1. This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Nephrology Consultant. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

2. SAMIAH S. AL-ANGARI

3.  Glomerulopathies vs. glomerulonephritis  Classification of Glomerulopathies  Pathology  Aetiology  Clinical features  Investigations  Complications  Management  Prognosis

5.  Glomerular disease includes glomerulonephritis, i.e. inflammation of the glomeruli and glomerulopathies when there is no evidence of inflammation.  Glomerulonephritis is a subset of glomerulopathies

6.  Nephrotic syndrome.  Acute glomerulonephritis (acute nephritic syndrome).  Rapidly progressive glomerulonephritis.  Asymptomatic urinary abnormality (haematuria, proteinuria or both).

8. Diseases commonly associated with acute GN:  Post streptococcal GN  Non- streptococcal post- infectious GN.  Infective endocarditis  Visceral abscess  SLE  Henoch-schonlein syndrome  cryoglobulinemia

10. Immune complex disease  Neutrophils: Protease GBM degradation O₂ free readicals cell damage AA metabolites ↓ GFR Complement- dependentComplement-leukocyte- mediated mechanism  Activation of the complement pathway Recruitment of neutrophils and monocytes C₅- C₉ (MAC)  Epithelial cell detachment.  (+) epithelial & mesangial cells to secrete damaging chemical mediators.  Upregulates TGF receptors on epithelial cells, excessive synthesis of extracellular matrix which leads to GBM thickening

11. Diffuse proliferative GN (PGN)  proliferation of cells within the glomeruli, accompanied by leukocyte filtrate  typical features of immune complex disease : - hypocomplimentemia - granular deposits of IgG & complement on GBM  Implicated antigens seem to be endostreptosin and nephritis – plasmin- binding ptn

15.  Abrupt onset of :  glomerular haematuria (RBC casts or dysmorphic RBC).  non-nephrotic range proteinuria ( < 2 g in 24 hrs).  oedema ( periorbital, sacral ).  hypertension.  transient renal impairment (oliguria, uraemia).

16. Base line measurements: - ↑ Urea - ↑ Creatinine - Urinalysis (MSU) : a) Urine microscopy (red cell cast) b) proteinuria

17. Diagnostically useful tests :  Culture (swab from throat or infected skin)  Serum anti-streptolysin-O titre  Hepatitis B surface antigen  Hepatitis C antibody  anti DNA, ANCA  ↓C3,4  Renal biopsy

18.  Nephrotic syndrome  HTN  AKI  Volume overload  Pulmonary edema  Chronic glomerulonephritis and CKI

19. Post streptococcal GN - Has a GOOD prognosis. - Supportive measures until spontaneous recovery. - Control HTN. - Fluid balance. - Oliguric with fluid overload. - GN complicating SLE or systemic vasculitides : immunosuppression with prednisolone, cyclophosphamide or azathioprine/ MMF.

20. THANK YOU