Minimal Change Disease

Minimal Change Disease: Pathogenesis and clinical findings

Minimal Change Disease: Pathogenesis and clinical findings
Authors: Jessica Krahn Reviewers: Timothy Fu Brooke Fallis Yan Yu* Juliya Hemmet* * MD at time of publication
Damage induced by cytokines, not immunocomplexes
Lack of abnormal immunocomplexes (antibody-antigen complexes) present in serum
Immunofluorescence test negative
Idiopathic/Primary Minimal Change Disease
No identifiable extraglomerular disease process causes this condition
Secondary Minimal Change Disease
Infections, NSAIDS, neoplasms via unclear mechanisms
Minimal change to glomerulus seen on light microscopy
Podocyte effacement seen on electron microscopy
Abnormal T Cell activation and release of cytokines (sometimes called permeability factors) that are toxic to podocytes
Podocyte foot processes efface (become flattened) or fuse together
Damage to negatively charged foot processes damages the charge barrier of the glomerulus that repels negatively charged molecules
↑ filtration of larger negatively charged molecules, such as low-molecular weight proteins like albumin, from the blood into the renal tubular filtrate
Induces ↑ hepatic lipoprotein synthesis and ↓ lipoprotein catabolism
(↑ serum LDL, VLDL, and triglycerides)
↑ lipid filtration through glomerulus
Lipiduria (fatty casts)
↓ oncotic pressure in capillaries
Fluid leaks into interstitial space
↑ Filtration of Proteins C and S and antithrombin
Hypercoagulable state
↑ Filtration of immunoglobulins
↑ Filtration of Plasminogen
Plasminogen converted to plasmin in the cortical collecting duct via urokinase- type plasminogen activator
Plasmin activates the epithelial sodium channel
↓ intravascular volume
Pre-Renal Acute Kidney Injury
Underfill edema
(see slide)
Thrombosis Edema (especially peri-
orbital, scrotal, labial, and extremities)
(see slide)
↑ Na+ and water reabsorption
Sign/Symptom/Lab Finding
Published December 30, 2021 on