Hazem.K.Al-Khafaji FICMS Department of internal medicine College of medicine Al-Qadissyia University

is a tuft of capillaries branching from afferent arteriole & drained via efferent arteriole, enclosed by Bowman ` s capsule.. The Glomerulus

3 Capillary Space Endothelium Urinary Space GBM Podocyte ` MD consult

Filtration Blood--›Glomerular filtration membrane -- ›Fluid Like plasma without protein & little lipid(low molecular weight)) --› Bowman’s space --› Renal tubules

 1-The commonest cause is immunologically mediated;  A- Antibodies directed against glomerular basement membrane(Anti GMB) as in Goodpasture’s syndrome.  B- Immune complex deposition as in post infectious G.N & IgA nephgropathy.  C- direct effect of T.lymphocyte & macrophage. 2- metabolic disease as diabetes mellitus & amyloidosis.  3- Familial diseases as Alport’s syndrome. 5

Extensive inflammatory damage to glomeruli can cause a fall in GFR and eventually produce uremic symptoms with salt and water retention, leading to oedema and hypertension. Leakage of cells & large molecular weight molecules,leading to haematuria (dysmorphic RBCs) & proteinuria.

Clinical presentations:

GN:inflammation of the glomeruli,classified according to histopathological findings.e.g focal,diffused.segmental & crescentic (crescent means accomulation of large pale cells within the Bowman's capsule forming semicircular structure & this indicate the worst prognosis. Mostly due to immunological injury. Glomerulopathy : the term used when there is no features of inflammation as in morbid obesity, Drugs,& HIV infection

Oliguria ≤ 500cc urine/ day Hypertension Oedema usually started as periorbital oedema at morning Haematuria(red or smoky appearance) Reduction of GFR Urinanalysis: dysmorphic red cells &Red cell casts Proteinuria (mild, moderate or may be in nephrotic range of >3.5 g/24hours)

Classification based on histopathological examination of renal biopsy. Examination by: Light microscopy. Electronic microscopy. Immunofluorescence microscopy

Post streptococcal Glomerulonephritis Subacute Bacterial Endocarditis Lupus Nephritis( diagnostic criteria of SLE) Anti-glomerular Basement Membrane Disease(Goodpasture ΄ s syndrome) IgA Nephropathy(henoch-Sch Ö n lein purpura) ANCA Small Vessel Vasculitis Membranoproliferative Glomerulonephritis Mesangioproliferative Glomerulonephritis

Membranous nephropathy: The most common cause of idiopathic (no evident cause) nephrotic syndrome in adults.

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Post-streptococcal glomerulonephritis is acute proliferative glomerulonephritis. Immune-mediated, follow infection with certain strains of ß-haemolytic streptococci. Following impetigo by 2–6 weeks (after skin infection) & following Streptococcal pharyngitis by 10 days up to 2weeks after infection. It can follow other infection with other bacteriae as salmonella,pneumococcus & staphylococcus.So it is called post-infectious glomerulonephritis. Acute post-streptococcal GN 90% of cases affect children between the ages of 2 and 14 years. 10% of cases are adults.

The classic presentation is an acute nephritic picture with haematuria(smoky colored urine), red blood cell casts, oedema mostly peri-orbital early in the morning, hypertension, oliguria & renal impairment(increased B.urea & S.creatinine), which may be severe enough to appear as RPGN ( development of renal failure within days to weeks). Systemic symptoms of headache, malaise, anorexia, and flank pain (due to swelling of the renal capsule) are reported in as many as 50% of cases.

GUE(Urinalysis):RBCs,dysmorphic RB C,RBC casts, granular casts &mild-moderate albuminuria. Evidences of streptococcal infection: Antistreptolysin O titre(ASOT):increasing or very high. Culture of throat swab. Swab from any site of infection(skin in case of impetigo). Assessment of renal function: reduced GFR,increased B.urea & S.creatinine. Serum complement(C3 & C4):both are reduced. Renal biopsy :rarely indicated(RPGN).

 If pt not improving within 2 weeks or there is progressive uremia then consider biopsy  Biopsy examined by 3 microscopes : immunofluorescent microscope, electronic microscope (EM) & light microscope.  Biopsy vital for 3 purposes : definite diagnosis, treatment modlity & assessment of prognosis. 18

Treatment is supportive, with salts & fluids restriction, control of hypertension with diuretics & other hypotensive agents, and dialysis as needed. Antibiotic treatment for streptococcal infection( penicillin group or macrolides) should be given to all patients but prolonged prophylactic treatment not indicated. Self limiting disease in most children & many adults. No role for immunosuppressive therapy in most cases.

Overall, the prognosis is good, with permanent renal failure being very uncommon (1–3%), and even less so in children. Renal function begins to improve within 2 weeks. But complete resolution of the hematuria and proteinuria in children occurs within 3–6 weeks of the onset of nephritis.

Bacterial sepsis, acute or subacute bacterial endocarditis, visceral abscess, infected ventriculoperitoneal shunt, osteomyelitis,Malaria(Plasmodium malariae),hepatitis B,hepatitis C& others. Treatment is aimed at eradicating the primary disease.

To be continued Thank you