The shrunken pore syndrome is associated with declined right ventricular systolic function in a heart failure population – the HARVEST study

Abstract

The close relationship between heart and kidney diseases was studied with respect to the ‘Shrunken pore syndrome’ that is characterized by a difference in renal filtration between cystatin C and creatinine. Patients were retrieved from the HeARt and brain failure inVESTigation trail (HARVEST) which is an ongoing study undertaken in individuals hospitalized for the diagnosis of heart failure. Ninety-five of 116 patients who underwent transthoracic echocardiograms (TTE) were eligible for this study. We used four different formulas for estimated glomerular filtration rate (eGFR); CKD-EPI_creatinine, CKD-EPI_{cystatin C}, LMrev and CAPA. Presence of the syndrome was defined as eGFR _{cystatin C} ≤ 60% of eGFR _creatinine and absence of the syndrome as eGFR _{cystatin C} >90% and <110% of eGFR _creatinine. In a linear regression model, adjusted for age and sex, and the ‘Shrunken pore syndrome’ defined by the equation pair CAPA and LMrev and the equation pair CKD-EPI_{cystatin C} and CKD-EPI_creatinine, echocardiographic parameters were studied. The ‘Shrunken pore syndrome’ showed statistically significant associations with measurements of right ventricular (RV) systolic function; (TAPSE and RV S’) (according to the equation pair CKD-EPI_{cystatin C} and CKD-EPI_creatinine). In conclusion, heart failure patients with the ‘Shrunken pore syndrome’ are at increased risk of having RV systolic dysfunction whilst heart failure patients without ‘Shrunken pore syndrome’ seem protected. These findings may indicate common pathophysiological events in the kidneys and the heart explaining the observed increased risk of mortality in subjects with the ‘Shrunken pore syndrome’.

Keywords:

• Cardio-renal syndrome
• creatinine
• cystatin C
• echocardiography
• glomerular filtration rate

Acknowledgements

We thank the research nurses Hjördis Jernhed, Dina Chatziapostolou and Malin Ståhl for valuable contributions.

Disclosure statement

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.

Funding

Dr Magnusson was supported by grants from the Medical Faculty of Lund University [ALFSKANE-432021] [ALFSKANE-436111], Skane University Hospital, the Crafoord Foundation, the Ernhold Lundstroms Research Foundation, the Region Skane, the Hulda and Conrad Mossfelt Foundation, the Southwest Skanes Diabetes Foundation, the Kocksa foundation, the Research Funds of Region Skåne and the Swedish Heart and Lung foundation [2015-0322].

Dr Christensson was supported by funding from the Medical Faculty of Lund University (ALFSKANE), Fulbright Commission, the Research Funds of Region Skåne, the Research Fund of Skåne University Hospital, and the Swedish Kidney Association.