BIOL 031 Lecture Notes - Lecture 26: Transforming Growth Factor Beta, Chemotaxis, Thrombosis
22 Dec 2020
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Document Summary
Certain common non-immunologically-mediated glomerular diseases, and discuss the mechanisms related to their pathogenesis and clinical presentation. Minimal change disease - common in children, males>females. Selective proteinuria initially, but can progress to non-selective. Morphology: loss of sgps (charge-selectivity) from podocytes, extensive foot process fusion, villous transformation and increased lipid droplets in tubular epithelia. Morphology: laminated-trabeculated appearance of the gbm, fetal glomeruli and foam cells. Initially high filtration (super hyper), but then progresses to nephrotic proteinuria and lower gfr. Initially selective proteinuria (microalbuminuria) then becomes nonselective. Tgf-b plays a role in diabetic lesions, especially in mesangial cells. Non-enzymatic glycation of proteins lead to loss of hs-pgs and damage to the gbm and mm. Diffuse intercapillary glomerulosclerosis - thickened gbm and increased mm (remember tgf-b may play a role) Nodular glomerulosclerosis (kimmelstiel wilson lesions) - nodules and cellular proliferation. Nephrotic proteinuria and secondary amyloidosis (75%, 25% respectively)
