Clinicopathological Review of Renovascular Hypertension and Hypertensive Emergency-related Nephropathy Based on Case Series

Renal complications resulting from persistent, uncontrolled hypertension include renovascular hypertension (RVH) and hypertensive emergency (crisis)-related nephropathy (HEN), both of which are characterized by hyperreninemia and are involved in the progression of nephropathy. In RVH, renal artery stenosis leads to increased renin secretion from the affected kidney, which induces focal segmental glomerulosclerosis (FSGS) lesions in the contralateral kidney, resulting in proteinuria. In HEN, severe hypertension (>200/120 mmHg) induces endothelial cell proliferation in renal arterioles, resulting in edematous thickening of the intima and narrowing of the lumen. This process increases renin secretion from the juxtaglomerular apparatus (JGA), further worsening hypertension and resulting in glomerular collapse and rapidly progressive renal impairment. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) suppress aldosterone activity and promote renin activity, respectively. Prolonged administration has been suggested to lead to JGA hyperplasia and smooth muscle cell proliferation in the renal arterioles.