Clinical Background: Poly- and perfluorinated compound (PFCS) pollution has been found to be the driver of different diseases, including glucose intolerance, hyperlipidemia, thyroid diseases, gestational diabetes mellitus and hypertension, testicular and genitourinary cancer, as well as impaired kidney function. This review focuses on the renal effects of PFCS, intending to clarify their occurrence and pathogenetic mechanisms. Epidemiology: Between October 31st, 2017, and March 31st, 2020, most frequently analyzed PFCS were perfluorooctane sulfonate, perfluorooctanoic acid, sodium perfluoro-1-hexanesulfonate, perfluoro-n-nonanoic acid, and perfluoro-n-decanoic acid. Unfortunately, the novel replacement compounds (e.g., perfluoroether carboxylic acid) are unregulated, and they are not under study. PFCS are linked with an impaired kidney function: the kidney is a target of PFCS because it is involved in their excretion. Inter- and intra-species variations exist and affect PFCS pharmacokinetics, leading to different risk profiles of adverse effects, even at similar exposures, and influencing the risk of renal damage in case of concomitant exposure to PFCS and some heavy metals. Challenges, Prevention and Treatment: In the last 20 years, much effort has been made to stop the PFCS production in Europe and USA. However, human exposure remains persistently high due to PFCS long half-life, the large-scale production in some countries and the unregulated novel compounds. This context makes further studies mandatory to understand the pathogenetic mechanisms of old and new PFCS and the effective strategies to remove PFCS from the human blood in the most affected areas of the world.
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