Glomerular lesions in acute GN are the result of glomerular deposition or in situ formation of immune complexes.

On gross
appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and
infiltration with polymorphonucleocytes (see Histologic Findings). Immunofluorescence reveals deposition of immunoglobulins
and complement.
Except in PSGN, the exact triggers for the formation of the immune complexes are unclear. In PSGN, involvement of derivatives
of streptococcal proteins has been reported. A streptococcal neuraminidase may alter host immunoglobulin G (IgG). IgG
combines with host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the glomeruli. In addition,
elevations of antibody titers to other antigens, such as antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase,
provide evidence of a recent streptococcal infection.

Structural and functional changes

Acute GN involves both structural changes and functional changes.
Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft because of the proliferation of
endothelial, mesangial,[1] and epithelial cells. The proliferation may be endocapillary (ie, within the confines of the glomerular
capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial cells). In extracapillary proliferation, proliferation
of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive GN.
Leukocyte proliferation is indicated by the presence of neutrophils and monocytes within the glomerular capillary lumen and
often accompanies cellular proliferation.
Glomerular basement membrane thickening appears as thickening of capillary walls on light microscopy. On electron
microscopy, this may appear as the result of thickening of basement membrane proper (eg, diabetes) or deposition of electrondense material, either on the endothelial or epithelial side of the basement membrane. Electron-dense deposits can be
subendothelial, subepithelial, intramembranous, or mesangial, and they correspond to an area of immune complex deposition.
Hyalinization or sclerosis indicates irreversible injury.
These structural changes can be focal, diffuse or segmental, or global.
Functional changes include proteinuria, hematuria, reduction in GFR (ie, oligoanuria), and active urine sediment with RBCs and
RBC casts. The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular volume,
edema, and, frequently, systemic hypertension.

Poststreptococcal glomerulonephritis
Streptococcal M-protein was previously believed to be responsible for PSGN, but the studies on which this belief was based
have been discounted. Nephritis-associated streptococcal cationic protease and its zymogen precursor (nephritis-associated
plasmin receptor [NAPlr]) have been identified as a glyceraldehyde-3-phosphate dehydrogenase that functions as a
plasmin(ogen) receptor.
Immunofluorescence staining of renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in earlyphase acute PSGN, and glomerular plasmin activity was almost identical to NAPlr deposition in renal biopsy tissues of acute
PSGN patients. These data suggest that NAPlr may contribute to the pathogenesis of acute PSGN by maintaining plasmin
activity.[2]
Antibody levels to nephritis-associated protease (NAPR) are elevated in streptococcal infections (group A, C, and G) associated
with GN but are not elevated in streptococcal infections without GN, whereas anti-streptolysin-O titers are elevated in both
circumstances. These antibodies to NAPR persist for years and perhaps are protective against further episodes of PSGN. In a
study in adults, the two most frequently identified infectious agents were streptococci (27.9%) and staphylococci (24.4%). [3]
Acute glomerulonephritis is a disease characterized by the sudden appearance of edema, hematuria, proteinuria, and
hypertension. It is a representative disease of acute nephritic syndrome in which inflammation of the glomerulus is manifested
by proliferation of cellular elements secondary to an immunologic mechanism (see the following image). [1, 2]

Schematic representation of proposed mechanisms involved in the development of acute

poststreptococcal glomerulonephritis (APSGN).MES: mesangial cell; END: endothelial cell; PMN: polymorphonuclear cell; M: macrophage; T:
T lymphocyte; GMB: glomerular basement membrane; C: complement; Anti-NAPlr-Ab: Anti-NAPlr-antibody.Courtesy of open access article,
"The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection." Oda T, Yoshizawa
N, Yamakami K, et al. Journal of Biomedicine and Biotechnology, 2012; doi: 10.1155/417675.

Acute poststreptococcal glomerulonephritis (APSGN) results from an antecedent infection of the skin (impetigo) or throat
(pharyngitis) caused by nephritogenic strains of group A beta-hemolytic streptococci. [3, 4, 5] The concept of nephritogenic
streptococci was initially advanced by Seegal and Earl in 1941, who noted that rheumatic fever and acute poststreptococcal
glomerulonephritis (both nonsuppurative complications of streptococcal infections) did not simultaneously occur in the same
patient and differ in geographic location.[6] Acute poststreptococcal glomerulonephritis occurs predominantly in males and often
completely heals, whereas patients with rheumatic fever often experience relapsing attacks.
The M and T proteins in the bacterial wall have been used for characterizing streptococci. Nephritogenicity is mainly restricted to
certain M protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that have shown nephritogenic potential. These may
cause skin or throat infections, but specific M types, such as 49, 55, 57, and 60, are most commonly associated with skin
infections. However, not all strains of a nephritis-associated M protein serotype are nephritogenic. [7] In addition, many M protein
serotypes do not confer lifetime immunity. Group C streptococci have been responsible for recent epidemics of APSGN
(eg, Streptococcus zooepidemicus). Thus, it is possible that nephritogenic antigens are present and possibly shared by
streptococci from several groups.[2]
In addition, nontypeable group A streptococci are frequently isolated from the skin or throat of patients with glomerulonephritis,
representing presumably unclassified nephritogenic strains.[7] The overall risk of developing acute poststreptococcal
glomerulonephritis after infection by these nephritogenic strains is about 15%. The risk of nephritis may also be related to the M
type and the site of infection. The risk of developing nephritis infection by M type 49 is 5% if it is present in the throat. This risk
increases to 25% if infection by the same organism in the skin is present.

Washer machine of the body the kidneys help to wash the blood from toxins, chemicals but
mainly drugs that you take.
The easiest way to remember what the kidney do is a little acronym that call fre the pee
F- filter- filter three things H ydrogen(acidic to the body) Urea (by product of protein
metabolism)Creatinine( another by product of protein)
R-reabsorb( we are talking about the reabsorption of the water
E-eliminate (eliminate 2 things that is toxins but mainly drugs