Case Files Paediatrics Chapter 29 Acute Poststreptococcal Glomerulonephritis

Front 1

1. Glomerulonephritis?

Back 1

a. Glomerular inflammation resulting in the triad of:
1. Haematuria
2. Proteinuria
3. HTN

Front 2

2. Red Cell casts?

Back 2

a. Injured glomeruli that increased permeability and leak red cells and proteins into the PCT.
b. The material subsequently clumps in the DCT and in the collecting ducts.
c. When passed, these cell clumps retain the shape of the tubule in the urine.
d. Red cell casts are markers for glomerular injury.

Front 3

3. Note: Acute poststreptococcal glomerulonephritis (APSGN) is the most common of the postinfectious nephritides, comprising 80-90% of cases.
a. Other bacteria, viruses, parasites, and fungi also have been implicated.
b. Males more commonly are affected.

Back 3

3. Note: Acute poststreptococcal glomerulonephritis (APSGN) is the most common of the postinfectious nephritides, comprising 80-90% of cases.
a. Other bacteria, viruses, parasites, and fungi also have been implicated.
b. Males more commonly are affected.

Front 4

4. Which strep causes APSGN and from what type(s) of infection?

Back 4

a. Group A β-haemolytic strep.
b. Can be from either Pharyngitis or impetigo (superficial skin lesion).
c. Note all GABHS infections results in APSGN. Certain GABHS strains “Nephritogenic” and are more likely to result in Acute Poststreptococcal glomerulonephritis?.

Front 5

5. Benefit of Abx use for GABHS?

Back 5

a. May reduce rheumatic fever risk.
b. Has NOT been shown to prevent Acute Poststreptococcal glomerulonephritis?.
c. The nephritis risk after infection w/nephritogenic strain of GABHS remains 10-15%.

Front 6

6. Interval between GABHS pharyngitis and Acute Poststreptococcal glomerulonephritis??

Back 6

a. 1-2 weeks.

Front 7

7. Interval between Impetigo and Acute Poststreptococcal glomerulonephritis??

Back 7

a. 3-6 weeks.

Front 8

8. Presentation of Acute Poststreptococcal glomerulonephritis?

Back 8

a. Symptoms onset is usually abrupt.
b. Although almost all pts have microscopic haematuria
c. Only 30-50% develop gross haematuria
d. 85% Present w/oedema
e. 60-80% develop HTN.

Front 9

9. Most important lab test for Acute Poststreptococcal glomerulonephritis?!?!?!?!?!?!?!?!?!?

Back 9

a. Serum C3 and C4 levels.
b. C3 is low in 90% of APSGN cases
c. C4 is usually normal.
d. Documentation of a recent strep infection is helpful

Front 10

10. If both C3 and C4 are low?

Back 10

a. An alternate diagnosis is considered.

Front 11

11. UA for Acute Poststreptococcal glomerulonephritis?

Back 11

a. Typically reveals:
1. High specific gravity
2. Low pH
3. Haematuria
4. Proteinuria
5. Red cell casts.

Front 12

12. Other important serum markers for Acute Poststreptococcal glomerulonephritis?

Back 12

1. ASO enzyme antibodies
2. Anti-DNase B antibodies
b. ASO antibodies are found in 80% of children w/recent GABHS pharyngitis but <50% of children w/recent GABHS skin infection.
c. ASO titres are positive in 16-18% of normal children.

Front 13

13. More reliable test than ASO antibodies?

Back 13

a. Anti-DNase B antibodies assay.
b. They are present in almost all pts after GABHS pharyngitis and in the majority of pts after GABHS skin infection.

Front 14

14. Note: antibodies to other strep antigens may also be assayed:
a. NADase
b. Hyaluronidase
c. Streptokinase.

Back 14

14. Note: antibodies to other strep antigens may also be assayed:
a. NADase
b. Hyaluronidase
c. Streptokinase.

Front 15

15. Should you do a renal biopsy for Acute Poststreptococcal glomerulonephritis?

Back 15

a. No, it is no longer routine.

Front 16

16. Tx of Acute Poststreptococcal glomerulonephritis?

Back 16

a. Generally supportive
b. Fluid balance is crucial
c. Diuretics, fluid restriction, or both may be necessary.
d. Sodium and potassium may require restriction.
e. HTN usually is easily controlled w/Ca-channel blockers.
f. Strict bed rest and steroids are NOT helpful.
g. Dialysis is rarely required.

Front 17

17. Prognosis of Acute Poststreptococcal glomerulonephritis?

Back 17

a. Resolution is usually rapid and complete.
b. The oedema resolves in 5-10 days and pts usually are normotensive w/in 3 weeks.
c. C3 levels usually normalize in 2-3 months.
d. A persistently low C3 level is uncommon and suggests an alternate diagnosis.
e. UA may be persistently abnormal for several years.

Front 18

18. Recurrent painless gross haematuria, frequently associated w/an upper respiratory tract infection, think of what?

Back 18

a. IgA nephropathy.
b. These pts may develop chronic renal disease over decades.
c. If proteinuria, HTN, or impaired renal function are found, a biopsy would be necessary.

Front 19

19. Benign familial haematuria inheritance?

Back 19

a. Autosomal dominant.

Front 20

20. Presentation of Benign familial haematuria?

Back 20

a. Persistent or intermittent haematuria w/o progression to chronic renal failure.

Front 21

21. Renal biopsy of Benign familial haematuria reveals?

Back 21

a. A thin basement membrane.
b. Can be normal.

Front 22

22. In what 2 conditions is Immune complex deposition w/IgA in the mesangium seen?

Back 22

a. HSP and IgA nephropathy!

Front 23

23. In what condition is Endothelial cell swelling w/fibrin deposition seen?

Back 23

a. HUS

Front 24

24. In what condition are crescentic glomeruli seen?

Back 24

a. Rapidly progressive glomerulonephritis.

Front 25

25. In what condition are C3 and C4 low?!?

Back 25

a. SLE

Front 26

26. Alport syndrome pathophys and presentation?

Back 26

a. Genetic defect in collagen synthesis that leads to abnormal basement membrane formation.
b. Presents w/haematuria, proteinuria, and renal failure.

Front 27

27. Denys-Drash syndrome?

Back 27

a. A group of findings composed of:
1. Wilms tumour
2. Gonadal dysgenesis
3. Nephropathy

Front 28

28. Complete.

Back 28

28. Complete.