## Non-proliferative or nephrotic syndrome class include the following:
_There are no microscopically visible changes in the glomerulus on microscopy
_It is the most common cause of the nephrotic syndrome in children
_It is managed with corticosteroids
_It does not progress to chronic renal disease
_This is associated with sclerosis (hardening) of parts of some glomerulus
_Its causes include HIV, heroin abuse and idiopathic
_Corticosteroids can provide some relief
_50% of cases will end up with renal failure
_It can manifest either nephrotic or a nephritic features
_It is caused by auto-antibodies to phospholipase A2 receptor (2/3 of cases), cancers of the lungs, cancers of GIT, hepatitis B virus infection, malaria, penicillamine, systemic lupus erythematosus and cerebral shunts among others.
_The pathology of MGN involves thickening of glomerular basement membrane with minimal hyperproliferation of the glomerular cells. Features of Type III hypersensitivity reaction are also evident.
_1/3 of patients remain with the disease, 1/3 remit, and 1/3 progress to end-stage kidney failure.
_This is an autosomal dominant inherited disease characterized by thin glomerular basement membranes
_It is a benign disease with key presentations of persistent microscopic hematuria as well as mild proteinuria.
_It shows very good prognosis.
## Proliferative or nephritic syndrome class include the following:
_It is the dominant type of glomerulonephritis
_Its pathology involves deposition of IgA in the space between glomerular capillaries
_Its clinical presentation include isolated visible or occult hematuria with or without a low-grade proteinuria
_It occurs as a late complication of pharyngitis or skin infections mainly due to a nephritogenic strain of β-hemolytic streptococci (although other bacterial infections can as well)
_It is the main cause of Acute Glomerulonephritis (AGN). For the details refers to disease description “Glomerulonephritis, Acute Post-streptococcal, APSGN” in this publication.
_Its main clinical features include microscopic hematuria, brown/pink and foaming urine, proteinuria, edema (with puffiness of the face), and hypertension
_RPGN is characterized by a rapid, progressive deterioration in renal function presenting as a nephritic syndrome
_It shows very prognosis
_There are 3 main types of RPGN: Type 1, Type 2 and Type 3
_Type 1 (or Goodpasture syndrome): it is an autoimmune disease of the lung where IgG antibodies directed against the glomerular basement membrane are produced. These IgG antibodies trigger an inflammatory reaction that culminates to the nephritic syndrome as well as the coughing up of blood. It managed with high dose methylprednisolone (or any other steroid), cyclophosphamide and plasmapheresis.
_Type 2 RPGN is caused by the immune-complex-mediated reaction associated with systemic lupus erythematosus, post-infective glomerulonephritis, IgA nephropathy, and IgA vasculitis
_Type 3 RPGN (Pauciimmune type): It is associated with vascular inflammation
_The pathology of this disease involves increased number of cells in the glomerulus and changes in the glomerular basement membrane
_Two primary subtypes exist namely Type 1 MPGN and Type 1 MPGN
_Type 1 MPGN (caused by circulating immune complexes) is caused by diseases such as systemic lupus erythematosus, hepatitis (B & C) infection among other infections. Circulating immune complexes may activate the complement system, leading to inflammation and an influx of inflammatory cells
_Type 2 MPGN (Dense Deposit Disease) is caused by an excessive activation of the complement system.
_It presents with features of nephritic syndrome as well as hypocomplementemia.
_The condition has a poor prognosis
## Nephrotic syndrome: