High levels of cholesterol (hypercholesterolemia), specifically elevated LDL
Electrolytes, urea and creatinine (EUCs): to evaluate renal function
Biopsy of kidney
Excessive permeability of plasma proteins - >> heavy proteinuria
Depletion of plasma proteins , mainly albumin - hypoalbuminaemia
Liver compensates but not successful - >> reversed A:G ratio
Reduced albumin -> decreased colloid oncotic pressure of the blood -> oedema
ADH is stimulated - >> oedema
Increased Lipoprotein synthesis and decreased catabolism by liver ->> Hyperlipidaemia (mainly VLDL and /or LDL)
HDL is also lost in urine when heavy proteinuria occurs
Loss of body proteins (immunoglobulins /complement) -> frequent infection
Loss of anticoagulants antithrombin III , antiplasmin - > thrombotic and embolic phenomenon
Major cause of NS in adults
Characterised by presence of electron-dense immune deposits along the epithelial side of GBM (subepithelial )
Idiopathic in 85% of patients
The 15% remaining GN is associated with malignant tumors , SLE , drugs , infections or metabolic disorders
Membranous GN Sub-epithelial immune Complex deposits Thickened GBM
Membranous GN H&E
Membranous GN IF
Capillary Lumen GBM GBM Membranous GN EM
MINIMAL CHANGE DISEASE
the major cause of nephritic syndrome in Children
normal glomeruli on light Microscopy
uniform and diffuse effacement of the foot Processes of visceral epithelial cells on electron microscopy
Immunofluorescence shows no immune deposits
The cause and pathogenesis are unknown
dramatic response to corticosteroid therapy.
long-term prognosis is excellent.
MINIMAL CHANGE DISEASE Foot Process Fusion
sclerosis of some, but not all, glomeruli (thus, it is focal)
FSG can be.
* A secondary evernt, refecting glomerular scarring, consequent to another primary glomerular disease (e.g., IgA nephropathy).
* associated to other known disorders (e.g. heroin abuse, HIV infection, obesity).
* The result of inherited mutations of proteins present in podocytes (podocin, a –actinin) or in the slit diaphragm between podocytes (nephrin).
1- Light Microscopy:
Normal and diseased glomeruli (Focal)
Segmental tuft sclerosis in diseased glomeruli
Deposits of IgM and C3
Focal fusion of foot processes
Thickness of capillary loops and glomerular cell proliferation
Glomeruli have a lobular appearance because of mesangial proliferation
Capillary walls often have a double-counter or tram-track appearance
Type 1 has subendothelial electron-dense deposits of immunoglobulins and complements
It occurs in patients with SLE , hepatitis B and other diseases
Type 2 has electron-dense GBM deposition in a confluent ribbon-like fashion
Type 2 is due to activation of alternative pathway of complement activation
Figure 8. Pathology of membranoproliferative glomerulonephritis type I. (a) Light microscopy shows a hypercellular glomerulus with accentuated lobular architecture and a small cellular crescent (methenamine silver).
IGA NEPHROPATHY (BERGER DISEASE)
the most common type of glomerulonephritis worldwide
major cause of recurrent glomerular hematuria
By light microscope, the glomeruli can appear nearly normal, showing only subtle mesangial hyprcellularity, or can reveal focal proliferative or sclerotic lesions
The pathogenesis is nuclear
although a genetic or acquired defect in immune regulation leading to increased mucosal IgA secretion. There isalso decreased clearance of IgA complexes by the liver.
Similar IgA deposits are seen in Henoch-Schönlein purpura in children
hematuria typically lasts for several days
chronic renal failure develops in 50% over a period of 20 years