Glomerulonephritis akut post streptococcus

Glomerular disease : Most often in children ( 3 and 7 ages ) Usually appear 1 2 weeks post infection ( follows streptococcal skin infection than streptococcal pharyngitis )
Elevated Antistreptolysin O ( ASO ) during the nephritic stage ( specific nephritogenic strain of group A streptocuccus )

Bacteri do not enter the blood, urine and kidney but streptococcal circulated and elicits the formation of anti body -> immune complex -> deposit in the glomeruli and active complement -> damage glomerular basement membrane -> obstruction of the glomerular capillaries by endothelial proliferation and swelling.

Tubular function is less severely impaired than glomerular function. The disease heal spontan or conservative therapy ( 95% children ) The rapidly progressive form of GNA and another small slow progression to GNC with CRF ( a small minority paediatric patien )

Laboratory findings
Cultur throad of streptococcal infection Increased : ASO 1 - 3 weeks post infection peaks 3-5 weeks 50 % show no rise in ASO titer, thus height of the titer dost not reflect severity of the renal disease

Urine : hematuria macro and microscopic 1-2 weeks and last 2 12 months Lekocytoria Sediment : RBC, WBC, granular, hyalin, fatty Proteinuria ( < 3 gr / day ) diappears before hematuria dan oliguri

Blood : increased BUN and Creatinine decreased creatinine clearence increased sediment rate ( ESR ) leukocytosis neutrophyl dominant normocytic anemia due to hemodilution,

Blood marrow depression or increase RBC depression Decrease serum complement occurs 24 hours before the onset hematuria Decreased albumin increase alfa 2 globulin the former reflect urinaria loss -> indicate acute inflamation

Nephrotic sindrome
Characterized : by marked proteinuria, decrease plasma protein, generalized edema, rise in serum lipids

Renal and systemic disease might be associated with the nephrotic syndrome Glomerulonephritis, circulatory disturbances ( renal vein thrombosis ), toxin, Systemic disease , infection, malignancy Primary renal disease causing nephrotic syndrome is membranous nephritis

Proteinuria : Glomerular protein leaked -> failure of tubular protein reabsorption -> protein loss in the urine consist albumin ( 1/3 Ig G ) -> hipoalbunemia

Edema : Hipoproteinemia -> the loss of colloid oncotic pressure-> fluids to leak from blood vessels into the intertitial space -> reduce plasma volume and cardiact out put -> releasing renin -> stimulates aldosterone -> retention of sodium and water -> water leak into the intertitial space -> edema

Hyperlipidemia and lipiduria Increase plasma lipid -> due to increased lipid synthesis and decreased lipid -> result from increased glomerular permeablity

Laboratorium findings
Increased urine protein ( albumin ) ( > 3,5 gr / 24 hr -- > 20 gr / hr ) Decrease albumin ( usually < 2,5 gr/dl ), Increased : cholesterol ( 350mg/dl ) if to be come decreased or normal, occurs -> with poor nutrition and or poor prognosis , increased triglycerides, lipoprotein Increased alfa and beta globulins Decreased gama globulin ( IgG )

Urine ; Oval fat bodies ( are lipid containing renal tubular epithelial cell ) Increased sedimentation rate due to increased fibrinogen Decreased serum calcium reflect fall in serum albumin, ( Ca ion normal )