ACUTE GLOMERULONEPHRITIS DOCUMENT.pptx

Notes for acute glomerulonephritis for students

1. ACUTE GLOMERULONEPHRITIS IN CHILDREN DR. MWENDWA

2. Objectives Introduction Definition Epidemiology Aetiolgy Pathophysiology Clinical features Investigations Treatment Complications

3. INTRODUCTION AGN is the term reserved for the variety of renal diseases in which inflammation of the glomerulus , manifested by proliferation of cellular elements , is secondary to an immunologic mechanism. In earlier years, AGN was known inappropriately as Bright disease , and almost any clinical presentation of gross hematuria was labeled as Bright disease.

4. DEFINITION Acute glomerulonephritis is a non suppurative immune mediated inflammatory lesion of the glomerulus . Is usually of sudden onset Charaterised by accumulation of nitrogenous waste in the blood, fluid & electrolyte derangement

5. EPIDEMIOLOGY In the tropics, children of the preschool age are commonly affected, while elsewhere children of the school age are commonly affected. Predominantly affects children from ages 2 to 12, average 6 to 10 year olds.

6. Cont.. No racial predilection appears to exist The male-to-female ratio range is 2:1. Incubation period is 1 to 4 weeks after infection thus the bacteria cannot be cultured from the sites or in blood.

7. AETIOLOGY. Most incidents of AGN appear to be associated with a post infectious state. Several bacterial and viral infections e.g staphylococcus and pneumonococcus, Coxsackie virus B, Echovirus type 9, Influenza virus, and mumps

8. CONT.. The most commonly recognized clinical picture (i.e, PSAGN) follows infection with group A beta hemolytic streptococci. It is also called Acute Nephritis, Glomerulonephritis and Post-Streptococcal Glomerulonephritis

9. CONT.. It may result from throat infection, impetigo or scabietic infection with GABHS. Transmission: -respiratory droplets or direct contact with mucus secretions -transmission via fomites is possible but less common

10. Impetigo

11. Cont..

12. Throat examination

13. PATHOPHYSIOLOGY Most forms of AGN are mediated by an immunologic process. For PSAGN, the evidence suggests that immune complexes, preformed by the combination of specific antibodies against streptococcal antigens, localize on the glomerular capillary wall and activate the complement system.

14. Cont.. Current evidence suggests that the inflammatory lesion in the glomerulus is associated with the fixation of soluble streptococcal antigen-antibody complexes. Immunoglobulin G (IgG) and complement (C3) complexes are found on the capillary basement membrane. The finding of C3 in the renal glomerulus usually is associated with decreased serum concentrations of C3 and total hemolytic complement.

15. Cont.. PSAGN can occur in epidemics but more commonly, it is sporadic. In patients with pharyngitis-related AGN, the latent period is approximately 10 days, and more than 80% of patients exhibit a significant rise in serum titer of antistreptolysin-O (ASO). But, a latent period is difficult to define in patients with impetigo-related AGN, and a rise in the titer of ASO is observed in only 50% of patients .

16. Cont.. Other streptococcal indicators (eg, antihyaluronidase [AH] titer, antideoxyribonuclease B titer [anti-DNase B]) are elevated in individuals with PSAGN secondary to either pharyngeal or skin infections. When a variety of antibody titers is used, almost 95% of patients with PSAGN demonstrate evidence of a prior streptococcal infection.

17. CLINICAL FEATURES Oedema: Facial puffiness usually in the periorbital area later it becomes more generalized Oliguria due to reduction in glomerular filtration < 400ml/ day. Hypertension; is the third cardinal feature of PSAGN and is reported in 50-90% of children who are hospitalized with AGN may rage from mild to moderate.

18. Facial oedema

19. BP measurement

20. CONT.. Altered urine colouration: -Gross hematuria occurs at onset in 3 0-50 % of children -The urine usually is described as being smoky, cola colored, tea colored, or rusty, dark brown or frankly bloody

21. Cont.. Difficulty in breathing: Dyspnea, orthopnea, and cough may be present. Pulmonary rales often are audible. At times, the only evidence of congestion is detected on chest radiograph. In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual

22. Cont.. Constitutional symptoms like malaise, lethargy, anorexia, fever, abdominal pain, and headache. History of the siblings and/or household contacts of children affected with PSAGN is important

23. Bimanual palpation

24. INVESTIGATIONS Urinalysis: -red cell cast or granular casts -proteinuria evidence nd by dip stick of +1/+2 corresponding to less than 2 g/m2/d -specific gravity elevated Full blood count: platelets and Hemoglobin are decreased Urea/creatinine –elevated Serum protein: low

25. Cont.. renal U/S renal shows normal to slightly enlarged kidneys bilaterally with some evidence of increased echogenicity. ASO titre should be documented to look for evidence of streptococcal infection in all patients.

26. Normal vs inflammed kidneys

27. Cont.. Cultures from either the pharynx or skin may be positive. other antibodies tests to a variety of streptococcal antigens (eg, ASO, AH, anti-DNase B ) or to combinations of antigens (eg, streptozyme test). NB: a rise in the titer of the antibody, measured at an interval of 2-3 weeks, is more meaningful than a single measurement.

28. Cont .. C3/C4 levels help to differentiate post streptococcal from other postinfectious forms of AGN. Reduced serum concentrations of C3 have been demonstrated in 80-92% of children with PSAGN. Values return to normal in most children within 6-8 weeks. The fourth component of complement (C4) value also may be depressed; however, this is an inconsistent finding. Chest radiograph: pulmonary oedema

29. Others Hepatitis B surface antigen Hepatitis C antibody Renal biopsy for selected patients

30. TREATMENT Prognosis is good and mostly management is supportive until spontaneous recovery occurs: Bedrest helps in maintaining adequate blood flow to the kidney. decreased sodium and protein intake may be recommended in the initial phase Fluid restrictions are adjusted according to the patient's urinary output and body weight.

31. Cont.. An accurate daily record of the patient's weight, fluid intake and urinary output. If residual infection is suspected, antibiotic therapy may be needed. Diuretics in the presence of fluid overload. Iron supplements for correction of anemia

32. Cont.. Antihypertensives to control high blood pressure. GN complicating SLE or systemic vasculitides : immunosuppression with prednisolone, cyclophosphamide or azathioprine may be used.

33. COMPLICATIONS Pulmonary edema CCF ARF Hypertensive encephalopathy UTI Chronic Glomerulonephritis and CRF

34. NB Hypertensive encephalopathy in approximately 5% of hospitalized children - May be accompanied by headache, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions. -Hypertensive encephalopathy has been reported in the occasional individual with minimal or no edema and with minimal urinary abnormalities.