Journal of Rare Cardiovascular Diseases

ISSN: 2299-3711 (Print) e-ISSN: 2300-5505 (Online)

The Impact of glomerulonephritis on cardiovascular disease: Exploring pathophysiological links and clinical implications

1College of Health and Medical Technology, Al-Ayen Iraqi University, Thi-Qar, 64001, Iraq
2College of Dentistry, Al-Ayen Iraqi University, Thi-Qar, 64001, Iraq
3Department of Physiology and Pharmacology, College of Veterinary Medicine, University of AL-Qadisiyah, Iraq
1College of Health and Medical Technology, Al-Ayen Iraqi University, Thi-Qar, 64001, Iraq
2College of Dentistry, Al-Ayen Iraqi University, Thi-Qar, 64001, Iraq
3Department of Physiology and Pharmacology, College of Veterinary Medicine, University of AL-Qadisiyah, Iraq
Corresponding Email: dr.maytham@alayen.edu.iq

Full Text:

Abstract

Background: Glomerulonephritis (GN) is an inflammatory renal disorder that significantly contributes to chronic kidney disease (CKD) and end‐stage renal failure, and is increasingly recognized as a major risk factor for cardiovascular disease (CVD). The mechanisms linking GN and CVD involve chronic inflammation, endothelial dysfunction, hypertension, oxidative stress, and dysregulation of the renin-angiotensin-aldosterone system (RAAS). \textbf{Objective:} This study aims to explore the pathophysiological links between GN and CVD, evaluate the associated cardiovascular risks, and review therapeutic strategies addressing both renal and cardiovascular health. It also identifies gaps in current risk stratification models and suggests directions for future research. Methods: A systematic review was conducted using PubMed, Scopus, Web of Science, Google Scholar, and the Cochrane Library to identify clinical trials, cohort studies, and meta-analyses published between 2000 and 2024. The risk of bias was assessed using the Newcastle-Ottawa Scale and the Cochrane Risk of Bias Tool. Results: Analysis of 52 studies revealed that GN patients have a 2.5- to 4-fold increased risk of cardiovascular events compared to the general population. Specifically, the risk of myocardial infarction increased by 3.2 times (HR: 3.2, 95% CI: 2.6–3.8, p<0.001), stroke risk by 2.8 times (95% CI: 2.2–3.4, p<0.001), and heart failure risk by 4.1 times (HR: 4.1, 95% CI: 3.5–4.9). Proteinuria and RAAS dysregulation were major contributors to cardiovascular pathology. Therapeutic interventions such as RAAS inhibitors and SGLT2 inhibitors significantly reduced cardiovascular mortality and heart failure hospitalization rates, while intensive blood pressure control lowered stroke risk, although overly aggressive management adversely affected kidney function in some patients. Conclusion: GN is a significant contributor to CVD, driven by systemic inflammation, hypertension, and endothelial dysfunction. Early intervention and comprehensive management—including pharmacological treatment and multidisciplinary care—are essential to mitigate adverse cardiovascular outcomes. Current cardiovascular risk models do not adequately predict risk in GN patients, underscoring the need for GN-specific risk assessment tools and further research into tailored cardioprotective therapies.

key word
glomerulonephritis, cardiovascular disease, chronic kidney disease, hypertension, inflammation, proteinuria, RAAS dysregulation, endothelial dysfunction

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