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Flashcards in nephrotic pathology Deck (19):
1

Complications of nephrotic syndrome

Protein deficiency- antithrombin III, HD lipoprotein, Ig, complement, albumin. Hypercholesterolemia, hyponatremia, hypokalemia, progression to chronic renal failure

2

Describe how nephrotic syndrome leads to increased infections

Increased glomerular permeability leads to loss of immunoglobulins

3

Describe how nephrotic syndrome leads to thrombosis

Loss of coagulation factors via increased glomerular permeability PLUS, hypoalbuminemia causes increased lipoprotein synthesis > hyperlipidemia > increased platelet aggregation

4

Describe how nephrotic syndrome leads to edema

increased glomerular permeability > albuminuria > hypoalbuminemia > edema > hypovolemia > Na and water retention > more edema

5

pathogenesis of glomerular injury

non inflammatory: 1) Circulating factors/Ig’s bind to GEC membranes &/or GBM without fixing complement causing loss of polyanion, GEC detachment from GBM. Ie. Minimal change disease/focal sclerosis. 2) complement fixing anti-GEC Abs (alternative pathway) leads to increased permeability of GBM and may involve oxidants/proteases from GEC. ie. membranous nephropathy
non inflammatory: 1) Circulating factors/Ig’s bind to GEC membranes &/or GBM without fixing complement causing loss of polyanion, GEC detachment from GBM. Ie. Minimal change disease/focal sclerosis. 2) complement fixing anti-GEC Abs (alternative pathway) leads to increased permeability of GBM and may involve oxidants/proteases from GEC. ie. membranous nephropathy

6

Minimal change nephropathy: clinical, morphology, pathogen therapy and prognosis

nephrotic syndrome with non change in morphology. Pathogen is unknown but thought to be a circulatory factor. EM shows foot process effacement, IF is negative. Therapy is steroids and prognosis is good

7

Focal sclerosis clinical, morphology, pathogen therapy and prognosis

Nephrotic syndrome with focal segmental glomerular sclerosis morphology. Pathogen is unknown but thought to be circulatory factor with hereditary forms. Therapy is steroids, but high relapse rate and some progress to end stage renal disease

8

Classifications of focal segmental glomerulosclerosis

idiopathic/hereditary (primary), HIV-associated nephropathy, heroin nephropathy or secondary FSGS (hyperfiltration) which is seen with either reduced renal mass (advanced renal diseases) or initially normal renal mass (diabetes mellitus, HTN, obesity, sickle cell)

9

Membranous glomerulonephritis clinical, morphology, pathogen, therapy and prognosis

Nephrotic syndrome with GBM thickening and spikes. Caused by chronic immune complex. EM shows subepithelial deposits and IF shows granular GBM. Therapy is steroids and some progress to ESRD

10

Is membranous glomerulopathy more common in adults or kids?

adults

11

membranous glomerulopathy associations

malignant tumors (lung, colon, melanoma), drugs, SLE, infections

12

Membranoproliferative glomerulonephropathy clinical, morphology, pathogen, therapy and prognosis

Usually nephritic/nephrotic with cell proliferation and GBM thickening-double contours. Caused by chronic immune complex. EM shows subendothelial deposits and IF shows granular GBM. Treated with steroids, possibly interferon. Some progress to ESRD

13

Membranoproliferative glomerulonephropathy associated conditions

chronic infection, neoplasms, systemic connective tissue diseases, miscellaneous (cirrhosis, sickle cell, heroin)

14

Renal amyloidosis presentation, histology

Presents with proteinuria. Histology shows amorphous fluffy pink material in glomeruli and vessels. Positive on congo red stain with apple green birefrigence
Presents with proteinuria. Histology shows amorphous fluffy pink material in glomeruli and vessels. Positive on congo red stain with apple green birefrigence

15

What is the number one cause of end stage renal disease

diabetes

16

Kidney manifestations of Diabetes Mellitus

Hyaline arterolar disease that resembles HTN but more severe and diabetic glomerulosclerosis with diffuse or nodular expansion of mesangium, mesangial lysis, BM thickening. Results from nonenzymatic glucosylation of proteins and hyperfiltration

17

Hypertensive renal disease pathology

•Finely granular surface (scarred glomeruli). Blood vessels show medial and intimal thickening, plus hyaline deposition

18

Malignant hypertensive renal disease pathology and intial event

Initial event is renal vasculature injury. Result is fibrinoid necrosis and hyperplastic arteriolitis . Kidneys respond by secreting more renin and perpetuating the problem

19

What is uremia and what conditions does it lead to?

A group of manifestations which occur when there is severe loss of all renal functions. Acidosis (pH), fluid retention/edema/CHF/HTN (Na and water), cardiac arrythmias (K), secondary hyperparathyroidism (PO4), azotemia (BUN, creatinine), toxicity (drugs), anemia (EPO), HTN (renin-angiotensin), osteomalacia (vit D activation)