ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO220

Salt Sensitivity and Hypertensive Nephropathy: A Link to Be Discovered

Session Information

Category: Hypertension and CVD

  • 1602 Hypertension and CVD: Clinical


  • 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

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.


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.


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.


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