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Infection-Related Glomerulonephritis

Infection-Related Glomerulonephritis: Pathogenesis & clinical findings Viral or bacterial infections (most commonly streptococcus & staphylococcus) trigger the inflammatory cascade Common infection sites include pharyngitis (infection of the mucous membranes in the oropharynx) & endocarditis (inflammation of the endocardium) but bacterial infections can originate anywhere in the body In streptococcal infections, bacteria release nephritis (inflammation of the kidney) associated plasmin receptor antigens (NAPlr) & streptococcal pyrogenic exotoxin B antigens (SPeB) into the systemic circulation from the infection site. Other bacterial infections may have different pathophysiology Immune response generated against circulating NAPlr & SPeB antigens includes ↑ production of IgG antibodies (critical for immune response & memory) IgG antibodies bind with self-antigens (molecules recognized by the immune system as belonging to the host) including plasmin & glomerular proteins (proteins found in the kidney’s filtering unit, the glomerulus) IgG antibodies activate plasmin (enzyme responsible for breaking down protein in the kidneys) Plasmin degrades protein in the kidneys IgG antibodies bind to glomerular proteins in the kidney & form immune complexes in glomeruli basement membrane & sub- epithelial podocytes (highly specialized cells in the glomerular filtration barrier) Degradation of key glomerulus components, including the glomerular basement membrane (GBM) & mesangial matrix Damage to key glomerulus components leads to abnormal regulation of blood filtration ↓ Selective permeability of the glomerular membrane IgG antibodies bind with NAPIr & SPeB antigens & form immune complexes (antibody & antigen combinations involved in immune system signalling) Immune complexes circulate & deposit in glomeruli basement membrane & sub-epithelial podocytes RBCs escape through the glomerulus into renal tubules & progress into the urine Dysmorphic hematuria (blood in the urine characterized by misshapen RBCs) Author: Joanna Keough Reviewers: Britney Wong Luiza Radu Jessica Revington Veronica Hammer* Louis Girard* *MD at time of publication **See corresponding Calgary Guide slide Legend: Pathophysiology Mechanism Immune complexes activate complement (C3, oxidizing agents, proteases) Complement activation helps ↑ proliferation of glomerular mesangial cells (cells with specialized proteins capable of producing motile forces) Mesangial cells produce extracellular matrix in the glomerulus Excess extracellular matrix blocks glomerular capillaries Mesangial cells release chemoattractants (signalling molecules) into the glomerulus & attract various immune cells Lymphocytes follow chemoattractants to the glomerulus & activate Neutrophils follow chemoattractants to the glomerulus & release lysosomal enzymes Lymphocytes accumulate in the glomerulus & obstruct glomerular capillaries Impaired blood flow through glomerular capillaries Capillary injury Podocyte injury or death Infection-Related Glomerulonephritis Glomerular kidney damage sustained after a bacterial or viral infection ↓ Glomerular filtration rate (GFR) Creatinine builds up in the blood ↑ Glomerular membrane permeability allows large molecules to pass through the membrane (e.g., red blood cells (RBCs), protein) ↓ GFR impairs the kidney’s ability to filter & excrete fluid ↓ Estimated GFR Prolonged (eGFR) renal damage Protein escapes into renal tubules & progresses into the urine Chronic kidney disease Proteinuria (loss of protein through the urine) ↑ Fluid retention in systemic circulation & ↓ renal blood flow Impaired potassium excretion ↓ Urine output Impaired acid waste product excretion Urine contains ↑ large proteins (e.g., albumin) Activation of the intrarenal renin- angiotensin-aldosterone system (RAAS)** Hyperkalemia (↑ serum potassium) Oliguria (↓ urine volume) Metabolic acidosis** Albuminuria (loss of albumin through the urine) Intrarenal RAAS activation leads to ↑ angiotensin II (Ang II) production ↑ Sodium & water retention in systemic circulation & ↓ excretion in urine (↓ GFR) Hypertension** Edema (swelling due to ↑ fluid in body tissues) Circulating blood volume exerts ↑ pressure on blood vessels & forces the heart to pump harder Left ventricle thickens & enlarges over time & demonstrates progressive cardiac injury (e.g., fibrosis, loss of cardiac muscle cells) Impaired cardiac output Heart failure Sign/Symptom/Lab Finding Complications Published November 15, 2025 on www.thecalgaryguide.com