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Flashcards in Glomerulonephropathies Deck (57)
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1

Nephritic 3 VS Nephrotic 3

What would you find in the urine?

Nephritic Characteristics:
1. +red cells - white blood cells
2. red cell or mixed cellular casts
3. variable degrees of proteinuria

Nephrotic Characteristics
1. proteinuria > 3.5 g/day
2. lipiduria
3. fatty casts

2

Nephritic Causes
9

1. Postinfectious glomerulonephritis
2. IgA nephropathy
3. Henoch-Schönlein purpura (HSP also termed IgA vasculitis [IgAV])
4. Mesangial proliferative glomerulonephritis
5. Lupus nephritis
6. Thin basement membrane disease
7. Hereditary nephritis
8. Membranoproliferative glomerulonephritis
9. Rapidly progressive (crescentic) glomerulonephritis

3

Nephrotic Causes
4

1. Systemic…Diabetic nephropathy, amyloidosis, systemic lupus
2. Minimal change disease (children)
3. Focal segmental glomerulosclerosis (FSGS)
4. Membranous nephropathy

4

What are the two patterns of nephritic disease? 2

1. Focal nephritic
2. Diffuse nephritic

5

1. What is a focal nephritic pattern?

2. What does the UA show? 3

3. Example? 1

1. Inflammatory lesions in less than ½ of glomeruli

2. UA shows
-RBCs,
-occasional RBC casts,
-mild proteinuria

3. Example: IgA nephropathy

6

1. What is a diffuse nephritic pattern?

2. What does the UA show? 4

3. Example? 1

1. Affects > ½ of the glomeruli

2. UA similar to focal,
-but w/ more proteinuria,
-also edema,
-HTN, and/or
-renal insufficiency

Example: post-streptococcal glomerulonephritis (PSGN)

7

1. Nephrotic syndrome affects how much of the glomeruli?

2. What is it lacking? 2

3. What will it cause? 3

4. Example?

1. Affects many of the glomeruli

2. Without obvious
-inflammation or
-immune complex deposition

3.
-edema,
-hyperlipidemia,
-hypoalbuminemia

4. Example: diabetic nephropathy

8

1. Poststreptococcal glomerular nephritis (PSGN) is the most common cause of what?

2. Primarily occurs where?

3. What age are at greatest risk?

1. Most common cause of acute nephritis worldwide

2. It primarily occurs in the developing world.

3. The risk of PSGN is greatest in children between 5-12 years of age.

9

Poststreptococcal glomerular nephritis (PSGN)

1. Occurs after what? 2

2. What does not necessariliy protect pts from this?

1.
-Usually occurs 1-3 weeks post strep throat
-3-6 weeks post skin infection with group A beta-hemolytic strep (GABS)

2. Antibiotic treatment does not always prevent glomerular disease

10

Poststreptococcal glomerular nephritis (PSGN)
Pathophysiology:

1. Caused by?

2. Can be associated with? 2

3. What does the resulting glomerular immune complex disease trigger? 2

1. Caused by glomerular immune complex disease induced by specific nephritogenic strains of group A beta-hemolytic streptococcus (GABS). ALMOST ALWAYS!

2. Can also be be associated with various
-viral illnesses and
-parasitic infections

3.
-complement activation and
-inflammation.

11

Poststreptococcal glomerular nephritis (PSGN):
Clinical Signs/Symptoms
9

1. Often asymptomatic
2. Microscopic hematuria leading to Gross hematuria
3. Proteinuria (can reach nephrotic range)
4. Edema
5. Hypertension
6. Increased serum creatinine
7. Variable decline in GFR
8. Hypocomplementemia (C3, C4)
9. Acute Renal Failure and need for dialysis is uncommon

12

Poststreptococcal glomerular nephritis (PSGN):
What lab test should we do if we suspect this?

Serology… for elevated titers of antibodies to extracellular streptococcal products is evidence of a recent GABS infection.

The streptozyme test!!!!

13

Poststreptococcal glomerular nephritis (PSGN):
The streptozyme test measures 5 streptococcal antibodies, & is positive in 95% of patients due to pharyngitis and about 80% of those with skin infections
What are the 5 antibodies?

1. Anti-streptolysin (ASO)*****
-many people will just order this
2. Anti-hyaluronidase (AHase)
3. Anti-streptokinase (ASKase)
4. Anti-nicotinamide-adenine dinucleotidase (anti-NAD)
5. Anti-DNAse B antibodies

14

Poststreptococcal glomerular nephritis (PSGN). When is a renal biopsy perfomred?
2

1. other glomerular disorders are being considered because they deviate from the natural course of the PSGN
2. presents late without a clear history of prior streptococcal infection

15

1. Persistently low C3 levels beyond 6 weeks are suggestive of a diagnosis of what?

2. Recurrent episodes of hematuria are suggestive of what?

1. membranoproliferative glomerulonephritis.

2. IgA nephropathy and are rare in PSGN.

16

Poststreptococcal glomerular nephritis (PSGN) treatment?
3

Management is supportive and focused upon treating the volume overload
1. sodium and water restriction
2. diuretic therapy Lasix (furosemide) - will also treat what- HTN
3. In patients with acute renal failure, dialysis may be required

17

Poststreptococcal glomerular nephritis (PSGN) prognosis?
2 paths

1. Most patients, particularly children, have complete clinical recovery, and resolution of their disease process begins within the first 2 weeks.

2. A small subset of patients have late renal complications (hypertension, increasing proteinuria, and renal insufficiency

18

1. IgA Nephropathy aka Berger’s Disease most common lesion to cause what?

2. Commonly in what races? 2

3. Gender?

4. Commonly in what age?

1. to cause primary GN in the developed world
2. Higher frequency in Asians and Caucasians—relatively rare in blacks
3. Male to Female ratio of 2:1
4. Age—80% are between 15-35YO at diagnosis

19

IgA Nephropathy/Berger’s Disease
1. Etiology?
2. What is the initiating event?
3. Dysregulated synthesis and metabolism of IgA results in ?

4. Environmental factors that drive the generation of pathogenic IgA? 2

1. The etiology of primary IgA nephropathy is generally unknown.

2. The initiating event is the mesangial deposition of IgA.

3. IgA immune complexes with characteristics that favor mesangial deposition and accumulation.

4.
-dietary antigens and
-mucosal infections

20

IgA Nephropathy Presentation
Typically presents in one of three ways: First way?
3

50% present with:
1. Gross hematuria*****
-May be recurrent
-Usually after URI "synpharyngitic hematuria."
2. Flank Pain
3. Fever

21

IgA Nephropathy Presentation
Typically presents in one of three ways: Second way?
2

30% present with:
1. Microscopic hematuria
--May eventually lead to gross hematuria
2. Mild proteinuria

22

IgA Nephropathy Presentation
Typically presents in one of three ways: Third way?
5

10% present with:
1. Nephrotic syndrome (proteinuria, lipiduria, fatty casts)- Which looks like=

2. Edema
3. Renal insufficiency
4. Hypertension
--Rare malignant hypertension
5. Hematuria

23

IgA Nephropathy Diagnosis
2


What else may mesangial IgA be seen with? 3


IgA nephropathy may rarely be seen with other glomerular diseases such as? 2

1. Suspicion based on clinical history, and urinalysis
2. Confirmation is by kidney biopsy

3. Mesangial IgA deposition may also be seen with
-cirrhosis,
-celiac disease and
-HIV infection

4.
-minimal change disease and
-granulomatosis with polyangiitis (Wegener's)

24

IgA Nephropathy Diagnosis.
Confirmation is by kidney biopsy. What will we see? 2

1. Prominent IgA deposits in the mesangium and along glomerular capillary walls
2. C3 and IgG are also deposited

25

Treatment of IgA Nephropathy
General intervention?
2

1. Blood pressure control (all)
2. ACEIs and/or ARBs

26

In which IgA nephropathy pts should we make sure are on an ACE and ARB? 3


Pts with severe or progressive disease need to be on what? 2

For patients w/
1. persistent proteinuria,
2. slightly reduced GFR and
3. mild/mod changes on biopsy

Look for reduction in protein excretion


1. Corticosteroids and/or
2. immunosuppressants

27

IgA Nephropathy Prognosis
1. What happens to most pts?
2. Some have persistant, low grade what? 2
3. Slow progression to what occurs in 50% of individuals?

4. Clinical predictors of progression include? 3

5. What pts are at low risk for progressive kidney disease?

1. Most patients enter a sustained clinical remission

2. hematuria and/or proteinuria

3. end-stage renal disease

4. Clinical predictors of progression include:
-elevated serum creatinine
-hypertension
-persistent protein excretion above 1000 mg/day.

5. Patients who have recurrent episodes of gross hematuria without proteinuria

28

Henoch-Scholein Purpura (HSP)/ IgA Vasculitis‏ is characterized by what?

Usually occurs in what ages?

Systemic vasculitis characterized by the tissue deposition of IgA-containing immune complexes

HSP usually occurs between ages of 3-15

29

The underlying cause of HSP is unknown, but the main theory is?

HSP represents an immune-mediated vasculitis that may be triggered by a variety of antigens

30

Henoch-Scholein Purpura (HSP)/ IgA Vasculitis‏
Tetrad of clinical manifestations?

What is present?

Can develop over what time?

1. Palpable purpura without thrombocytopenia or coagulopathy
2. Arthritis/arthralgias
3. Abdominal pain

Renal disease (GN)

Can develop over days to weeks and manifestations can vary in order of presentation