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REVIEW article

Front. Med.
Sec. Nephrology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1526090

Advances in Kidney Disease: Pathogenesis and Therapeutic Targets

Provisionally accepted
Vincent BOIMA Vincent BOIMA 1Alex Baafi Agyekum Alex Baafi Agyekum 2Khushali Ganatra Khushali Ganatra 2Francis Agyekum Francis Agyekum 1*Edward Kwakyi Edward Kwakyi 1Jalil Inusah Jalil Inusah 1Elmer Ametefe Elmer Ametefe 1Dwomoa Adu Dwomoa Adu 1
  • 1 University of Ghana, Accra, Ghana
  • 2 Korle Bu Teaching Hospital, Accra, Ghana

The final, formatted version of the article will be published soon.

    ABSTRACT： Chronic kidney disease (CKD) is a global public health issue characterized by progressive loss of kidney function, of which end-stage kidney disease (ESKD) is the last stage. The global increase in the prevalence of CKD is linked to increasing prevalence of traditional risk factors, including obesity, hypertension, and diabetes mellitus, as well as metabolic factors, particularly insulin resistance, dyslipidemia, and hyperuricemia. Mortality and comorbidities, such as cardiovascular complications, rise steadily as kidney function deteriorates. Patients who progress to ESKD require long-term kidney replacement therapy, such as transplantation or hemodialysis/peritoneal dialysis. It is now understood that a crucial aspect of CKD involves persistent, low-grade inflammation. In addition, increased oxidative and metabolic stress, endothelial dysfunction, vascular calcification from poor calcium and phosphate metabolism, and difficulties with coagulation are some of the complex molecular pathways underlying CKD and ESKD-related issues. Novel mechanisms, such as microbiome dysbiosis and apolipoprotein L1 gene mutation, have improved our understanding of kidney disease mechanisms. Africa's high kidney disease risk has been linked to APOL1 high-risk alleles. The threefold increased risk of ESKD in African Americans compared to European Americans is now mainly attributed to variants in the APOL1 gene in chromosome 22q12 locus. Additionally, the role of new therapies such as SGLT2 inhibitors, mineralocorticoid receptor antagonists, and APOL1 channel function inhibitors offers new therapeutic targets in slowing down the progression of chronic kidney disease. This review describes recent molecular mechanisms underlying CKD and emerging therapeutic targets.

    Keywords: advances, kidney disease, Pathogenesis, therapy, APOL1 gene

    Received: 11 Nov 2024; Accepted: 30 Jan 2025.

    Copyright: © 2025 BOIMA, Agyekum, Ganatra, Agyekum, Kwakyi, Inusah, Ametefe and Adu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Francis Agyekum, University of Ghana, Accra, Ghana

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.