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Step One > Renal-Pathology > Flashcards

Renal-Pathology Flashcards

1
Q

What does the presence of casts in urine indicate? What causes RBC casts? WBC casts? Fatty casts? Granular casts? Waxy? Hyaline?

A

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
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2
Q

Concerning glomerular disorders, what does the term focal mean? Diffuse? Proliferative? Membranous? Primary? Secondary?

A 
focal? 50%
Proliferative? hypercellular glomeruli
Membranous? Thickening of GBM
Primary? primarily of kidney
Secondary? systemic disease impacting glomerulus
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3
Q

What is the overall cause of nephritic syndrome? Lab findings? Specific causes?

A

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
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4
Q

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?

A

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.

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5
Q

What is nephritic-nephrotic syndrome? Pathophys? Lab findings? Specific causes? Most common?

A

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

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6
Q

What is seen in LM in acute PSGN? IF? Antibodies involved/location/type of HSR? EM? Epid? Prognosis? Presentation? Lab findings?

A

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

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7
Q

What is seen in LM and IF of RPGN? What is the composition? Prognosis? Causes? Findings/treatment/presentation in the specific causes?

A

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

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8
Q

What are the causes of DPGN? What is seen on LM? EM? AB involved? Type HSR? IF?

A

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

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9
Q

What is seen on LM/EM/IF in IgA nephropathy? AB/Type of HSR? Causes? Presentation?

A

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.

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10
Q

What is the pathophys of alport syndrome? Genetics? Presentation? EM?

A

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

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11
Q

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?

A

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

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12
Q

What its seen on LM/EM/IF in FSGS? What is deposited? Epid? Causes? Treatment? Prognosis?

A

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

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13
Q

What is seen on LM/IF/EM in minimal change disease? epid? Causes? Complications? Treatment/prognosis?

A

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)

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14
Q

What is seen on LM/IF/EM in membranous nephropathy? Epid? Causes? Treatment/prognosis?

A

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

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15
Q

What is seen on LM in amyloidosis? Associations?

A

LM: Congo red stain shows apple=green birefringence under polarized light

Kidney is most commonly involved organ in system. amyloidosis

Mult. Myeloma, TB, RA

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16
Q

What is seen on LM of diabetic glomerulonephropathy? Pathophys?

A

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.

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17
Q

How do kidney stones present? What are some severe complications? What is the main method of treatment/prevention?

A

Unilateral flank tenderness, colicky pain radiating to groin, hematuria

Hydronephrosis, pyelonephritis

Encourage fluid intake

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18
Q

At what pH do calcium kidney stones precipitate? In what form? x ray findings? Crystal description? Causes? Most common presentation (lab findings)? Treatment?

A

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

19
Q

At what pH do ammonium magnesium phosphate kidney stones precipitate? x ray findings? Crystal description? Causes? Most common presentation (lab findings)? Treatment?

A

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

20
Q

At what pH do uric acid kidney stones precipitate? x ray findings? Crystal description? Risk factors? Imaging? Associations? Treatment?

A

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

21
Q

At what pH do cystine kidney stones precipitate? x ray findings? Crystal description? Pathophys? Epid? Possible presentation? Diagnosis? Treatment?

A

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

22
Q

What is hydronephrosis? Usual cause? Other causes? Results? When does serum creat. become elevated?

A

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

23
Q

Histo of Renal cell CA? Epid? Risk factors? Presentation? Spread? treatment? Mutation? ASsociated PNP sydromes? Why is it “silent” cancer?

A

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

24
Q

What is a renal oncocytoma (cell make up)? Histo? Presentation? Treatment?

A

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

25
Q

What is another name for a wilms tumor? Epid? Cellular make up? Presentation? Mtation? What are two syndromes that it can be part of?

A

Nephroblastoma

Most common renal malignancy of ages 2-4

Embryonic glomerular structures

Large palpable, unilateral flank mass and/or hematuria

Loss of function mutations of TSGs WT1 or WT2 on chrom. 11

Beckwith-Wiedemann
WAGR

26
Q

What are the symptoms of beckwith-wiedemann syndrome? WAGR complex?

A

Wilms tumor
macroglossia
organomegaly
hemihypertrophy

Wilms tumor
aniridia
genitourinary malformation
mental retardation

27
Q

Epid of transitional cell CA? Location? What suggests bladder cancer? Risk factors? Histology?

A

Most common tumor of urinary tract system

Renal calyces, pelvis, ureters, and bladder

Painless hematuria (no casts) suggests bladder cancer

Pee SAC

Phenacetin
Smoking
Aniline Dyes
cyclophosphamide

papillary growth lined by transitional epithelium with mild nuclear atypia and pleomorphism

28
Q

What is the pathophys of squamous cell CA of the bladder? Risk factors? Presentation?

A

Chronic irritation of urinary bladder leading to squamous metaplasia to dysplasia and squamous cell CA

Schistosoma haematobium, chronic cystitis, smoking, chornic nephrolithiasis

Painless hematuria

29
Q

What is an acute bacterial cystitis? Presentation? Risk factors? Causes? Lab findings? What does sterile pyuria and negative urine cultures suggest for a cause?

A

UTI=inflammation of urinary bladder

Suprapubic pain, dysuria, urinary frequency, urgency
Systemic signs absent

Female, sexual intercourse, indwelling catheter, diabetes mellitus, impaired bladder emptying

E. Coli (most common)
Sapro
Klebsiella
proteus mirabilis (ammonia scent of urine)

Positive leukocyte esterase
Positive nitrites for gram neg. organisms

N. gonorrhoeae or chlamydia

30
Q

What is the pathophys of acute pyelonephritis? Location? Presentation? Causes? Urine findings? CT findings? Risk factors? Complications? Treatment?

A

Neutrophils infiltrate renal interstitium

Cortex w/ relative sparing of glomeruli/vessels
Fevers, flank pain

Acending UTI
Hematogenous spread to kidney

WBCs in urine, possibly with casts

Striated parenchymal enhancement

Indwelling urinary catheter
Urinary tract obstruction
vesicoureteral reflux
DM
pregnancy

Chronic pyelo
renal papillary necrosis
perinephric abscess
urosepsis

Antibiotics

31
Q

What is the pathophys of chronic pyelonephritis? Usual underlying cause? Histo?

A

recurrent episodies of acute pyelo

Vesicoureteral reflux or chronically obstructing kidney stones (a chronic predisposition)

Course, asymmetric corticomedullary scarring, blunted calyx. tubules contain eosino cats resembling thyroid tissue (thyroidization of kidney)

32
Q

What is the pathophys/timetable of drug induced interstitial nephritis? Another name? Lab findings? Which drugs? Presentation?

A

tubulointerstitial nephritis

Acute interstitial renal inflammation

Pyuria (classically eosinophils)
Azotemia
Associated w/ fever, rash, hematuria, and flank tenderness, but can be asymptomatic

Drugs act as haptens, induce HSR leading to inflammation. 1-2 weeks after most drugs
Could be months after NSAIDs

Diuretics, penicillin derivatives, PPIs, sulfonamides, rifampin

33
Q

What is diffuse cortical necrosis? Pathophys? Associations?

A

Acute generalized cortical infarction of both kidneys

Due to combination of vasospasm and DIC

Obstetric catastrophies
Septic shock

34
Q

What is the epid. of acute tubular necrosis? Prognosis? Lab findings? What are the 3 stages like? Timetable for them? Describe the two different pathophysiologies. Histo?

A

Most common cause of acute kidney injury in hospitalized patients.

Often spontaneously resolves
Can be fatal, especially during initial oliguric phase

Incr. FENa (fractional excretion of sodium)
Granular (muddybrown) casts

Inciting event
Maintenance phase=oliguric; 1-3 weeks; risk of hyperkalemia, metabolic acidosis, uremia
Recovery phase=polyuric; BUN and serum creatinine fall; risk of hypokalemia

Ischemic: Secondary to decr. RBF (hypotension, shock, sepsis, hemorrhage, HF).
Death of tubular cells that may slough into tubular lumen (PCT and thick ascending limb are highly susceptible)

Nephrotoxic: Secondary to injury resulting from toxic substances (Aminoglycosides, radiocontrast agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria. PCT is particularly susc. to injury

Sloughed tubular cells w/i tubular lumen

35
Q

What is the pathophys of renal papillary necrosis? Findings? Triggers? Associations?

A

Sloughing of necrotic renal papillae leading to gross hematuria and proteinuria.

Recent infection or immune stimulus

SAAD papa
Sickle cell disease or trait
Acute pyelonephritis
Analgesics (NSAIDS)
Diabetes Mellitus
36
Q

How is acute kidney injury defined? What is another name for it? What is the pathophys of prerenal azotemia? Findings? What is the pathophys of intrinsic renal failure? Findings? Causes? What is the pathophys of postrenal azotemia? Causes?

A

Acute renal failure

Abruput decline in renal funciton as measured by incr. Cr and BUN

PRERENAL

Decr. RBF leads to decr. GFR
Na/H20 and BUN are retained by kidney to conserve V
Incr. BUN/Cr ratio
Decr. FENa

INTRINSIC

Due to ATN or ischemia/toxins; less commonly due acute glomerulonephritis

Patchy necrosis leads t debris obstructing tubule and fluid backflow acrss necrotic tubule leading to decr. GFR.
BUN is impaired
Decr. BUN/Cr ratio

POSTRENAL

Outflow obstruction (stones, BPH, neoplasia, cong. anom)
Only with bilateral obstruction
37
Q

Compare and contrast prerenal, intrinsic renal and postrenal acute kidney injury concerning urine osmolality, urine Na, FENa, and Serum BUN/Cr.

A

PRERENAL

Urine Osmol: >500
Urine Na: 20

INTRINSIC

Urine Osmol: 40
FENa: >2%
Serum BUN/Cr: 40
FENa: >1%=mild; >2%=severe
Serum BUN/Cr: Varies
38
Q

What are the two forms of renal failure? Causes of each? What are the consequences of renal failure? What are the symptoms of Uremia?

A

Acute (ATN, prerenal, postrenal)

Chronic (hypertension, DM, congenital anomalies

MAD HUNGER

Meta Acid
Dyslipidemia (incr. TGs)
Hyperkalemia
Uremia (Incr. BUN=Nausea and anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction)
Na/H20 retention
Growth retardation and devel. delay
EPO failure (anemia)
Renal Osteodystrophy
39
Q

Describe the pathophys of renal osteodystrophy. Presentation?

A

Failure of Vit D Hydroxylation (decr. Ca absorption)
Failure to preserve Calcium (hypocalcemia)
Failure to excrete Phosphate (tissue calcifications leads to decr. Ca)

All this leads to Secondary hyperparathyroidism which causes:

Subperiosteal thinning of bones.

40
Q

How does ADPKD present? Mutation? Chrom? How does death occur? Associations?

A

Numerous cysts causing bilateral enlarged kidneys ultimately destroying kidney parenchyma

Flank pain, hematuria, hypertension, urinary infection, progressive renal failure.

PKD1 (16) PKD2 (4)

complications of chronic kidney disease or hypertension (Incr. renin production)

Berry aneurysms, mitral valve prolapse, benign hepatic cysts

41
Q

How does ARPKD present? ASsocation?

A

In infancy: systemic hypertension, progressive renal insufficiency and portal hypertension
Potters sequence in Utero

Congenital hepatic fibrosis

42
Q

What is the pathophys of medullary cystic disease? Imaging findings? Prognosis?

A

Tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

Medullary cysts nt visualized
Shrunken kidneys on U/S

Poor prognosis

43
Q

What are simple cysts filled with? What are they like on U/S? Prognosis? What are complex cysts like? Prognosis?

A

Ultrafiltrate (Anechoic on U/S). Very common; most of all renal masses. Incidental finding, asymp

Complex Cysts: Septated, enhanced, or have solid components.
Follow up or removal due to risk of RCC.

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