1. Nephrology Division King Khalid University
Acute
Glomerulonephritis
Tutorial Med Course 441
Prof. Jamal Alwakeel
Nephrology Division King Khalid University

2. 14 year old Saudi Male c/o fever-headache for 10 days General malaise
Dark urine x 3 days

3. HPI Fever intermittent Muscular joint pain Urine character Edema
No skin rash

4. PH & Med
Antibiotic and NSAID
Social Hx
S. review FH

5. Examination BP : 160/90 mmHg and Look Sick Pale Puffiness in face
Pulse rate: 120/min
Temperature : 39 ºC
Respiration: 25/min,
Look Sick
Pale
Puffiness in face
Head and neck
JVP

6. Chest Examination Normal percussion Normal TVF Normal breath sound
Vesicular breathing
S1 increase
S2 N
S3 positive
Pansystolic murmur
Radiation to axilla
Grade III

7. Abd CNS M.S. /Normal Burbic rash in the leg Tend epigastic Tend loins
BS +ve
CNS
Normal
M.S. /Normal
Burbic rash in the leg

8. Urine Sample with hematuria
Initial Diagnosis
Fever? Infection vs autoimmune Disease
Murmur; M R vs VSD
HEAMATURIA
Urine Sample with hematuria

9. Initial Diagnosis Systemic Surgical Medical Hematuria Hemolytic Anemia
Embolization
Anti-coagulant
Surgical
Stone
Tumor
Papillary
APKD
Medical
Acute kidney injury
Glomerulonephritis
Rapid progressive glomerulonephritis
Initial Diagnosis

10. Differential Diagnosis of Hematuria
ARF-AKI-ATN
Acute glomerulonephritis (post-infection)
RPGN
IgA
Hemolytic uremic syndrome
NSAID
Hemolytic Anemia
IgA Nephropathy
Hemolytic uremic

11. Investigation WBC 15,000 cells/microliter Hb – 100 g/L Plat – 150 g/L
ESR 90
PT normal
PPT normal Sec
BI normal Sec

12. U&E S.cr - 210µmol/L K – 6mmol/L Ca – 1.9 mmol/L Urea – 20mmol/L
Na – 125 mmol/L
Ca – 1.9 mmol/L
Albumin – 28 g/L

13. Urine Analysis
Many RBC
Red cell cast absent
Protein – 1.2 g/24 hr

15. U/S : kid size ENLARGE 12.2 cm

18. Patient receive ceftriaxone IV and IV fluid
Treatment
Patient receive ceftriaxone IV and IV fluid
TREAT HYPERKALEMIA

20. Follow – up:
S Cr – 300 µmmol/L
JVP
Oliguria
Edema

21. Investigations for Glomerulonephritis
Regular follow-up and U&E
Antistreptolysin O (ASO)
ANA, Anti-DNA
C3-C4
ANCA (p,c)
HCV Antibody (HBsAg)
HIV RF
Cryoglobulin
Anti-basement membrane anti-body (with lung hemorrhage

22. Management IV Lasix Repeat urine analysis RBC cast
Kidney biopsy : RPGN-infection
Serology test : C3 low
RF: -negative
Final diagnosis: Infection glomerulonephritis- RPGN
Anti-glomerular basement membrane anti-bodies

23. Glomerular Disease – Acute Glomerulonephritis
Post infectious glomerulonephritis
Group A Strep Infection
Infective endcarditis
Membranoproliferative glomerulonephritis:
Systemic lupus erythematosus
Hepatitis C virus
IgA Nephropathy (Buerger’s Disease)
Rapidly progressive glomerulonephritis
Type I RPGN (direct antibody)
Good Posture syndrome
Type II RPGN (immune complex)
Post infectious
Systematic lupus erythematosus
Henoch – Schonlein pupura (IgA)
Type III RPGN (pauci-immune)
Vasculitis (Wegener granulomatosis; poiyarteritis nodosa-microscopic polyangitis)

24. Complications of acute glomerulonephritis
Hypertension
Pulmonary edema
Hyperkalemia
Encephalopathy convulsion
Electrolyte disturbance
Pericaditis
Gastroentritis
Peptic ulcer

25. Management of Glomerulonephritis
Treat the cause
Conservative management
Dialysis

26. Acute post-infection glomerulonephritis
Often associated with group A
B-hemolytic streptococcal type 12 infection
Also staphylococcus or viruses

27. Acute Glomerulonephritis
Symptoms occur days after infection
Hematuria
Proteinuria (<1gm/24 hr)
Decreased GFR, oliguria
Hypertension
Edema around eyes, feet and ankles
Ascites or pleural effusion
Antistreptolysin O (ASO), Low C3, normal C4
Kidney biopsy immune complexes and proliferation

29. Proliferative GN-post streptococcal
This glomerulus is hypercellular and capillary loops are poorly defined
This is a type of proloferative glomerulonephritis known as post-streptococcal glomerulonephritis

30. Post-streptococcal GN
Post-streptococcal glomerulonephritis is immunologically mediated, and the immune deposits are distributed in the capillary loops in a granular, bumpy pattern because of the focal nature of the deposition process

32. Post-streptococcal glomerunephritis
Conservative Treatment (acute kidney injury
Improves 1 – 4 weeks, C3 normalizes in 1 – 3 months, hypertension improves 1 – 3 months, intermittent hematuria x 3 years
99% complete recovery in children and 85% in adult

33. IgA nephropathy (Buerger’s Disease)
Most common acute glomerulonephritis in US, South East Asia
Associated with H.S. Purpura
Upper respiratory (50%) in 1 – 2 days (synpharyngitic hematuria)
Primary versus secondary (IBD, Liver disease, SLE, vasculitis)
50% risk of CRF
Proteinuria, hypertension, renal insufficiency predict worse prognosis
50% increase IgA, normal compliments
TREATMENT OF CONSERVATIVE ACEi
HIGH RISK: patient prednisone and alkylating agent
Cyclophosphamide-azothroprim & ASA & ACEi & tosilectomy

34. Rapid Progressive GN Type I RPGN (direct antibody)
Good pasture syndrome
Type II RPGN(immune complex)
Post infectious
Systematic lupus erythematosus
Henoch-schonlein purpura (IgA)
Cryoglobulinemia
Type II (pauci-immune)
Vasculitis (Wegener granulomatosis, microscopic polyangitis, poplyarteries nodosa)

35. Rapidly progressive GN
Develops over a period of days and weeks
Primarily adults in 50’s and 60’s
Progresses to renal failure in a few weeks or months
Hematuria is common, may see proteinuria, edema or hypertension

36. Rapidly progressive (Crescentic) Glomerulonephritis
Morphology
Crescent formation
Crescents are formed by proliferation of parietal cells
Infiltrates of WBC’s & fibrin deposition in Bowman’s space
EM reveals focal ruptures in the GBM

41. Goodpasture Syndrome TREATMENT Early treatment is essential
Antibody formation against pulmonary and glomerular capillary basement membranes
Damage glomerular basement membrane
Men – 20 to 30 years of age
Pulmonary hemorrhage and renal failure
TREATMENT
Early treatment is essential
Pulse steroid (10 mg/kg/day for 3 – 5 days)
Cyclophosphamide
Plasmapheresis

42. Goodpasture’s syndrome
This immunoflourescence micrograph shows positivity with antibody to IgG has a smooth, diffuse, linear pattern that is characteristic for glomerular basement antibody with Goodpasture’s syndrome

43. Microscopic Polyangitis
Necrotizing vasculitis of small – and medium – sized vessels in both the arterial and venous circulations
Frequently involves the lung and the kidney with typical complications of hemorrhage and glomerulonephritis
Usually positive p-ANCA (anti-myeloperoxidase)
Usually positive c-ANCA (ant-proteinase 3)

45. Treatment Initial Therapy
Combination cyclophosphamide-corticosteroid therapy
Pulse methyl prednisone (10 mg/kg/day for 3-5 days)
A slow steroid taper, with the goal of reaching 20 mg of prednisone per day by the end of two months and an overall glucocorticoid course of between 6 and 9 months
Either daily oral or monthly intravenous cyclophosphamide

46. Treatment Plasmapheresis
Severe manifestations of pulmonary hemorrhage on presentation
Dialysis – dependent renal failure upon presentation
Concurrent anti-GBM antibodies

47. Thank you…