Autoimmune-mediated renal disease and hypertension

Abstract

Hypertension is a major risk factor for cardiovascular disease, chronic kidney disease (CKD), and mortality. Troublingly, hypertension is highly prevalent in patients with autoimmune renal disease and hastens renal functional decline. Although progress has been made over the past two decades in understanding the inflammatory contributions to essential hypertension more broadly, the mechanisms active in autoimmune-mediated renal diseases remain grossly understudied. This Review provides an overview of the pathogenesis of each of the major autoimmune diseases affecting the kidney that are associated with hypertension, and describes the current state of knowledge regarding hypertension in these diseases and their management. Specifically, discussion focuses on Systemic Lupus Erythematosus (SLE) and Lupus Nephritis (LN), Immunoglobulin A (IgA) Nephropathy, Idiopathic Membranous Nephropathy (IMN), Anti-Neutrophil Cytoplasmic Antibody (ANCA)-associated glomerulonephritis, and Thrombotic Thrombocytopenic Purpura (TTP). A summary of disease-specific animal models found to exhibit hypertension is also included to highlight opportunities for much needed further investigation of underlying mechanisms and novel therapeutic approaches.

Meta‐analysis on the association between the frequency of tooth brushing and hypertension risk

“…Activated T cells infiltrate tissues and produce cytokines, including interleukin 17A, 48 which promotes renal and vascular dysfunction and end‐organ damage leading to hypertension. 49 Periodontitis and inflammatory bowel disease (IBD) share common dysbiotic and immunological features. 50 Thus, periodontitis can activate the chronic inflammatory state associated with autoimmunity.…”

“…Thus, periodontitis can activate the chronic inflammatory state associated with autoimmunity. Prevalent hypertension in autoimmune disease with the impact of immune system dysfunction on vascular dysfunction and renal hemodynamics as primary mediators, with oxidative stress as the main contributor 49 …”

Cardiovascular Complications in Systemic Lupus Erythematosus

“…Hypertension (HT) is an essential predisposing factor for CVDs, and it is highly common in autoimmune diseases that have an impact on the kidneys such as SLE [ 53 ]. Sabio et al worked on a study in 2011 that included 335 women (112 with SLE and 223 healthy controls).…”

Should Renal Inflammation Be Targeted While Treating Hypertension?

“…Autoimmune diseases are characteristic of overactivation of immune cells, and chronic inflammation. Coincidently, autoimmune diseases with a renal component are associated with hypertension and cardiovascular morbidities ( Boesen and Kakalij, 2021 ). Examples include systemic lupus erythematosus (SLE), Goodpasture syndrome, idiopathic membranous nephropathy, immunoglobulin A nephropathy, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, idiopathic thrombocytopenic purpura, rheumatoid arthritis and psoriasis ( Panoulas et al, 2007 ; Coumbe et al, 2014 ; Giannelou and Mavragani, 2017 ; Liu and Kaplan, 2018 ; Tumurkhuu et al, 2019 ; Boesen and Kakalij, 2021 ).…”

“…Coincidently, autoimmune diseases with a renal component are associated with hypertension and cardiovascular morbidities ( Boesen and Kakalij, 2021 ). Examples include systemic lupus erythematosus (SLE), Goodpasture syndrome, idiopathic membranous nephropathy, immunoglobulin A nephropathy, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, idiopathic thrombocytopenic purpura, rheumatoid arthritis and psoriasis ( Panoulas et al, 2007 ; Coumbe et al, 2014 ; Giannelou and Mavragani, 2017 ; Liu and Kaplan, 2018 ; Tumurkhuu et al, 2019 ; Boesen and Kakalij, 2021 ). The renal pathological mechanisms involved in autoimmune-induced hypertension are still not completely understood; however, we do know that the loss of self-tolerance leads to autoantibody production and these autoantibodies form complexes, deposit into tissues like the kidneys and promote activation of other immune cells and the complement system.…”