Kidney Diseases Glomerulopathies Flashcards
Glomeruli are responsible for
Filtration of blood
Produce ultra-filtrate
Endothelial fenestrae
Pores that allow filtration of blood to occur
Kidney is a
Bunch of glomeruli and tubules that controls electrolyte balance and acid base balance and produces renin
Define Glomerulonephritis
Inflammation
Primary disease =
Affects the glomerulus FIRST
Autoimmune
Chronic glomerulonephritis =
Most common cause of CKD
Primary Glomerulopathies (high potential to progress to chronic)
Rapidly progressive (crescentic) Membranous glomerulopathy Minimal-change disease Focal segmental glomerulosclerosis Membranoproliferative IgA nephropathy
Acute proliferative
Associated with infection
Last for a few weeks and then goes away
No serious consequences
Amyloidosis
Disease in which you have deposition of certain stage proteins in different parts of the body
Leads to an inflammatory reaction
Systemic disease with glomerular involvement
Lupus
DM
Amyloidosis
Glomerulus Pathology
Blood enters through afferent arteriole
Blood leaves through the efferent arteriole
Primary ultra-filtrate accumulates in the Bowman’s capsule
When blood leaves it has to pass through endothelial basement membrane and podocytes
Juxtaglomerular cells produce
Renin after sensing a change in BP
(Stretch = increase BP –> they act
Kidney filtration barrier
Between podocytes there is space which is where the filtrate occurs
Pathogenesis Main
Antibody-Mediated Injury (in situ immune complex deposition)
Antibody-Mediated Injury
Immune complexes formed inside you leads to circulating antibodies and antigens in the kidney
A lot of immune complexes in the plasma and kidney
Cytotoxic antibodies go and kill certain cells
Complement Pathway
T cells go to the kidney and destory some of the kidney structure –> complement is activated –> destroy cells via cell lysis through terminal complement complex which leads to holes in the cytoplasmic membrane
Where do antibodies deposit
Within the filtration barrier (under the endothelium, within basement membrane, under the epithelium)
Testing for Antibody-Mediated Injury
Use antibodies to detect antibody complexes
Important bc glomerularnephritis is very harsh
Epithelial injury Pathogensis
After deposition, destruction of components of the barrier (basement membrane, podocytes) –> process are becoming flat –> podocyte effacement –> barrier is leaky and proteinuria
Mediator of Injury Pathogenesis
Immune complexes can active classical branch of complement
C5b-9
Incorporate themselves into the membrane and make holes –> cell lysis
C5a
Potent inflammatory mediator
Attracts chemokines greatly and causes production of oxidants, cytokines, chemokines
What disease progress to chronic glomerulonephritis?
Crescentic GN
Focal segmental glomerulosclerosis
Membraneoproliferative GN
Membranous nephropathy
Clinical manifestations:
Nephritic syndrome Rapidly progressive Nephrotic syndrome Chronic Renal Failure Isolated urinary abnormalities
Nephritic syndrome Symptoms
HEMATURIA Azotemia Proteninuria Oliguria Edema HTN
Nephrotic syndrome Symptoms
PROTEINURIA >3.5 g/d Hypoalbuminemia Hyperlipidemia Lipiduria Edema
Nephritic syndrome Etiology
Primary Glomerular Disease (acute proliferative GN) Systemic disease (SLE)
Nephrotic syndrome Etiology
Primary: Membranous GN, minimal change disease (children- given steroids and everything goes back to normal = nephrotic)) and focal segmetnal
Nephrotic Syndrome Systemic Disease
DM
Amyloidosis
SLE
Malignancy
