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Renal manifestations of SLE

Systemic Lupus Erythematosus (SLE): Renal Manifestations Authors: Madison Turk Reviewers: Modhawi Alqanaie Mao Ding Luiza Radu Glen Hazlewood* * MD at time of publication Genetic susceptibility and potential environmental triggers (smoking, silica, Epstein-Barr Virus, hormones, ect) ↓Clearance of dead cell debris in the body (exact mechanisms unknown; See slide on pathogenesis of SLE) Extracellular exposure of nuclear proteins (which bind DNA and regulate gene expression) Immune cells respond to nuclear proteins as if they are non-self, as they usually don’t ‘see’ them Systemic Lupus Erythematosus An autoimmune disease characterized by anti-nuclear-antibody production resulting in widespread inflammation and tissue damage in varying affected organs, including one, or a combination of, joints, skin, brain, lungs, kidneys, and blood vessels Production of auto-antibodies against self nuclear proteins IC deposition in renal vessels Activation of inflammatory cells against IC’s causing vascular injury/inflammation ↑Clot formation in vessels leading to ↓vessel lumen diameter and ↓blood flow ↑Reninàcleavage of angiotensinogen to angiotensin Ià cleavage by angiotensin converting enzyme into angiotensin II Vessel constriction to ↑blood pressure (to ↑ renal blood flow) IC deposition in tubule basement membrane of the kidney Formation of immune complexes (IC) (collections of antigen(s), antibodies, and/or complement proteins bound together) Tubulointerstitial nephritis: (Inflammation of the renal tubules and interstitium, sparing the glomeruli) Renal ischemia IC deposition in the glomerulus Activation of complement, initiating an inflammatory response Recruitment of myeloid cells (monocytes/ neutrophils) Production of reactive oxygen species, cytokines and release of cytotoxic granules Tubular inflammation and damage resulting in ↓sodium reabsorption Renal release of reninà ↑ angiotensin I/II and resulting ↑ aldosterone ↑Sodium reabsorption, and potassium excretion in the collecting duct ↓Potassium secretion from the Distal Convoluted Tubule Hyperkalemia Hypokalemia ⍺-intercalated cell damage ↓Acid excretion Metabolic acidosis End stage kidney disease (all manifestations can result in this) Hypertension Tissue damage from the inflammatory response Glomerular nephritis (inflammation/damage of the filtering part of the kidneys) Fibrosis (thickening or scarring of tissue) Mesangial and parietal cell proliferation Podocyte injury ↑blood and protein excretion due to damage to the glomerular filtration membrane ↓protein in blood Edema Proteinuria Hematuria ↓Functional renal tissue to filter creatinine from blood ↓ Glomerular filtration rate ↑ Plasma creatinine Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Nov 11, 2024 on www.thecalgaryguide.com