Abstract: TH-PO220
Salt Sensitivity and Hypertensive Nephropathy: A Link to Be Discovered
Session Information
- Hypertension and CVD: Clinical - I
November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Tunesi, Francesca, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- D'Urbano, Luca, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- Simonini, Marco, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- Citterio, Lorena, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- Zagato, Laura, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- Manunta, Paolo, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
- Lanzani, Chiara, IRCCS Ospedale San Raffaele, Milano, Lombardia, Italy
Background
Sodium sensitivity (SS) is a change in blood pressure (BP) depending on Na+ intake, 30% of population has it. Either a salt load test or a sodium dietary protocol can be used to stratify the population into 3 groups based on BP variation: sodium sensitive (SS), sodium resistant (SR), inverse sodium sensitivity (ISS), based on an increase, a non-significant variation or a decrease in BP following the administration of Na+. SNPs located in genes related with Na+ metabolism, aldosterone synthesis and kidney tubular Na+ reabsorption are related to this phenotype.
Methods
We analyzed data collected from the follow-up (FUP) of 127 subjects with a new diagnosis of hypertension, categorized by their profile through acute salt load test. We analyzed the kidney damage by annual decline of eGFR and development of microalbuminuria. Genetic polymorphism analysis has been executed.
Results
No differences in the decline of eGFR are observed among the groups (-1.3084 ml/min ± 0.16 p= 0.372). SR subjects seem to be more prone to develop earlier microalbuminuria (χ 2 10.682, p= 0.005) even with an adequate BP control (P-Anova SBP 0.766; P-Anova DBP 0.856). An inverse correlation exists between pressure-natriuresis ratio and decline in eGFR (R -0.194 p= 0.016). Polymorphism in CYP11B2 (0.72 OR p= 0.045) and NEDD4L (0.74 OR p=0.027) are protective against eGFR decline. ADD3 polymorphism (3.73 OR p= 0.049) is a risk factor for development of microalbuminuria. KL (0.15 OR p= 0.034), PKD and TRPC6 (p-Value 0.037, p-Value 0.009) polymorphism are protective factor against microalbuminuria.
Conclusion
SR patients are more at risk of developing hypertensive nephropathy earlier than other groups; steeper pressure natriuresis ratio is involved in quicker decline in renal function possibly accelerating development of hypertensive nephropathy. Further studies with larger sample and standardization in salt sensitivity test are needed to translate this knowledges into clinical setting.
A) salt load test; B) microalbuminuria