Salt Sensitivity Hypertension and Lens Opacities
Salt Sensitivity Hypertension and Lens Opacities
Salt-sensitive hypertension (SSH) accounts for about the half of all Hypertension (HT) cases
 .In SSH, Na+/K+-ATPase activity is impaired. Impaired Na+/K+-ATPase activity in the lens
 epithelium results in cortical opacities in the peripheral equator of the lens.

 This study analyzed 305 patients with hypertension aged between 40 and 80 years and 124
 non-HT controls. A total of 163 patients with HT who were admitted to the emergency service
 at least once with a minimum increase of 10% in their systolic and diastolic blood pressure
 after consuming salted food met the eligible criteria for HT and were included in the SSH
 group. A total of 142 patients who were previously diagnosed with HT but had no previous
 history were considered non-SSH. Two researchers examined the presence of cortical lens
 opacities biomicroscopically using the diffuse, direct, Scheimpflug, and retroillumination
 from fundus methods.
The number of patients with hypertension (HT) worldwide is estimated to reach 1.56 billion by
 2025.HT accounts for almost 50% of deaths due to stroke and coronary artery disease.
 Salt-sensitive hypertension (SSH) accounts for about the half of all HT cases. Na+ /K+-ATPase
 activity is impaired in patients with SSH . Impaired Na+ /K+-ATPase activity in the lens
 epithelium results in cortical opacities in the peripheral equatorial region of the lens.A
 definite diagnosis of salt sensitivity is difficult, expensive, and associated with low
 patient compliance. Salt sensitivity is a risk factor for cardiovascular mortality and
 morbidity regardless of blood pressure and for other diseases such as asthma, gastric
 carcinoma, osteoporosis, and renal dysfunction. The present study is the first to investigate
 the potential of using lens opacity to predict SSH.

 The transparency of the whole lens is largely based on epithelial cell permeability and Na+
 /K+-ATPase activity. Circulation is activated by Na+ /K+-ATPases, which are present at
 20-fold normal concentrations, particularly in the equatorial than in the anterior epithelial
 cells.

 The mechanisms associated with SSH pathogenesis, such as signaling pathways involving Src
 family kinase (SFK), endothelin, connexin, brain natriuretic peptide (BNP), aldosterone,
 transient receptor protein V4 (TRPV4) ion channel, with-no-lysine kinase-Ste20-like
 proline/alanine rich kinase/oxidative stress-responsive kinase 1 (WNK-SPAK/OSR1), and
 Ras-related C3 botulinum toxin substrate (Rac1) , are important to the physiology of the lens
 epithelium. Compelling studies suggest that inhibition of these pathways may facilitate
 opacity.
Inclusion Criteria:

 Salt Sensitivity Hypertension patients Non-SSH, salt-resistant HT (SRH) patients Control
 patients without HT, aged 40-80 years.

 Exclusion Criteria:

 Cataracts Diabetes Mellitus Smoking Hypo/hypercalcemia Hyperparathyroidism Eye trauma
 Coronary artery disease Cardiac failure Renal failure

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