Radka Nuneva-Doncheva‡, Irena Gencheva-Angelova§Corresponding author: Radka Nuneva-Doncheva ( dr.nuneva@abv.bg ) Corresponding author: Irena Gencheva-Angelova ( irena.gencheva-angelova@mu-pleven.bg ) Academic editor: Nikolay Kyuchukov © Radka Nuneva-Doncheva, Irena Gencheva-Angelova. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Citation:
Nuneva-Doncheva R, Gencheva-Angelova I (2026) Association between high serum Lipoprotein(a) concentration and renal pathology: Mechanisms of Lipoprotein(a)-mediated kidney injury. Journal of Biomedical and Clinical Research 19: 11-24. https://doi.org/10.3897/jbcr.e181346 |  |
Abstract: A high serum level of Lipoprotein(a) [Lp(a)] is inherited, but various chronic kidney diseases (CKD) can cause its secondary elevation because the kidney is involved in its catabolism. These two facts form the basis for the two theories of the causal relationship between high Lp(a) levels and CKD.
Purpose: This review aimed to summarize the complex relationships between Lp(a) levels and renal function, focusing on the molecular and cellular mechanisms. Furthermore, it aimed to differentiate between primary (genetically determined) and secondary (non-genetic) elevations of Lp(a) in various forms of CKD.
Materials and Methods: We conducted a comprehensive literature search across the following databases: PubMed, Science Direct, Google Scholar, and Wiley Online Library, covering the period from January 2010 to February 2025. The search strategy employed keywords such as “Lipoprotein(a)”, “chronic kidney disease”, “renal catabolism”, and “Lp(a) pathophysiology”. Inclusion criteria focused on peer-reviewed meta-analyses, cross-sectional studies with Mendelian randomization, and prospective clinical trials published in English. Studies with fewer than 50 participants or lacking clear markers of renal function were excluded. Data were synthesized through a thematic analysis of molecular mechanisms and a comparative review of clinical outcomes to ensure a robust overview of both genetic and secondary Lp(a) elevations. The research approach follows narrative literature review methodologies. The selection of studies focused on their relevance, the strength of their evidence, and temporal relevance.
Results: There is a complex feedback loop between high primary Lp(a) levels, CKD, and the secondary increase in Lp (a). Renal health influences Lp(a) levels, which in turn can further damage the kidney.