L9- CKD Pathology Flashcards
In general, what kind of histological changes do you see in CKD?
Lots of collagen and fibrin!!!
[Trichrome stain in picture - collagen pink and fibrin green]
Renal Atrophy and Fibrosis
What are the most common causes of CKD?
HTN/Nephrosclerosis
Diabetes
Progression of other diseases leading to fibrosis/scaring
Adult (AD) PKD
Multiple Myeloma Kidney (AMyloidosis)
Chronic HTN leads to ______________ causing CKD?
What changes to you see in the kidney Grossly?
What changes do you see in the kidney histologically?
Benign Nephrosclerosis - sclerosis of renal arterioles and small arteries w/ hyalinosis
Grossly: SMALL (or normal) kidneys, surface is granular w/ fibrotic scarring, loss of cortical mass
Histo: Hyaline Arteriolosclerosis / Hyalinosis (incresed deposition of ECM in sub-endothelial layer so can NOT contract and relax in response to simtulus)
and
Medial Hypertrophy/Fibroelastic Hyperplasia (hypertrophic media of the artery and wall is thick, lumen smaller, and Multiple layers of elastin)
What renal changes occur w/ Malignant HTN? What do you see grossly? What do you see histologically?
What are some other manifestations you can see in addition to the kidney ones?
Malignant HTN = episodes of BP so high causes damage
Other manifestations: Retinal Hemorrhages and Papilledema
Grossly: Rupture of arterioles and capillaries leads to small hemorrhages **“flea-bitten kidney” **
Histo: fibrinoid necrosis of Arterioles ( can look like thrombotic microangiopathy; brigh eosinophilic material replacing wall of artery; LOSS OF STRUCTION and collection of amorphous pink material)
and
Hyperplastic Arteriolosclerosis - Onion skinning (concentric laminated thickening of the wall and progressive narrowing of lumen)
Quick Summary: Vascular Changes in HTN benign vs Malignant?
Benign Nephrosclerosis - slower
- Hyalinosis
- Medial Hypertrophy
Malignant Nephrosclerosis - faster and more immediate
- fibrinoid necrosis
- onion skinning
2 different processes leading to renal artery stenosis….
1) Atherosclerosis - Fibrous intimal thickening, cholesterol, and Ca deposition, related to HTN and hyperlipidemia
2) Medial Fibromuscular Dysplasia - thickened fibromuscular ridges alternating w/ areas of wall thinning - CAN OPERATE AND FIX!
What kinds of things do you see w/ renal infarcts?
Atheromatous plaques cn have cholesterol crystals etc
Ischemia/infarctoin and lead to Wedge-Shaped areas of ischemic necrosis (see picture)
What else is Diabetic Glomerulosclerosis associated with?
Microalbuminuria
Non-nephrotic and Nephrotic Proteinuria
Micrioangiopathy - disease of small vessels
RETINOPATHY!
What is the pathogenesis of DM and Diabetic Glomerulosclerosis?
Glycosylation of proteins and then when advanced and glucose constantly elevated stable glucosylation of proteins results in Vascular BM becoming thick and leaky and having increased ECM production
What glomerular abnormalitieis can you see in Diabetic Glomerulosclerosis?
Increased Mesangial Matrix - NODULES!!! diabetic nodules in the glomerulus from amorphous, thick, mesangial matrix
Thick GM
Hyalinosis - involvement of both afferent and efferent glomerular arterioles Pathognomonic!!!
What is Adult PKD? Genetics? Pathogenesis?
Autosomal dominant trait w/ high penetrance
PKD1 Chromosome 16 and PKD2 Chromosome 4
Gene products are **Polycystin 1 and 2 **
Gene products involved in cell-cell matrix interactions (tubular epithelial cell growth and differentiation) so that when normal remodeling and replacing cells occur - here it happens abnormally- and instead no cross talk and inadequate differentiation causes cysts to form
Presentation of Adult PKD?
Gross changes?
Histology?
Presentation: Cysts arise at ALL levels of the nephron in BOTH kidneys - bilateral
Progressive compression of parenchyma leads to renal failure in 30s/40s
*Hematuria!!!
Gross: HUGE KIDNEYS w/ lots of cysts
Histo: big cystic spaces and less parenchyma
Clinical Associations w/ PKD?
Cerebral Aneurysms - Berry Aneurysm, can be life threatening
Hepatic Cysts
Splenic, pancreatic and pulmonary cysts
Causes/ pathogenesis and presentation of renal amyloidosis?
Can be secondary to plasma cell tumors (ALL) or inflammatory conditions (AA) and get accumulatoin of amyloid protein - light chain and the proteins spontaneously aggregate and form fibrils!!
Presentation - heavy proteinuria/nephrotic syndrome
Renal Amyloidosis Histology to know?
Deposits in Mesangium and replace all glomerular structure
*Congo-Red to see - stains amorphous orange/pink
Use polarized light on congo-red and turns Apple Green Bifrenges
On EM: see amyloid deposits as **non-branching fibrils **
