nephrotic pathology

Question 1

Complications of nephrotic syndrome

Answer 1

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

Question 2

Describe how nephrotic syndrome leads to increased infections

Answer 2

Increased glomerular permeability leads to loss of immunoglobulins

Question 3

Describe how nephrotic syndrome leads to thrombosis

Answer 3

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

Question 4

Describe how nephrotic syndrome leads to edema

Answer 4

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

Question 5

pathogenesis of glomerular injury

Answer 5

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

Question 6

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

Answer 6

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

Question 7

Focal sclerosis clinical, morphology, pathogen therapy and prognosis

Answer 7

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

Question 8

Classifications of focal segmental glomerulosclerosis

Answer 8

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)

Question 9

Membranous glomerulonephritis clinical, morphology, pathogen, therapy and prognosis

Answer 9

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

Question 10

Is membranous glomerulopathy more common in adults or kids?

Answer 10

adults

Question 11

membranous glomerulopathy associations

Answer 11

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

Question 12

Membranoproliferative glomerulonephropathy clinical, morphology, pathogen, therapy and prognosis

Answer 12

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

Question 13

Membranoproliferative glomerulonephropathy associated conditions

Answer 13

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

Question 14

Renal amyloidosis presentation, histology

Answer 14

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

Question 15

What is the number one cause of end stage renal disease

Answer 15

diabetes

Question 16

Kidney manifestations of Diabetes Mellitus

Answer 16

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

Question 17

Hypertensive renal disease pathology

Answer 17

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

Question 18

Malignant hypertensive renal disease pathology and intial event

Answer 18

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

Question 19

What is uremia and what conditions does it lead to?

Answer 19

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)