Overfill Edema: Pathogenesis
Nephrotic Syndrome
Damage to the glomeruli of the kidneys (See Nephrotic Syndrome: Pathogenesis and Clinical Findings Slide)
Aberrant filtration of proteins including plasminogen
(glycoprotein in the systemic circulation involved in the dissolution of fibrin blood clots)
↑ Plasminogen concentration in tubular fluid
Conversion of plasminogenà plasmin by urokinase-type plasminogen activator in the cortical collecting tubule
Plasmin activates epithelium
sodium channels (involved in Na+ reabsorption) in principal cells of the cortical collecting duct
Nonsteroidal Anti-inflammatory Drugs
Inhibition of cyclooxygenase throughout body (enzyme that converts arachidonic acidàprostaglandins)
↓ Prostaglandins throughout body
Thiazolidines
↓ Prostaglandin- mediated inhibition of Na+ and Cl- transport in ascending loop of Henle and collecting ducts
↑ Na+ reabsorption from kidney tubules back into blood
↓ Prostaglandin-mediated vasodilation in kidneys
↓ Pressure of blood perfusing kidneys → ↓ pressure gradient between glomerulus and bowman’s capsule
↓ Glomerular filtration rate
↓ Renal excretion of salt & water
↑ Salt and water retention
↑ Effective arterial blood volume
↑ blood pressure in veins
Unclear mechanism but possible theories include upregulation of epithelium sodium channels in the cortical collecting tubule and involvement of other transporters in the proximal tubule and cortical collecting tubule
Acute Renal Failure Chronic Renal Failure
↑ Hydrostatic pressure within capillariesàexceeds hydrostatic pressure within interstitial spaceàfluid moves from capillaries into interstitial space
Overfill Edema
Abnormal accumulation of fluid in the interstitial space where urine Na+ >40meq/L
Authors: Samin Dolatabadi Reviewers: Meena Assad, Jessica Krahn, Brooke Fallis, Ran (Marissa) Zhang, Yan Yu*, Juliya Hemmett* * MD at time of publication
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published January 23, 2022 on www.thecalgaryguide.com