ASN QBank Pearls - Glomerular and Vascular Disorders Flashcards
have often been associated with increased risk for progression of diabetic
nephropathy
smoking and HTN
which genetic screening test is likely to detect a mutation in more than 5% of sporadic FSGS in adolescents?
mutations in NPHS2 (podocin) gene, including p.R229Q variant
possible kidney biopsy findings in MM nephropathy
- fractured tubular casts
- Congo red–positive glomerular and tubular deposits
- acute tubular injury/necrosis
- plasma cell infiltrates
amyloidosis fibril size
9 to 12 nm
cryoglobulinemic GN microtubule shape and size
- curved
- 25-35 nm
immunotactoid glomerulopathy microtubule pattern and size
- parallel arrays
- > 30 nm
fibrillary GN fibril pattern and size
- RANDOM
- 15-30 nm
lupus nephritis IG pattern
“fingerprint”
treatment for idiopathic MCD
- sodium and fluid restriction
- furosemide
- statins
- ACEI
- high-dose prednisone daily or on alternate days
spontaneous remission rate of nephrotic syndrome in iMCD
1/3, but may take up to 2 years or more
treatment of steroid-resistant FSGS
cyclosporine A often in combination with low-dose prednisone
lesion associated with highest response rate to treatment with steroids and has the BEST prognosis in nephrotic patients with FSGS
tip lesion
has not been shown to be effective treatment in patients with idiopathic membranous glomerulonephritis (iMGN)
prednisone alone
multiple myeloma with acute cast nephropathy clues
- very low anion gap
- hypercalcemia
- anemia
- presence of trace urine protein by dipstick
- elevated UPC on direct measurement
- protein electrophoresis shows IgG kappa paraprotein
HIVAN
collapsing FSGS
HIVAN bp
rarely hypertensive
hepatitis B–induced membranous GN is usually associated with
hepatitis BeAg immune complexes in the subEPIthelial space
hepatitis BsAg-induced MPGN is usually associated with
subENDOthelial deposits due to the different sizes of molecules
hepatitis C leads to what type of cryoglobulinemia
type 2
hepatitis C leads to what type of MPGN
type 1 MPGN
cryoglobulins activate which complement pathway
classical complement pathway
HIV directly infects renal tissue including the
- podocytes
- mesangial cells, and
- renal tubular cells
associated renal lesion;
- hepatitis A
postinfectious GN (PIGN)
associated renal lesion;
- HIV
collapsing FSGS
associated renal lesion;
- hepatitis C
MPGN
associated renal lesion;
- hepatitis B
membranous GN
HIVAN or collapsing FSGS is due to
active viral replication in the podocyte –> podocytes change to proliferative macrophages
treatment that may lead to an improvement in renal function and nephrotic syndrome in HIVAN
- HAART
- ACEI or ARB, and
- steroids