Renal artery stenosis causes kidney ischemia, reducing the size of the affected kidney, which eventually results in atrophy. Although renal atrophy is considered irreversible, resolution of the ischemia occasionally restores kidney size when the cause is renal artery stenosis. Angioplasty is effective in patients with nonatherosclerotic renovascular diseases (non-ARVDs). Nevertheless, renal enlargement after angioplasty has not been fully examined. We conducted a retrospective study to examine this phenomenon in non-ARVD patients. Ten patients with a <100-mm pole-to-pole length of the poststenotic kidney were treated with angioplasty. Data were collected up to 12 months after angioplasty. The mean age was 28 years; the estimated glomerular filtration rate was 92 ± 7 mL/min/1.73 m2 (mean ± SEM); blood pressure was 150/99 mmHg; 80% were women; and fibromuscular dysplasia was present in 90% of the patients. All patients had hypertension. The lengths of the poststenotic and contralateral kidney before angioplasty were 91 ± 1 and 111 ± 3 mm, respectively. After angioplasty, the length of the poststenotic kidney gradually increased during the 3 months after treatment (+5.4 mm) and that of the contralateral kidney decreased over the same time course (-3.7 mm). Enlargement was also found in the moderate atrophy subgroup (length < 92 mm), and it was greater in the <30 years old group. In a noteworthy case, renal size in the poststenotic kidney recovered from 87 to 102 mm after angioplasty. Our findings demonstrated that reduced renal size can be reversed after optimal angioplasty in non-ARVD patients, especially young patients, suggesting reversibility of the ischemic kidney.
Keywords: Angioplasty; Fibromuscular dysplasia; Ischemic nephropathy; Renal artery stenosis; Renovascular hypertension.