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Acute glomerular disease
- 1. G l om e r u l o n e p h r I t I s HELLO K I D N E Y
- 2. ANATOMY OF MRKIDNEY LET’S CHECK IT OUT!!!
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- 5. Functions of ME(MR.KIDNEY) Without me, YOU will UNABLE to: Remove wastes and water from the blood Balanced chemicals in your body Release hormones Help to control blood pressure Help to produce red blood cells Produce vitamin D, which keeps the bones strong and healthy
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- 7. What is glomerulonephristis? Glomerulonephritisis is a kidney condition that involves damage /inflammation to the glomeruli.
- 8. Types of glomerulonephritis Acute glomerulonephritis - begins suddenly Chronic glomerulonephritis -develops gradually over several years.
- 9. Approach to patientwith glomerular disease
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- 12. Acute Glomerulonephritis Acute glomerulonephritis(AGN) is an abrupt onset of one or more features of an Acute Nephritic Syndrome : • Oedema e.g. facial puffiness • Microscopic / macroscopic haematuria • Decreased urine output (oliguria) • Hypertension • Azotemia
- 13. Presenting features ofAGN Acute nephritic syndrome (most common) Nephrotic syndrome Rapidly progressive glomerulonepritis Hypertensive encephalopathy Pulmonary oedema Subclinical (detected on routine examination)
- 14. Causes of AcuteNephritis Post streptococcal AGN Post-infectious acute glomerulonephritis (other than Grp A B-Haemolytic Stretococci) Subacute bacterial endocarditis Henoch- Schoelein Purpura IgA nephropathy Hereditary nephritis SLE Systemic vasculitis
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- 16. In children, thecommonest cause of acute nephritic syndrome is post-infectious AGN, mainly due to post-streptococcal infection of the pharynx or skin. Post streptococcal AGN is commonest at 6-10 years age.
- 17. Definition AGN that followsan infection with a nephritogenic strain of group A beta hemolytic streptococci. The classic example of the acute nephritic syndrome. Nelson Textbook of Pediatrics, 7th Edition
- 18. Streptococcal infection ofthe throat ( strep throat) or skin ( impetigo)
- 19. epiDemiology Most commonly– sporadic. Peak incidence - age 2-14 y/o, uncommon <3y/o. Males are commonly affected than females.
- 20. etiology anD pathogenesis Mtypes of streptococci (nephritogenic strains) M types 47, 49, 55, 2, 60, and 57 - following impetigo M types 1, 2, 4, 3, 25, 49, and 12 – pharyngitis Incubation period: 2–6 weeks after skin infection 1–3 weeks after streptococcal pharyngitis.
- 21. etiology anD pathogenesis Antibodiesto streptoccocus (eg antistreptolysin O) are formed in the circulation Antigen-antibody circulating immune complexes are subsequently deposited along the glomerular basement membrane (GBM).
- 22. Streptococcal infection immune complexformation + deposited in GBM complement system activated immune injuries cellular proliferation GBM fracture capillary lumen narrowed hematuria glomerular blood flow decreased proteinuria oliguria GFR↓ distal sodium reabsorption retention of water & sodium blood volume ↑ edema hypertension Low serum complement
- 25. light microscope not specificfor post streptococcal nephritis •Glomeruli appear enlarged and hypercellular. •Diffuse mesangial cell proliferation with an increase in mesangial matrix. •Polymorphonuclear leukocytes are common in glomeruli during the early stage of the disease.
- 26. Deposits localize inthe mesangium and along the capillary wall in a subepithelial pattern and stain dominantly for C3 and to a lesser extent for IgG
- 27. typical manifestation 1. Edema 75%of the patients Face, periorbital area lower extremities generalized (ascites, pleural effusions) 2. Proteinuria – usually normalize after 4 weeks 3. Oliguria
- 28. Sign and symptoms Kidneypain normally happens in the “flank” region, which is just below the bottom of rib cage.
- 29. Sign and symptoms Cola-coloredor diluted, iced- tea-colored urine from red blood cells in your urine (hematuria) Foamy urine due to excess protein (proteinuria)
- 30. Sign and symptoms High blood pressure (hypertension) Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen Fatigue/SOB from anemia or kidney failure. Less frequent urination than usual.
- 31. Clinical course Spontaneous improvementtypically begins within 1 wk with resolution of edema in 5-10 days and hypertension in 2-3 wk, but urinalysis may be abnormal (persistent microscopic hematuria) for a year.
- 32. InvestIgatIons Urinalysis and culture •Haematuria – present in all patients. • Proteinuria (trace to 2+, but may be in the nephrotic range; usually associated with more severe disease.) • Red blood cell casts (pathognomonic of acute glomerulonephritis). • Other cellular casts. • Pyuria may also be present.
- 33. InvestIgatIons Urinalysis and culture •Red blood cell casts (pathognomonic of acute glomerulonephritis) • Other cellular casts • Pyuria may also be present
- 34. InvestIgatIons Bacteriological andserological evidence of antecedent streptococcal infection: • Raised ASOT ( > 200 IU/ml ). • Increased anti-DNAse B (if available) – a better serological marker of preceding streptococcal skin infection. • Throat swab or skin swab.
- 35. InvestIgatIons Renal functiontest • The BUN - elevated in 75% of patients, • serum creatinine level is increased in one half of the patients • Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic acidosis are seen only in severe patients. Full blood count • A mild normochromic anemia may be present from hemodilution and low-grade hemolysis. • Leucocytosis may be present.
- 36. InvestIgatIons Complement levels •C3 level – low at onset of symptoms, normalizes by 6wks • C4 is usually within normal limits in post-streptococcal AGN. Ultrasound of the kidneys • Not necessary if patient has clear cut acute nephritic syndrome.
- 37. IndIcatIons for renal BIopsy Severeacute renal failure requiring dialysis. Features suggesting non post-infectious AGN as the cause of acute nephritis. Delayed resolution • Oliguria > 2 weeks • Azotaemia > 3 weeks • Gross haematuria > 3 weeks • Persistent proteinuria > 6 months
- 38. dIagnosIs Acute onset Symptoms: edema,oliguria, dark urine, hypertension Urinalysis: RBCs, protein, casts Evidences of streptococcal infection: – Elevated serum titers of Abs to streptozymes(ASO) Serum C3 - Reduced
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- 42. ManageMent Strict monitoring -fluid intake, urine output, daily weight, BP (Nephrotic chart) Penicillin V for 10 days (give erythromycin if penicillin is contraindicated) Fluid restriction
- 43. MANAGEMENT Diuretic (e.g. Frusemide)should be given in children with pulmonary oedema. Diet – no added salt to diet.
- 44. COMPLICATIONS Look out forcomplications of post- streptococcal AGN: • Hypertensive encephalopathy usually presenting with seizures • Pulmonary oedema (acute left ventricular failure) • Acute renal failure
- 45. MANAGEMENT fOr COMPLICATIONS Significant asymptomatic hypertension symptomatic,severe hypertension or hypertensive emergency / encephalopathy
- 47. Prehypertension is definedas a blood pressure in at least the 90th percentile, but less than the 95th percentile, for age, sex, and height, or a measurement of 120/80 mm Hg or greater. Hypertension is defined as blood pressure in the 95th percentile or greater.
- 49. Acute pulmonary edema MANAGEMENTfOr COMPLICATIONS
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- 51. fOLLOw-uP For atleast 1 year. Monitor BP at every visit Do urinalysis and renal function to evaluate recovery. Repeat C3 levels 6 weeks later if not already normalised by the time of discharge.
- 52. OuTCOME Short termoutcome: Excellent, mortality <0.5%. Long term outcome: 1.8% of children develop chronic kidney disease following post streptococcal AGN. These children should be referred to the paediatric nephrologists for further evaluation and management.
- 53. KIDNEY SAY !!!! Thanksfor watching
Editor's Notes
- #5 Normal histological structure of a glomerulus. On the right, is a 3-D illustration of a glomerulus. Left one shows AA = affrent arteriole, EA= Efferent arteriole, BC= Bowman’s capsule, US= Urinary space