Key result
Fontan circulation linked to ~10 mL/min/1.73 m2 lower cystatin C-based eGFR versus healthy controls.
Why the study?
Do patients with Fontan circulation have identifiable differences in renal biomarkers and intrarenal hemodynamics compared to healthy controls?
Case-Control (n=50)
No
Do patients with Fontan circulation have identifiable differences in renal biomarkers and intrarenal hemodynamics compared to healthy controls?
In patients with a Fontan circulation, creatinine-based eGFR overestimates kidney function due to reduced muscle mass, whereas cystatin C and intrarenal flow measurements effectively unmask progressive glomerular injury and reduced renal compliance.
Cystatin C eGFR and albuminuria may better detect masked kidney dysfunction in Fontan patients; leaves open whether routine use alters outcomes or risk stratification.
Background Kidney dysfunction is prevalent but insufficiently understood in Fontan patients. We aimed to investigate Fontan‐Associated Renal Disease (FARD) through comprehensive phenotyping using biomarkers of renal function and injury, as well as ultrasound assessment of intrarenal hemodynamics. Methods We prospectively collected data on serum creatinine and cystatin C levels, and 24‐h urine creatinine clearance and albumin excretion in 25 Fontan patients, comparing them to healthy age‐ and sex‐matched controls. Additionally, we measured intrarenal venous and arterial flow patterns using Doppler ultrasonography. Results Median age was 28 (Q1–Q3: 19–35) years, with 48% female. Compared to controls, Fontan patients had similar creatinine‐based eGFR (eGFR cr ) (114 vs. 106 mL/min/1.73 m 2 ; p = 0.2), lower cystatin C‐based eGFR (eGFR cys ) (96 vs. 106 mL/min/1.73 m 2 ; p = 0.045), and lower 24‐h urinary creatinine excretion (10.0 vs. 13.7 mmol/24 h; p < 0.001). Additionally, patients had higher 24‐h urine albumin excretion (14 vs. 2 mg/24‐h; p < 0.001). In patients, both eGFR cys and urine albumin correlated with age ( r = −0.56 and r = 0.44, respectively; p < 0.05). Twenty‐‐four out of 25 patients and all controls had continuous intrarenal venous flow patterns. Venous impedance and arterial renal resistance indices were higher in patients than controls (0.44 vs. 0.14 and 0.67 vs. 0.60, respectively; p < 0.05). Conclusion FARD involves a progressive decline in kidney function and glomerular injury. eGFR cr masks kidney dysfunction in Fontan patients due to reduced muscle mass. Fontan intrarenal hemodynamics demonstrate decreased venous and arterial compliance. Moreover, continuous intrarenal venous flow persists in Fontan patients.
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Hassel et al. (2026) conducted a case-control in Fontan-Associated Renal Disease (n=50). Fontan circulation vs. Healthy controls was evaluated on Cystatin C-based estimated glomerular filtration rate (eGFR_cys) (p=0.045). Patients with a Fontan circulation had lower cystatin C-based eGFR (96 vs 106 mL/min/1.73 m2) and higher 24-h urine albumin (14 vs 2 mg) than healthy controls, indicating masked kidney dysfunction.
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