Impact of Cardiovascular Organ Damage on Cortical Renal Perfusion in Patients with Chronic Renal Failure

Author:

Lubas Arkadiusz1ORCID,Ryczek Robert2,Kade Grzegorz1,Smoszna Jerzy1,Niemczyk Stanisław1

Affiliation:

1. Department of Internal Diseases, Nephrology, and Dialysis, Military Institute of Medicine, Ulica Szaserów 128, 04-141 Warsaw 44, Poland

2. Department of Cardiology, Military Institute of Medicine, Ulica Szaserów 128, 04-141 Warsaw 44, Poland

Abstract

Introduction. Properly preserved renal perfusion is the basic determinant of oxygenation, vitality, nutrition, and organ function and its structure. Perfusion disorders are functional changes and are ahead of the appearance of biochemical markers of organ damage. The aim of this study was to evaluate a relationship between the renal cortex perfusion and markers of cardiovascular organ damage in patients with stable chronic renal failure (CKD).Methods. Seventeen patients (2 F; 15 M; age47±16) with stable CKD at 2–4 stages and hypertension or signs of heart failure were enrolled in this study. Blood tests with an estimation of renal and cardiac functions, echocardiographic parameters, intima-media thickness (IMT), renal resistance index (RRI), and total (TPI), proximal (PPI), and distal (DPI) renal cortical perfusion intensity measurements were collected.Results. DPI was significantly lower than PPI. TPI significantly correlated with age, Cys, CKD-EPI (cystatin), and IMT, whereas DPI significantly depended on Cystain, CKD-EPI (cystatin; cystatin-creatinine), IMT, NT-proBNP, and troponin I. In multiple stepwise regression analysis model only CKD-EPI (cystatin) independently influenced DPI.Conclusions. Cardiovascular and kidney damage significantly influences renal cortical perfusion. Ultrasound measurement of renal perfusion could be a sensitive method for early investigation of cardiovascular and renal injuries.

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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