Juarez-Villa JD, Zepeda-Quiroz I, Toledo-Ramírez S, Gomez-Johnson VH, Pérez-Allende F, Garibay-Vega BR, Rodríguez Castellanos FE, Moguel-González B, Garcia-Cruz E, Lopez-Gil S. Exploring kidney biopsy findings in congenital heart diseases: Insights beyond cyanotic nephropathy. World J Nephrol 2024; 13(1): 88972 [PMID: 38596269 DOI: 10.5527/wjn.v13.i1.88972]
Corresponding Author of This Article
Salvador Lopez-Gil, MD, Associate Professor, Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chavez, 1 Juan Badiano, Mexico City 14080, Mexico. salvadorlgil@gmail.com
Research Domain of This Article
Urology & Nephrology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Jose Daniel Juarez-Villa, Iván Zepeda-Quiroz, Sebastián Toledo-Ramírez, Victor Hugo Gomez-Johnson, Francisco Pérez-Allende, Brian Ricardo Garibay-Vega, Francisco E Rodríguez Castellanos, Bernardo Moguel-González, Edgar Garcia-Cruz, Salvador Lopez-Gil
Jose Daniel Juarez-Villa, Iván Zepeda-Quiroz, Sebastián Toledo-Ramírez, Victor Hugo Gomez-Johnson, Francisco Pérez-Allende, Brian Ricardo Garibay-Vega, Francisco E Rodríguez Castellanos, Bernardo Moguel-González, Salvador Lopez-Gil, Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chavez, Mexico City 14080, Mexico
Edgar Garcia-Cruz, Congenital Heart Disease, Instituto Nacional de Cardiología Ignacio Chavez, Mexico City 14080, Mexico
Author contributions: Juarez-Villa JD, Zepeda-Quiroz I, Toledo-Ramírez S, Gomez-Johnson VH, Pérez-Allende F, Garibay-Vega BR, Rodríguez Castellanos FE, Moguel-González B, Garcia-Cruz E, and Lopez-Gil S contributed to design of the study, data analysis, drafting and critical revision and editing, and final approval of the final version.
Institutional review board statement: The need for study approval was waived by the local Ethics Committee of The National Institute of Cardiology.
Informed consent statement: The need for informed consent was waived by the local Ethics Committee of The National Institute of Cardiology.
Conflict-of-interest statement: None of the authors have any conflict-of-interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Salvador Lopez-Gil, MD, Associate Professor, Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chavez, 1 Juan Badiano, Mexico City 14080, Mexico. salvadorlgil@gmail.com
Received: October 18, 2023 Peer-review started: October 18, 2023 First decision: December 7, 2023 Revised: December 20, 2023 Accepted: January 15, 2024 Article in press: January 15, 2024 Published online: March 25, 2024 Processing time: 155 Days and 12.3 Hours
Abstract
BACKGROUND
The association between congenital heart disease and chronic kidney disease is well known. Various mechanisms of kidney damage associated with congenital heart disease have been established. The etiology of kidneydisease has commonly been considered to be secondary to focal segmental glomerulosclerosis (FSGS), however, this has only been demonstrated in case reports and not in observational or clinical trials.
AIM
To identify baseline and clinical characteristics, as well as the findings in kidney biopsies of patients with congenital heart disease in our hospital.
METHODS
This is a retrospective observational study conducted at the Nephrology Department of the National Institute of Cardiology “Ignacio Chávez”. All patients over 16 years old who underwent percutaneous kidney biopsy from January 2000 to January 2023 with congenital heart disease were included in the study.
RESULTS
Ten patients with congenital heart disease and kidney biopsy were found. The average age was 29.00 years ± 15.87 years with pre-biopsy proteinuria of 6193 mg/24 h ± 6165 mg/24 h. The most common congenital heart disease was Fallot’s tetralogy with 2 cases (20%) and ventricular septal defect with 2 (20%) cases. Among the 10 cases, one case of IgA nephropathy and one case of membranoproliferative glomerulonephritis associated with immune complexes were found, receiving specific treatment after histopathological diagnosis, delaying the initiation of kidney replacement therapy. Among remaining 8 cases (80%), one case of FSGS with perihilar variety was found, while the other 7 cases were non-specific FSGS.
CONCLUSION
Determining the cause of chronic kidney disease can help in delaying the need for kidney replacement therapy. In 2 out of 10 patients in our study, interventions were performed, and initiation of kidney replacement therapy was delayed. Prospective studies are needed to determine the usefulness of kidney biopsy in patients with congenital heart disease.
Core Tip: Patients with congenital heart disease often have impaired kidney function, typically due to the presence of focal segmental glomerulosclerosis (FSGS). However, in many cases, this glomerular pathology is identified only once clinically established (nephrotic proteinuria). The aim of this study is to determine the presence of FSGS under baseline conditions (without proteinuria), and therefore, it could be speculated that a preventive treatment could delay the initiation of kidney replacement therapy.
