Renal - Pathology Flashcards
inferior mesenteric artery root implicated in this congenital problem
horseshoe kidney
most common congenital renal anomaly
Bilateral renal agenesis 1 problem w/3 complications
Also known as
oligohydraminos
- > lung hypoplasia, flat face w/ low set ears, developmental extremity problems
- potters syndrome
Unilateral renal agenesis complication
hypertrophy and later hyperfiltation later on leading to renal failure risk
Noninherited congenital renal malformation characterized by cysts
what histology seen
dysplastic kidney (usually unilateral)
Collagen adjacent to cysts
inherited defect w/ cysts in the renal cortex and medulla
Polycystic kidney disease
infantile and adults
inherited defect w/ cysts in the medullary collecting duct
Seen grossly
Medullary cystic disease (Auto Dom)
shrunken kidneys
ADPCK presents as (3)
associated w/(3)
Adults w/ HTN, hematuria and worsening renal failure
berry aneurisms
hepatic cysts
mitral valve prolapse
Infantile PCKD presents as
Auto recessive
presents as renal failure and infantile HTN
also have hepatic fibrosis w/ hepatic cyst formation
Acute renal failure seen as
Azotemia and oliguria seen w/in days
Divided into pre renal, post renal and infrarenal
Azotemia def
increased BUN and Creatinine in serum
Prerenal azotemia due to?
See:(3)
BUN:Creatinine
FENa ?
Osm?
decreased blood flow
See decreased GFR, azotremia and oliguria
BUN:Creatinine >15, low flow means BUN can resorb, renin aldosterone working to increase BUN level
FENa 500 mOSM/kg - tubes are fine
Postrenal azotremia ude to
See (3)
BUN:Creatinine
FENa
Osm
obstruction downstream
See low GFR, azotemia and oliguria
Depends:
Early
- BUN:Cr >15, BUN forced into serum w/ backpressur
-FENa 500 mOsm, tubes fine
Late - tubular damage - Can’t resorb as well
-BUN:Cr 1%
Osm <500mOsm
Intrarenal Tubular necrosis is
Types(2)?
Problem w/in the kidney(block) usually resulting in BUN:Cr < 15 ( overall increase in BUN and creatinine)
FENa >1%
Osm <500 mOSM
Acute Tubular Necrosis - tubes
Acute interstitial nephritis - surrounding tissue
Causes of Acute tubular necrosis (2)
Ischemia
- low blood supply, preceded by pre renal azotemia
Nephrotoxic
-aminoglycosides, heavy metals. myoglobinuria(crush injury), ethylene glycol, radio contrast die, urate (tumor lysis syndrome(
Brown granular cases in urine seen in
necrotic cells plugging the tubule in acute tubular necrosis
Tumor lysis syndrome
What is it and prevention?
acute leukemia treated w/ chemo -> increased nuclear material in the blood
Rx w/ hydration and allopurinol
Acute interstitial nephritis Due and causes (3)
Drug induced hypersensitivity of surrounding tissue
NSAIDs, penicillin and diuretics
Clinical features of acute tubular necrosis (3)
oliguria w/ brown granular casts
elevated BUN and Creatine
Hyperkalemia(reduced excretion) w/ metabolic acidosis (decreased organic acid excretion)
eosinophils seen in urine?
acute interstitial nephritis
Renal papillary necrosis
Presentation(2) and causes (4)
gross hematuria and flank pain w/ necrotic renal papillae
Due to: chronic analgesic use, DM, Sickle cell severe acute pyelonephritis
Nephrotic syndrome = what seen
4 complications
> 3.5 g.day filtered
leading to
hypoalbuminemia -edema
hypogammaglobinemia - infection risk
hypercoaguable - loss of anti thrombin III
Hyperlipidemai and hypercholesterolemia - fatty casts in urine (liver wants to thicken blood)
Most common syndrome in kids
Associated w/
minimal change disease
Hodgekin lymphoma - due to cytokine release leading the change
effacement of foot processes on electron microscopy (2)
Rx?
minimal change disease or focal glomerulosclerosis
Steroids, great response in KIDS,
not adults w/ FSGS -> renal failure
HIV, heroin and sickle cell associated nephrotic syndrome
Focal semental glomeulosclerosis
Usually idiopathic
MOST COMMON - hispanic and African americans
Membranous nephopathy is associated w/ (5)
used to be most common - usually idiopathic
HepB HepC solid tumors SLE - (diffuse prolifererative glomerulinephritis more common) Drugs (NSAIDs and penicillamine)
Thick glomeruli basement membrane on H and E w/ immune complex deposits (granular) (2)
Membranous nephropathy
Membranoproliferative glomerulonephritis
(can be nephritis too)
Deposits go to all 3 areas
- subepithelial - membranous nephropathy
- subendothelial - Type I membranoproliferative gom
- BM - type II membranoproliferative glom
Spike and dome appearance EM
Membranous nephropathy -
Podocytes like to be on BM and will lay down BL over subepithelial deposits
Tram Track appearance on Em
Associated w/
Membranoproliferative Glomerulonephritis Type 1
(HBV and HCV)
Mesangial cells adjacent proliferate w/ sub endothelial deposits and tries to split deposit w/ increased cytoplasm -> tram track
Associated w/ C3 nephritic factor
What is It?
membranoproliferative glomerulonephritis Type II
intramembranous deposit (BM)
Antibodies stabilize C3 convertase instead of destroying it -> hyperactive complement activation inflammation and decreased C
nonenzymatic glycosylation of vascular BM -> hyaline arteriolosclerosis
Diabetes mellatis nephrotic syndrome
Kimmelstiel Wilson nodules
Sclerosis of the mesangium seen in DM nephrotic syndrome
Protective agent in DM nephrotic syndrome
ACE inhibitors
Prevents further clamping of the efferent arteriole and associated hyper filtration (selected in the disease progression)
Nephrotic syndrome w/ apple green birefringence
deposits are what type and where?
Systemic Amyloidosis involves kidney most commonly
deposits in the mesangium
AL seen from original cause multiple myeloma
6 types of nephrotic syndrome
Minimal change disease
Focal segmental glomerulosclerosis
Membranous Nephropathy Membranoproliferative Glomerulonephritis (nephritic as well)
Diabetes Mellitus
Systemic Amyloidosis
Nephritic syndrome characterized by(2)
Also see
glomerular inflammation(hyper cellular) and bleeding
limited proteinuria periorbital edema and HTN
RBC casts
Hypercellularity in nephritic syndrome is due to
Immune complex deposition and activation of complement -> C5a recruitment of PMNs