Cardiovascular Disease in Kidney Transplant Recipients

Leave No Stone Unturned

Steven Van Laecke; Daniel Abramowicz


Nephrol Dial Transplant. 2019;34(5):727-730. 

In This Article

Concluding Remarks

The position paper by Rangaswami et al.[1] is a contemporary summary of the evidence on diagnostic and management strategies in KTRs. Although the authors handle existing flaws and shortcomings, gaps persist in the majority of review papers in the field. In particular, the role of inflammation in atherosclerosis and in destabilization of vulnerable coronary plaques merits further investigation in light of the findings of recent trials in the general population. In KTRs, it is conceivable that potential beneficial effects of anti-inflammatory drugs are offset by negative effects on classical risk factors (Figure 1). The time has come to liberate cardiovascular guidance and literature in KTRs away from general population recommendations and evolve into a field-specific approach with integration of genetic and immunological aspects relevant for both diagnosis and treatment. Likely, future clinical trials could benefit from precision medicine–based tools.

Figure 1.

Established (upper part) and upcoming (lower part) cardiovascular risk factors in KTRs. Red arrows reflect negative effects of risk factors in the development of CVD, with a central role for both systemic and local vascular inflammation. An ambiguous role of immunosuppressive drugs is reflected by negative effects on both traditional and non-traditional risk factors (for instance, CMV), whereas the blue arrows delineate potentially protective effects. The bidirectional relationship between HLA antibodies and inflammation needs further exploration. Effects of immunosuppressive drugs on blood pressure seem drug dependent and blood pressure–lowering effects of MPA in KTRs remain speculative. CNI, calcineurin inhibitors; Cs, corticosteroids; HLA-AB, human leukocyte antigen-antibodies; MPA, mycophenolic acid.