Renal: glomerular dzs, nephrotic, nephritic Flashcards
define glomerulopathies
significant cause of kidney disease
- acute and chronic
- group of diseases
Glomerulonephopathies can result from
- systemic inflammatory dz—>glomerulonephritis
2. non-inflammatory dzs–>metabolic dz–>DM, herediatary nephropathies like Alport’s
primary glomerulopathies occur where
kidney
secondary glomerulopathies occur
multisystem dz involving kidneys
–ex SLE
degree of proteinuria determisn?
if its nephrotic or nephritic
normal amt of protein in urine in 24 hrs?
100-200 mg/hr
how does protein get into the urine?
- inflammation alters GBM (podocytes) permeability (normally resitricts things by size and charge…aka proteins)
- incrs in GBM permeability= pore sizes enlarge and RBCs and protein can pass through
types of PU
- orthostatic or postural–>elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent posiiton
- overproduction
- tubular
- glomerular dysfunctino
nephritis versus nephrotic
- define each
- basic CM for each one
Nephritic=caused by systemic inflammation/ immune complex dz (SLE, vasculitis) or an infection
*inflammation in glomerulus=BLEEDING
*renal vascular changes that cause HTN
*Proteinuria <3,000
TYPES=post infectious glomerulonephropathy (post strep), IGA nephropathy, Memabnoproliferative
Nephrotic= damange to filterting mechanism–leading to protein wasting in urine—>protein waisitng causes decr serum protein (hypoproteinemia.MC seen as hypoalbuminemia),
*decr serum protein= causes HYPOTONIC surroundings–>so fluid flows OUT of HYPOtonic–>
- EDEMA**
- *liver tries to compensate by producing more proteins…. and in doing so makes more lipids too
- Proteinuria >3,000
- hypoproteinuria
- hyperlipidemia
TYPES=minimal change dz, focal segmental glomerulura sclerosis, membranous nephropathy, DM nephropathy
greater degree of proteinuria=?
nephrotic
>3,000
injury to podocytes
nephrotic
inflammation causing enalrged pores and “leaky” glomeruluar BM
nephritic
describe the sediment for nephrotic
urine bands
urine >3,000 PU in 24/hrs
+lipidemia
+hyperlipidemia—>seen as oval fat bodies and maltese cross
+/- microscopic hematuria
describe urine sed for nephritic
“acitve”
- hematuria
- RBC casts
- WBC casts
- Proteinuria variable… <3,000 BUT over >1 gram
MC causes for transient PU
stessful conditions–>fever, exercise, CHF,
major causes of nephritic syndrome
auto-immune or allergic interstitial inflammation
heavy metal intoxications
drug-induced intersitial injury
major causes of nephrotic syndrome
primary and secondary glomerular dzs
dm
htn
typical clinical findings in a pt with nephrotic syndrome
- **EDEMA (bc major loss of protein.. mainly albumin)
- hyperlipidemia
- hypoproteinemia-hypoalbuminemia
define abnormal amt of PU
over 200 about
Glomerulonephritis
-define
Inflammation/proliferation of glomerular tissue, scaring and fibrosis
-immune complexes (antigen/AB) form in ciruclation–>activation of compliment–>recruit and activate immune cells–>deposite in glomerulus–>cause damage to GBM, mesanial or capillary endothelium
ANTIGEN CAN BE TO:
- ->glomerular antigens
- ->glomerular BM
- ->trapped as circulating immune complexes
- ->cell mediated
**basically antigens/AB can be made directly against the GBM or there was an infection (strep) and those antigens/AB get trapped in glomerulus=inflammation
mechanisms contributing to decline in GFR for glomerulonephritis
- ***decr glomerular perfusion secondary to
1. inflammation
2. scarring/sclerosis
3. thickening of glomerular basememt membrane with increased permeability to proteins and RBC
causes of glomerulonephritis
- post infectious GN
- IgA nephropathy
- membranoproliferative glomerlunonephropathies (MPGN)
- Rapidly progresive crescentic GNs
MCC of nephritic syndrome
IGA nephropathy
Post-infectious Glomerulonephritis
- mcc
- other causes
MC etiologies= STREP 2nd to nephritic strain of B-hemolytic GAS
other causes= SKIN or respiratory sources, Hep B, Hep C, Malaria, Syphilis, HIV
IgA Nephropathy
- another name
- explain
- MC population and gender
- etiology
Berger Dz
abnormal IgA immune complexes binds to glomerular mesangial cells–>cause injury
*IGA is first line defense in respiratory and GI secretions—so infections cause an OVERPRODUCTION which then damage kidneys
MC affects young males
**24-48 HOURS after URI or GI infection
Membranoproliferative GN
- mcc
- typical lab finding and what it means
immune complex mediated
- involves mesanigal cell proliferation and complement deposition
- gives glomurli a lobular apperance due to mesangial proliferation
- the GBM splits–> causing Tram tracking or double counter apperance on histology
ASSOC WITH HEP C—tx the hep c— MPGN goes away
HUS Vasculitis
- often asoc with
- explina patho
HEMOLYTIC UREMIC SYNDROME
- *e. coli diarrhea shiga-toxin
- MCC of ARF in kids
- complement dysregulation via gene mutations
- antibodies to complement factor H
SECONDARY CAUSES
-infection: shiga toxin producing E. coli or strep pneumoniae or HIV
Lupus GN
- mc type
- pu levels
diffuse lupus nephritis class IV **alllllll over leads to progressive kidney dz
six types
PU mostly nephritic— but sometimes cna show nephrotic range
rapidly progressive GN (RPGN)
- characterized by?
- types
- crescent lesions–acute chronic or mixed
- cresents form from fibrin and plasma potein despotiion collapsing the cresecent shape of bowmans capsule
- crescents may be secondary to severe injury to glomerular capillary wall
- severity of dz correlates to degree of crescents
- ***ANY CAUSE OF AGN CAN PRESENT WITH RPGN–the following ONLY PRESENT WITH RPGN
TYPES
- anti-GBM–>goodpastures
- Pacui-immune–ANCA assoc vasculitis—> Wegners (granulomatosis polyangiitis and Microscopic polyangiitis
Wegners aka Granulomatosis Polyangiitis
- whart is it
- (+) ???
- classically involves what part of body
systemic vasculitis of MEDIUM AND LARGE size arteries
90% are ANCA (+)
—-> C-ANCA= 80%–> ANTI-PROTEINASE 3 ****
—-> P-ANCA=15%
involves–>upper and lower resps, kidneys
microscopic polyangiitis
renal small vessel vasculitis
-usually renal limited
*abesence of granulmatosis inflammation—how to tell the difference on biopy b.w this and wegners
70%= P-ANCA
Goodpastures
- type of rxn
- explain age distribution
Type 2 hypersensitivity—AB mediated
- ***ANTIBODIES TO: type IV collagen in lungs and kidney
1. anti-GBM—->GN (renal)
2. anti-alveolar BM—>alveolar hemorrhage (pulm) —>hemoptysis
BIOMODAL age distribution—> 3rd and 6th decade of life (can presnt in 30s,,, and then again in 60s)
M»>F
Nephrotic
- cause thought to be secondary to?
- primary etiologies
- secondary etiologies
podocyte malfunction or injury
PRIMARY ETIOLOGIES
- membranous
- Focal Segmental Glomerular Sclerosis
- Minimal Change dz
SECONDARY ETIOLOGY:
4. Diabetic Nephropathy
reason for hyperlipidemia in nephrotic syndrome
increased synthesis from liver and decreased catabolism
- hepatic lipoprotein synthsis is stimulated by decreased oncotic pressure–>hypercholesterolemia
- also acquired defect in LDL receptor that causes diminished clearance
- incrs trigs due to decreased catabolism NOT overproduction
why are PT at risk for thrombosis in nephrotic syndrome
-DVT, PE, renal vein thrombosis
-multifactorial etiology
*increase urinary loss of anti-thrombin III, protein C and S
*increased platelet aggregation
BUT BOTH CAN LEAD TO ANASARCA—– total body swelling
minimal change dz
-loss of negative charge of basement membrane promotes proteinuria
KIDS*
T-lymphocyte abnormalities that lead to increased glom. permeability—> effacement of visceral epithelial foot processes
membranous nephropathy
increased glomerular permeability and glomerulosclerosis
-idiopatic
or
-secondary forms
*circulating IGG against antigen PLA2R on GBM
Focal Segmental glomerulosclerosis (FSGS)
-
- idiopathic
- primary
- secondary
- genetic
2nd to circulating factor toxic to the podocyte–can be adaptive
“FOCAL” bc involves some glomeruli but not others
“SEGMENTAL” bc involves a segment of glomerulus
NOT THE WHOLE GLOMERULUS THO
