Hypertension is defined as average systolic blood pressure and/or diastolic blood pressure that are ≥95th percentile for gender, age, and height on ≥3 occasions (1). Renal parenchymal disease and essential hypertension are the most important causes in <12 and >12 years, respectively (2). Hypertension with hypokalaemia and suppression of plasma renin activity is known as mineralocorticoid hypertension. The most common cause of mineralocorticoid hypertension is probably primary aldosteronism. Monogenic forms of low renin hypertension are apparent mineralocorticoid excess (AME), Liddle syndrome, steroid 11β–hydroxylase (11β–OHD) and steroid 17–hydroxylase (17–OHD) deficiencies, glucocorticoid–remediable hyperaldosteronism (familial hyperaldosteronism type I), familial hyperaldosteronism type II, and primary hyperaldosteronism (Conn’s syndrome) (3). AME described by New et al. in 1977 in a Zuni girl, is a potentially fatal disorder that results in juvenile low–renin hypertension, hyporeninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thrive, poor growth and in many cases nephrocalcinosis (4). AME is caused by a deficiency of 11β–hydroxysteroid dehydrogenase type 2 (11β–HSD2) owing to autosomal recessive mutations in the HSD11β2 gene (5). Left ventricular hypertrophy (LVH) is the most prominent clinical evidence of target–organ damage caused by hypertension in children and adolescents’ and has been reported in 34% to 38% of children and adolescents with mild, untreated BP elevation. Abnormalities of the retinal vasculature have been reported in adults with hypertension. Very few studies of retinal abnormalities have been conducted in children with hypertension (1).