Nephrotic Syndromes

Question 1

Most Common Nephrotic Syndrome in Children

Answer 1

Minimal Change Disease (MCD) (lipoid nephrosis)

Question 2

MCD EM Findings and Cause

Answer 2

• Foot process Effacement (flattening) due to Cytokines from T-cells or possibly from Hodgekin Lymphoma Reid-Sternburg Cells.
• Selective Loss of Albumin from GBM polyanion loss.

Question 3

Treat MCD with….

Answer 3

Steroids (they knock out the cytokines!)

Question 4

Most common cause of Nephrotic Syndrome in Adults

Answer 4

Focal Segmental Glomerusclerosis

Question 5

FSGS LM and EM Findings

Answer 5

LM: Focal (only some of the glomeruli) and Segmental (only part of the glomerulus) Sclerosis and Hyalinosis
EM: Foot Process Effacement

Question 6

FSGS Associated with

Answer 6

HIV (severe collapsing FSGS), Heroin Abuse, Interferon Treatment, Sickle Cell, and Chronic Kidney Disease

Question 7

Interferon alpha treatment in FSGS can cause

Answer 7

Tubuloreticular Endothelial Inclusions

Question 8

Membranous Nephropathy LM, EM, and IF Findings

Answer 8

LM: diffuse capillary and GBM Thickening
EM: “Spike and Dome” with SUBEPITHELIAL deposits (Podocytes lay down more basement membrane to cover up deposits, which leads to the appearance of hills and valleys, or spikes and domes)
IF: GRANULAR, SLE’s Nephrotic Presentation

Question 9

Membranous Nephropathy Associated with

Answer 9

Infections (Hep B or C), SLE, idiopathic, or Drugs

Question 10

Membranoproliferative Glomerulunephritis (MPGN) Type I Findings

Answer 10

SUBENDOTHELIAL IC Deposits with GRANULAR IF give rise to the “tram-track” appearance due to GBM splitting caused by mesangial ingrowth. (Most common type)

Question 11

MPGN Type I Associated with

Answer 11

Hugely with Hep B or C

Question 12

MPGN Type II Findings

Answer 12

Intramembranous IC Deposits; “dense deposits” that are associated with CS Nephritic Factor.

Question 13

CS Nephritic Factor

Answer 13

Antibody that stabilizes C3 Convertase; the enzyme that activates Complement, leading to Inflammation (C3 —> C3a + C3b)

Question 14

Diabetic Glomerulonephropathy Findings

Answer 14

Nonenzymatic glycosylations of GBM leads to increased permeability and thickening, which develops into Hyaline Arteriosclerosis.
NEG of efferent arterioles –> increased GFR –> mesangial expansion –> Albumin leakage

Question 15

Diabetic Glomerulonephropathy LM Findings

Answer 15

Mesangial Expansion, GBM thickening, esosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson Lesions)

Question 16

Treat Diabetic Glomerulonephropathy with

Answer 16

ACE Inhibitors because they block Angiotensin II from constricting the efferent arterioles which would exacerbate the problem.

Question 17

Amyloidosis LM Findings

Answer 17

Congo Red stain shows apple-green birefringence under polarized light from deposits in the mesangium.

Question 18

Amyloidosis associated with

Answer 18

Chronic Conditions (multiple myeloma, TB, RA)