Cardiac functional consequences of chronic kidney disease: direct evidence of uraemic cardiomyopathy

Purpose: Uraemia is associated with increased cardiac morbidity and mortality. The present study aimed to test the hypothesis that patients with chronic kidney disease (CKD) without any known cardiovascular disease or diabetes mellitus have impaired cardiac and physical functional reserves compared to controls. Methods: We compared the cardiopulmonary exercise performance and non-invasive haemodynamics of 30 male patients with late CKD (stages 4&5) and 20 patients with early CKD (stages 2&3) against 101 healthy male volunteers. Physical and cardiac functional reserves were measured during treadmill exercise testing with standard respiratory gas analyses and a CO2-rebreathing method of non-invasively measuring cardiac outputs during peak exercise. As positive controls, data from 39 age- and gender-matched heart failure (HF) patients in NYHA class II&III were also obtained. The results are presented as mean±SD. Result: The mean eGFRs of early and late CKD patients were 54.4±18.2 and 16.2±5.8 ml/min respectively. Compared to healthy controls, the CKD patients showed a graded reduction in peak cardiac power output (CPOmax) with 92.4±12.2% (P<0.05) of predicted CPOmax in early CKD and 81.4±13.2% (P<0.001) of predicted CPOmax in late CKD, whereas their peak O2 uptake (VO2max) was preserved in early CKD (98.8±11.8% of predicted VO2max, P=NS) and mildly reduced in late CKD (87.6±18.1% of predicted VO2max, P<0.01). These values were not as impaired as in HF patients who had 58.2±14.4% and 45.5±10.7% of predicted VO2max and CPOmax respectively (both P<0.001). ![Figure][1] Conclusion: This novel study shows that CKD per se causes impaired cardiac functional reserve, thus confirming the identity of Uraemic Cardiomyopathy which requires further cardio-renal collaborative research. [1]: pending:yes