title: The pathophysiology of the chronic cardiorenal syndrome: a magnetic resonance imaging study.
abstract: OBJECTIVE
  To study the association of renal function with renal perfusion and renal parenchymal structure (T1 relaxation) in patients with chronic heart failure (HF).
  
  
  METHODS
  After IRB approval, 40 participants were enrolled according to HF and renal function status [10 healthy volunteers < 40 years; 10 healthy age-matched volunteers; 10 HF patients eGFR > 60 ml/min/1.73 m(2); 10 HF patients eGFR < 60 ml/min/1.73 m(2)] and assessed by MRI. To be eligible for enrolment all HF patients with renal dysfunction (RD) needed to be diagnosed as having chronic cardiorenal syndrome based on current guidelines. Patients with primary kidney disease were excluded.
  
  
  RESULTS
  Renal cortical perfusion correlated with eGFR values (r = 0.52;p < 0.01) and was similar between HF patients with and without RD (p = 0.27). T1 relaxation correlated negatively with eGFR values (r = -0.41;p > 0.01) and was higher in HF patients compared to volunteers (1121 ± 102 ms vs. 1054 ± 65 ms;p = 0.03). T1 relaxation was selectively prolonged in HF patients with RD (1169 ms ± 100 vs. HF without RD 1067 ms ± 79;p = 0.047). In linear regression analyses coronary artery disease (p = 0.01), hypertension (p = 0.04), and diabetes mellitus (p < 0.01) were associated with T1 relaxation.
  
  
  CONCLUSIONS
  RD in HF is not primarily mediated by decreased renal perfusion. Instead, chronic reno-parenchymal damage, as indicated by prolonged T1 relaxation, appears to underly chronic cardiorenal syndrome.
  
  
  CONCLUSIONS
  • The pathophysiology underlying chronic cardiorenal syndrome is not completely understood. • Chronic cardiorenal syndrome is independent of cardiac output or renal perfusion. • Renal T 1 relaxation appears to be prolonged in HF with renal impairment. • Renal T 1 relaxation is associated with classic cardiovascular risk factors. • Association of renal T 1 relaxation with parenchymal damage should be validated further.
authors.affiliation: Clinic of Internal Medicine and Clinic for Transplant-Immunology and Nephrology, University Hospital Basel, Basel, Switzerland, tobias.breidthardt@usb.ch.
authors.forename: Tobias
authors.initials: T
authors.lastname: Breidthardt
authors.forename: Eleanor F
authors.initials: EF
authors.lastname: Cox
authors.forename: Iain
authors.initials: I
authors.lastname: Squire
authors.forename: Aghogho
authors.initials: A
authors.lastname: Odudu
authors.forename: Nur Farhayu
authors.initials: NF
authors.lastname: Omar
authors.forename: Mohamed Tarek
authors.initials: MT
authors.lastname: Eldehni
authors.forename: Susan T
authors.initials: ST
authors.lastname: Francis
authors.forename: Christopher W
authors.initials: CW
authors.lastname: McIntyre
mesh_terms: D000328:Adult; D000368:Aged; D059347:Cardio-Renal Syndrome / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000150:complications; D002908:Chronic Disease; D005260:Female; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D007677:Kidney Function Tests; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D051437:Renal Insufficiency / Q000503:physiopathology; D012307:Risk Factors