Acute Glomerulonephritis

1. Acute Glomerulonephritis Tutorial Med Course 441 Prof Jamal Alwakeel Nephrology DivisionKing 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 • pulse rate: 120/min • Temperature : 39 ºC • Respiration: 25/min. pale • Look Sick • 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 IIII

7. Abd • Tend epigastic • Tend loins • BS +ve • CNS • Normal • M.S. /Normal

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

9. Initial Diagnosis Hematuria • Systemic • Hemolytic Anemia • Embolization • Anti-coagulant • Surgical • Stone • Tumor • Papillary • APKD • Medical • Acute kidney injury • Glomerulonephritis • Rapid pogressiveglomerulonephrtis • IgA Nephropathy

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 • Scr - 210µmol/L • Urea – 20mmol/L • K – 6mmol/L • Na – 125 mmol/L • Ca – 1.9 mmol/L • Albumin – 28 g/L

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

15. U/S : kid size ENLARGE 12.2 cm

18. 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 • Serology tesy : all negative • RF: -negative • Final diagnosis • 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 – Schonleinpupura (IgA) Type III RPGN (pauci-immune) • Vasculitis (, Wegener granulomatosis; poiyarteritisnodosa-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 10-21 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 (synpharyngitichematuria) • 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-schonleinpurpura (IgA) • cryoglobulinemia • Type II (pauci-immune) • Vasculitis (, Wegener granulomatosis, microscopic polyangitis,poplyarteriesnodosa)

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 • 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)

46. 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

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

48. Thank you…