Glomerulonephritis

Question 1

2 broad categories of glomerular disease

Answer 1

primary (intrinsic renal) or secondary (due to systemic disease)
nephrotic vs nephritic syndrome

Question 2

What broad mechanism usually causes GN?

Answer 2

immune mediated mechanisms

other…metabolic/hemodynamic disturbances

Question 3

Primary feature of GN and progression

Answer 3

impairment in selective filtration of blood, resulting in excretion of larger substances like plasma protein and blood cells. GFR eventually decreases leading to renal failure, necessitating dialysis/transplant if refractory to medical therapy

PROTEINURIA AND HEMATURIA

Question 4

How to diagnose GN

Answer 4

• urinalysis (hematuria, proteinuria, RBC casts)
• renal function tests
• needle biopsy of kidney

Question 5

Pathogenesis of nephrotic syndrome

Answer 5

abnormal glomerular PERMEABILITY due to a number of conditions

Question 6

pathogenesis of nephritic syndrome

Answer 6

inflammation of glomeruli due to any causes of GN

Question 7

MCC cause of nephritic syndrome

Answer 7

poststrep glomerulonephritis

Question 8

Lab findings in nephritic syndrome

Answer 8

hematuria
AKI - azotemia, oliguria
proteinuria (mild, less than 3.5g/day)

Question 9

Lab findings on nephrotic syndrome

Answer 9

Urine protein >3.5g/24hr (nephrotic range)
hypoalbuminemia
hyperlipidemia, fatty casts in urine

Question 10

Clinical findings in nephritic syndrome

Answer 10

HTN, edema

Question 11

Clinical findings in nephrotic syndrome

Answer 11

Edema, hypercoagulabe state, increased risk of infxns

Question 12

What are the primary glomerular disorders

Answer 12

minimal change, focal segmental glomerulosclerosis (fsgs), membranous glomerulonephritis, IgA nephropathy (Berger disease), herditary nephritis (Alport syndrome)

Question 13

Minimal change is associated with what two malignancies?

Answer 13

Hodgkin disease and non-Hodgkin lymphoma

Question 14

What does minimal change look like on light and electron microscopy?

Answer 14

light - NO CHANGES/ABNORMALITIES SEEN

electron - fusion of foot processes

Question 15

Prognosis and treatment of minimal change

Answer 15

excellent prognosis with 4-8 week steroid therapy, but relapses occur

Question 16

how does minimal change present?

Answer 16

nephrotic syndrome (MC presentation), most common in children

Question 17

FSGS accounts for _____% of cases of adult nephrotic syndrome

Answer 17

25

Question 18

Prognosis and course of FSGS

Answer 18

fair to poor prognosis, doesn’t usually respond well to steroids; renal insufficiency develops within 5-10 years of dx, progressive course

Question 19

Treatment regimen for FSGS

Answer 19

controversial; steroids, immunosuppressive therapy, cytotoxic agents, ACE/ARBs

Question 20

Presentation of membranous glomerulonephritis

Answer 20

usually presents with nephrotic syndrome; glomeruflar capillary walls are thickened

Question 21

Primary and secondary causes of membranous glomerfulnephritis

Answer 21

primary - idiopathic
secondary- infection (hepC, hepB, syphilis, malaria), drugs (gold, captopril, pencillamine)
neoplasm
lupus

Question 22

How does IgA nephropathy (Berger) usually present

Answer 22

asymptomatic recurrent hematuria/mild proteinuria (MCC cause of glomerular hematuria); can present with gross hematuria after infection/exercise
mesangial deposition of IgA and C3 are seen on electron microscopy

Question 23

How does IgA nephropathy affect renal function

Answer 23

RENAL FUNCTION USUALLY NORMAL

Question 24

Features of alport syndrome/herditary nephritis

Answer 24

• x-linked or autosomal dominant
• hematuria, pyuria, proteinuria, high frequency hearing loss without deafness, progressive renal failure

KIDNEY SHIT WITH HEARING LOSS

Question 25

2 MCC causes of ESRD

Answer 25

diabetic nephropathy and hypertensive nephropathy

Question 26

GN usually due to hepC, associated commonly with cryoglobunemia, poor prognosis

Answer 26

membranous GN

Question 27

Poststreptococcal GN occurs after what infection and after how many days, who does it affect most commonly?

Answer 27

occurs after GABS, 10-14 days after infection (even with antibiotic therapy), usually affects children 2-6 years old

Question 28

Features of post strep GN

Answer 28

• hematuria (cola colored urine)
• edema
• HTN
• low complement levels
• proteinuria
• elevated anti-streptolysin O

Question 29

Prognosis of post strep GN and treatment

Answer 29

good prognosis, usually self limiting (alhtough may progress rapidly in adults)

supportive therapy (anti HTN, loop diuretics for edema, abx controversial)

Question 30

Triad of proliferative GN (usually crescentic) + pulmonary hemorrhage + IgG antiglomerular basement membrane antibody

Answer 30

goodpasture syndrome

Question 31

How does goodpasture present?

Answer 31

rapidly progressive renal failure, hemoptysis, cough, and dyspnea….lung disease preceeds kidney disease by days-weeks

Question 32

What does renal biopsy show for goodpasture

Answer 32

linear immunofluorescene pattern

Question 33

How to treat goodpasture

Answer 33

plasmapharesis to remove circulating anti-IgG antibodies

- cyclophosphamide and steroids to decrease formation of new antibodies

Question 34

How does HIV nephropathy present?

Answer 34

proteinuria, edema, hematuria

resembles collapsing FSGS

Question 35

How to treat HIV nephropathy

Answer 35

prednisone, ACE inhibitors, antiretroviral therapy

Question 36

Which glomerular disorder is most commonly associated with development of renal vein thrombosis (RVT)?

Answer 36

membranous nephropathy

Question 37

Symptoms of RVT

Answer 37

nausea, vomiting, fever, FLANK PAIN, HEMATURIA