Fenofibrate Induced Nephrotoxicity and Paradoxical Low HDLC- A Boon or Bane?: A Review
Asian Journal of Research in Nephrology · pp. 94–106 · Published 26 Sep 2022
Abstract
Fenofibrate is the most common drug prescribed to treat atherogenic dyslipidaemia. The nephrotoxicity of fenofibrate, as characterised by the increased Serum Creatinine (SCr) and reduced estimated glomerular filtration rate (eGFR), though reported in literature, it's clinical awareness, and it's implications, seem to be low. Also reported is the paradoxical Low level of High-density lipoprotein cholesterol (HDLC) during fenofibrate therapy, as against the expected rise, as an isolated event and, in conjunction with the raised SCr. Perhaps such association occurred, in a small subset of cases of fenofibrate induced nephrotoxicity or it may be due to lack of awareness about the association or the association being overlooked, these might be the reasons for the paucity of reporting the same, in the literature. The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, and the Action to Control Cardiovascular Risk in Diabetes (ACCORD Lipid Study), it is confirmed that, the SCr levels decreased, eGFR improved and HDLC levels are raised on cessation of the fenofibrate therapy. The cause and effect is, thus proved. The CKD, triglyceredemia and the low HDLC. Each of the three, are know individual risk factors for cardiovascular disease (CVD). It would be the concern of any body, treating atherogenic dislipidema, as to whether to expose the patient to the risks of possible renal damage and the risks of low HDLC, in treating hypertriglyceridemia, with fenofibrate. It is imperative that these concerns, if any, be resolved. Awareness of fenofibrate causing the raised Scr and reduced eGFR, is essential for avoiding wrong diagnosis and treatment of an iotrogenic cause. Apart from the dark side of fenofibrate therapy, umpteen number of benefits of fenofibrate therapy are reported. Intriguingly, the greatest benefits are seen in those who experienced the most severe adverse effects mentioned above. Hence is the justification for the dilemma expressed in the tittle. A brief review of all the issues concerned, including the present status of the fenofibrate therapy, is being reviewed in this article.
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