tab Milestones in...

Era

Management of ARVD

1930s

Experimental RAS caused renal ischaemia and systemic hypertension [2]. Renovascular hypertension was reversed by unilateral nephrectomy [3].

1960s

Complex surgical revascularization techniques were developed to spare renal tissue given that renal angiography showed that ARVD was often a bilateral disease. Surgical revascularization however had limited success and was associated with a high mortality rate while improved pharmacological blood pressure control was noted to correlate with improved survival [4, 5].

1980–90s

Adequate pharmacological blood pressure control did not always prevent loss of renal function and ACEi were associated with AKI especially in patients with bilateral ARVD [6]. Enthusiasm for surgical revascularization increased especially with evidence that it could slow the rate of loss of renal function post-operatively [7].

Early 1990s

Percutaneous angioplasty techniques gained popularity in view of increasing patient age and comorbidity [8].

Late 1990s

PTRAS was shown to be technically superior to PTRA and became the preferred technique for revascularization [9]. There was further evidence that revascularization could improve the rate of decline of renal function post-intervention, but studies were uncontrolled [10].

Late 1990s to early 2000s

Three small RCTs (EMMA, DRASTIC and Scottish and Newcastle study) showed that PTRA was not associated with any clinical benefit. On the other hand, there was accumulating evidence that enhanced vascular protection, including the use of ACEi could slow the rate of progression of ARVD and improve clinical outcomes [11].

Current era

Larger RCTs (ASTRAL and CORAL) comparing optimal medical treatment with revascularization confirmed that revascularization does not confer further benefit to multi-targeted medical therapy [12, 13].

Future directions

Increasing evidence that revascularization may be beneficial in patients with a ‘high-risk’ phenotype who were not adequately represented in clinical trials [1]. Future management of ARVD will rely on modern imaging techniques to establish the haemodynamic significance of RAS and enable accurate identification of patients with a ‘hibernating parenchyma’ [14] (viable parenchyma with potential to recover function), and novel strategies (e.g. cell-based therapies) to protect the renal parenchyma and microvascular architecture [15, 16].

Table 1.

Open in new tab

Milestones in the history of management of ARVD

Era	Management of ARVD
1930s	Experimental RAS caused renal ischaemia and systemic hypertension [2]. Renovascular hypertension was reversed by unilateral nephrectomy [3].
1960s	Complex surgical revascularization techniques were developed to spare renal tissue given that renal angiography showed that ARVD was often a bilateral disease. Surgical revascularization however had limited success and was associated with a high mortality rate while improved pharmacological blood pressure control was noted to correlate with improved survival [4, 5].
1980–90s	Adequate pharmacological blood pressure control did not always prevent loss of renal function and ACEi were associated with AKI especially in patients with bilateral ARVD [6]. Enthusiasm for surgical revascularization increased especially with evidence that it could slow the rate of loss of renal function post-operatively [7].
Early 1990s	Percutaneous angioplasty techniques gained popularity in view of increasing patient age and comorbidity [8].
Late 1990s	PTRAS was shown to be technically superior to PTRA and became the preferred technique for revascularization [9]. There was further evidence that revascularization could improve the rate of decline of renal function post-intervention, but studies were uncontrolled [10].
Late 1990s to early 2000s	Three small RCTs (EMMA, DRASTIC and Scottish and Newcastle study) showed that PTRA was not associated with any clinical benefit. On the other hand, there was accumulating evidence that enhanced vascular protection, including the use of ACEi could slow the rate of progression of ARVD and improve clinical outcomes [11].
Current era	Larger RCTs (ASTRAL and CORAL) comparing optimal medical treatment with revascularization confirmed that revascularization does not confer further benefit to multi-targeted medical therapy [12, 13].
Future directions	Increasing evidence that revascularization may be beneficial in patients with a ‘high-risk’ phenotype who were not adequately represented in clinical trials [1]. Future management of ARVD will rely on modern imaging techniques to establish the haemodynamic significance of RAS and enable accurate identification of patients with a ‘hibernating parenchyma’ [14] (viable parenchyma with potential to recover function), and novel strategies (e.g. cell-based therapies) to protect the renal parenchyma and microvascular architecture [15, 16].

Era	Management of ARVD
1930s	Experimental RAS caused renal ischaemia and systemic hypertension [2]. Renovascular hypertension was reversed by unilateral nephrectomy [3].
1960s	Complex surgical revascularization techniques were developed to spare renal tissue given that renal angiography showed that ARVD was often a bilateral disease. Surgical revascularization however had limited success and was associated with a high mortality rate while improved pharmacological blood pressure control was noted to correlate with improved survival [4, 5].
1980–90s	Adequate pharmacological blood pressure control did not always prevent loss of renal function and ACEi were associated with AKI especially in patients with bilateral ARVD [6]. Enthusiasm for surgical revascularization increased especially with evidence that it could slow the rate of loss of renal function post-operatively [7].
Early 1990s	Percutaneous angioplasty techniques gained popularity in view of increasing patient age and comorbidity [8].
Late 1990s	PTRAS was shown to be technically superior to PTRA and became the preferred technique for revascularization [9]. There was further evidence that revascularization could improve the rate of decline of renal function post-intervention, but studies were uncontrolled [10].
Late 1990s to early 2000s	Three small RCTs (EMMA, DRASTIC and Scottish and Newcastle study) showed that PTRA was not associated with any clinical benefit. On the other hand, there was accumulating evidence that enhanced vascular protection, including the use of ACEi could slow the rate of progression of ARVD and improve clinical outcomes [11].
Current era	Larger RCTs (ASTRAL and CORAL) comparing optimal medical treatment with revascularization confirmed that revascularization does not confer further benefit to multi-targeted medical therapy [12, 13].
Future directions	Increasing evidence that revascularization may be beneficial in patients with a ‘high-risk’ phenotype who were not adequately represented in clinical trials [1]. Future management of ARVD will rely on modern imaging techniques to establish the haemodynamic significance of RAS and enable accurate identification of patients with a ‘hibernating parenchyma’ [14] (viable parenchyma with potential to recover function), and novel strategies (e.g. cell-based therapies) to protect the renal parenchyma and microvascular architecture [15, 16].

ACEi, angiotensin-converting enzyme inhibitor; ARVD, atherosclerotic renovascular disease; PTRA, percutaneous transluminal renal angioplasty; PTRAS, percutaneous transluminal renal angioplasty with stenting; RCTs, randomized controlled trials.

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