Renal-Pathology Flashcards
What does the presence of casts in urine indicate? What causes RBC casts? WBC casts? Fatty casts? Granular casts? Waxy? Hyaline?
Hematuria/pyuria originates in the glomerulus or renal tubules
RBC=glomerulnephritis, malignant hypertension WBC=tubulointerstitial inflammation, acute pyelonephritis, transplant rejection Fatty casts (Oval fat bodies)=nephrotic Granular (muddy brown) = acute tubular necrosis Waxy= ESRD/CRF Hyaline=Non specific, maybe normal, concentrated urine
Concerning glomerular disorders, what does the term focal mean? Diffuse? Proliferative? Membranous? Primary? Secondary?
focal? 50% Proliferative? hypercellular glomeruli Membranous? Thickening of GBM Primary? primarily of kidney Secondary? systemic disease impacting glomerulus
What is the overall cause of nephritic syndrome? Lab findings? Specific causes?
GBM disruption
Hypertensin Incr. BUN and creatinine oliguria hematuria RBC casts in urine Proteinuria in subnephrotic range (<3.5 g/day)
Acute PSGN Rapidly progressive glomerulonephritis IgA nephropathy (Berger disease) Alport syndrome Membranoproliferative GN
What is the overall cause of nephrotic syndrome? Lab findings? Specific causes? Are the causes primary or secondary? How can it lead to a hypercoag state? How can it lead to infection?
Podocyte disruption–>charge barrier impaired
Proteinuria (>3.5 g/day) Hypoalbuminemia Hyperlipidemia Edema Frothy urine Fatty casts
Focal Segmental Glomerulosclerosis (prim. or sec.) Minimal change disease (prim or sec) Membranous nephropathy (1 or 2) Amyloidosis (2) Diabetic glomerulonephropathy (2)
Loss of ATIII in urine
Loss of IGs in urine.
What is nephritic-nephrotic syndrome? Pathophys? Lab findings? Specific causes? Most common?
Severe nephritic syndrome w/ GBM damage so bad it damages charge barrier leading to protein loss and other nephrotic syndrome features.
Can be caused by any nephritic disease, but usually
Diffuse proliferative GN
MPGN
What is seen in LM in acute PSGN? IF? Antibodies involved/location/type of HSR? EM? Epid? Prognosis? Presentation? Lab findings?
LM: Glomeruli enlarged and hypercellular
EM: Subenpithelial IC humps
IF: “starry sky” granular appearance “lumpy bumpy” due to IgG, IgM, and C3 deposition along GBM and mesangium
Usually in children, psost group A strep (2 weeks)
Type III HSR
Peripheral and periorbital edema, coca colored urine, hypertension
self-limiting
Incr. anti-DNAase B titers
Decr. complement levels
What is seen in LM and IF of RPGN? What is the composition? Prognosis? Causes? Findings/treatment/presentation in the specific causes?
LM/IF: Crescent moon shape consisting of fibrin and plasma proteins, with glomerular parietal cells, monocytes, macrophages
Poor prognosis. Rapidly deteriorating renal function.
CAUSES
Goodpasture-type II HSR; Abs to GBM (type IV collagen) and alveolar BM. Linear IF
Hematuria/hemoptysis
Emergent plasmapheresis
Granulamatosis w/ polyangiitis (Wegener): c-ANCA
Microscopic polyangiitis: p-ANCA
What are the causes of DPGN? What is seen on LM? EM? AB involved? Type HSR? IF?
LM: Wire looping of capillaries
EM:Sub endothelial and sometimes intramembranous IgG based ICs often w/ C3 deposition
IF:Granular
Causes: SLE (most common cause of death)or MPGN
What is seen on LM/EM/IF in IgA nephropathy? AB/Type of HSR? Causes? Presentation?
LM: Mesangial prolif.
EM: mesangial IC deposits
IF: IgA-based IC deposits in mesangium
Causes: henoch schoenlein purpura
Presentation: Renal insufficiency or acute gastroenteritis
Episodic hematuria w/ casts.
What is the pathophys of alport syndrome? Genetics? Presentation? EM?
Pathophys: Mutatin in type IV collagen leading to thinning and splitting of GBM
X=linked
Eye problems (retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness
EM: Basket weave appearance
Can’t see, can’t pee, can’t hear a buzzing bee
What is the appearance of type 1 MPGN on EM? IF? LM? Causes of type 1? What are the EM findings of type II MPGN? Pathophys of type II?
Type I
LM: Tram track appearance
EM: Subendothelial immune complex deposits
granular IF
Causes: Idiopathic or secondary to HBV or HCV
Type II
Intramembranous IC deposits; “dense deposits:
C3 nephritic factor (stabilizes C3 convertase leading to decr. serum C3 levels
What its seen on LM/EM/IF in FSGS? What is deposited? Epid? Causes? Treatment? Prognosis?
LM: Segmental sclerosis and hyalinosis
EM: Effacement of foot process similar to MCD
IF: Focal deposits of IgM, C3, C1
Epid: Most common cause of nephrotic syndrome in AA and Hisp.
Treatment: Primary has inconsisten response to steroids
Prognosis: May progress to chronic kidney disease
Cause: Primary or HIV, SCD, Heroin abuse, obesity, IFN treatment, chronic kidney disease
What is seen on LM/IF/EM in minimal change disease? epid? Causes? Complications? Treatment/prognosis?
LM: Normal glomeruli (maybe lipid in PCT cells)
EM: Effacement of foot processes
IF: neg.
Causes: Often idiopathic, triggered by recent infection or immunization
Epid: Most common cause in children
Treatment: Corticosteroids (excellent response)
What is seen on LM/IF/EM in membranous nephropathy? Epid? Causes? Treatment/prognosis?
LM: Diffuse capillary and GBM thickening
EM: Spike and dome appearance w/ subepithelial deposits
IF: Granular (IC deposition)
Causes: Primary or antibodies t PLA2 receptor, NSAIDS/penicillamine, HBC/HCV, SLE, solid tumors)
Epid: Most common cause of primary nephrotic syndrome in caucasian adults
Treatment: Poor response to steroids
Prognosis: May progress to chronic renal disease
What is seen on LM in amyloidosis? Associations?
LM: Congo red stain shows apple=green birefringence under polarized light
Kidney is most commonly involved organ in system. amyloidosis
Mult. Myeloma, TB, RA
What is seen on LM of diabetic glomerulonephropathy? Pathophys?
LM: mesangial expansion, GBM thickening, Eosinophillic nodular glomerulsclerosis (Kimmelstein nodules)
Nonenzymatic glycosylation of GBM leads to thickening and incr. perm.
NEG of efferent arterioles laeds to incr. GFR and mesangial expansion.
How do kidney stones present? What are some severe complications? What is the main method of treatment/prevention?
Unilateral flank tenderness, colicky pain radiating to groin, hematuria
Hydronephrosis, pyelonephritis
Encourage fluid intake
At what pH do calcium kidney stones precipitate? In what form? x ray findings? Crystal description? Causes? Most common presentation (lab findings)? Treatment?
Incr. pH (calc phosphate)
Decr. pH (calc. oxalate)
Radioopaque
Envelope or dumbell shaped calcium oxalate
Ethylene glycol ingestion, vitamin C abuse, hypocitraturia, malabsorption (crohns)
Stone w/ hypercalciuria and normocalcemia
hydration, thiazides, citrate
At what pH do ammonium magnesium phosphate kidney stones precipitate? x ray findings? Crystal description? Causes? Most common presentation (lab findings)? Treatment?
Incr. pH
Radioopaque
Coffin lid
Struvite
Infection with urease + bugs (proteus, staph sapro, klebsiella) that hydrolyze urea to ammonia leading to urine alkalinization
Staghorn calculi
Eradication f underlying infection
Surgical removal of stone
At what pH do uric acid kidney stones precipitate? x ray findings? Crystal description? Risk factors? Imaging? Associations? Treatment?
Decr. pH
Radiolucent
rhomboid or rosettes
Decr. urine volume, arid climates, acidid pH
Visible on CT and U/S, not xray
Hyperuricemia
Diseases w/ incr. cell turnover, such as leukemia
Alkalinization of urine
Allopurinol
At what pH do cystine kidney stones precipitate? x ray findings? Crystal description? Pathophys? Epid? Possible presentation? Diagnosis? Treatment?
Decr. pH
RAdiolucent
Hexagonal
Autorecessive condition in which cystine reab PCT transporter loses function leading to cystinuria. Cystine is poorly soluble, thus forming stones
Children
Can form staghorn calculi
Sodium Cyanide Nitroprusside test
Alkalinization of urine
What is hydronephrosis? Usual cause? Other causes? Results? When does serum creat. become elevated?
Distention/dilation of renal pelvis and calyces
Urinary tract obstruction (renal stones, BPH, cervical cancer, injury to ureter)
Retroperi fibrosis, vesicoureteral reflux
Only if obstruction is bilateral
compression and possible atrophy of renal cortex and medulla
Histo of Renal cell CA? Epid? Risk factors? Presentation? Spread? treatment? Mutation? ASsociated PNP sydromes? Why is it “silent” cancer?
PCT cells become polygonal clear cells filled with accumulated lipids and carbs
Men 50-70
Smoking and obesity
Hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss
Invades renal vein then IVC then to lung and bone
Resection if localized
Immunotherapy or targeted therapy if spread
chemo and radiation doesn’t work
Most common rimary renal malignancy
VHL (chrom. 3 deletion)
EPO, ACTH, PTHrP
Commonly presents as metastases
What is a renal oncocytoma (cell make up)? Histo? Presentation? Treatment?
Benign epithelial cell tumor (well circumscribed mass w/ central scar
Large eosino cell w/ abundant mitochondria and no peirnuclear clearing
Painless hematuria, flank pain, abdominal mass
Resected to exclude malignancy