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Kidney Week

Abstract: PUB037

Nocturnal Blood Pressure Dipping Patterns and Kidney Disease Progression

Session Information

Category: Cardiovascular-Kidney-Metabolic Health

  • 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

  • Dekmak, Batoul, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
  • Leung, Christopher, Georgetown University, Washington, District of Columbia, United States
  • Han, Jona, Georgetown University, Washington, District of Columbia, United States
  • Han, Karina, Georgetown University, Washington, District of Columbia, United States
  • Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
Background

While office BP captures a single daytime snapshot, ABPM better detects nocturnal dipping patterns. Normal dipping —a 10–20% nocturnal BP decline — reflects physiological sympathetic withdrawal. CKD patients frequently exhibit non- or reverse-dipping, potentially accelerating disease progression. We investigated nocturnal dipping's relationship with the markers of CKD progression; eGFR decline and proteinuria.

Methods

This retrospective cohort study enrolled 17 adults with CKD stages II–IV who underwent 24-hour ABPM, classified as dippers (10–20% nocturnal decline), non-dippers (<10%), or reverse dippers (nocturnal rise). Primary outcome was annualized eGFR slope; secondary outcomes were proteinuria and clinical characteristics.

Results

The cohort (mean age 66.0 ± 17.6 years; 61% female) was predominantly CKD stage II–III (83%), with 71% showing abnormal dipping: 47% non-dippers, 24% reverse dippers, and 29% normal dippers. Counterintuitively, dippers showed steeper eGFR decline (−4.14 mL/min/1.73m2/year) versus non-dippers (−1.79) and reverse dippers (−1.88), likely confounded by older age (79.4 vs. ~63 years) and higher office SBP (157.0 vs. ~138 mmHg). Reverse dippers had the highest median UACR (145 mg/g) versus dippers (48) and non-dippers (26), suggesting nocturnal hypertensive glomerular injury. Notably, 18% had masked hypertension undetectable by office measurement.

Conclusion

Abnormal nocturnal dipping affected over two-thirds of this CKD cohort. Reverse dipping's association with proteinuria supports circadian hemodynamic disruption as a mechanism of kidney injury. The paradoxical faster eGFR decline in dippers likely reflects confounding by age and daytime BP burden. These findings reinforce ABPM's value in CKD, and raise important questions about whether dipping status alone, without accounting for age and comorbidities adequately captures cardiorenal risk. Larger prospective studies are needed to clarify these relationships and assess whether targeting nocturnal BP patterns can slow CKD progression.

Clinical characteristics