## Basic introduction:
## Primary causes of NS:
_There are no microscopically visible changes in the glomerulus on microscopy
_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 feature
_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.
## Secondary causes of NS:
_Diuretic therapy with Furosemide about 1 mg/kg/day with or without Spironolactone (2 mg/kg/day).
_IV albumin therapy in cases of extensive hypoalbuminemia (where the response to diuretic treatment is generally poor)
_Antibiotics (when infection is suspected or there is a need for prophylaxis)
_Corticosteroid therapy for 2-3 months may give some remission
_Immunomodulatory drugs such as cyclosporine, cyclophosphamide, and tacrolimus may be beneficial in patients who respond poorly to the steroid therapy.
_ACE inhibitors and ARBs can give provide some improvement of the outcome especially in adults
_Statins (for treatment of dyslipidemia)