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MQW U5 > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

Light/Immunoflourescence/Electron Microscopy Findings in Minimal Change Disease

A

Only EM finding: foot processes (podocyte) effacement

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2
Q

Disease: Associated w/ dense subendothelial immune complex deposits, granular IF, “tram-track” apparance

A

Type 1 Membranoproliferative Glomerulonephritis (MGN) – nephritic/nephrotic; GBM splitting by mesangial ingrowth

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3
Q

Disease: associated w/ C3 nephritic factor, intramembranouse dense deposits

A

Type 2 Membranoproliferative Glomerulonephritis (MGN) – C3NF stabilizes C3 convertase (C3bBb) –> low serum C3

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4
Q

Average adult kidney weight

A

150g

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5
Q

What cell is the major glomerular barrier to protein loss in the urine?

A

Podocytes

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6
Q

This congenital renal disease is associated with increased risk later inlife for developing 2ndary FSGS due to overwork of the nephron

A

Unilateral renal agenesis –> overwork of nephron –> progressive glomerular sclerosis

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7
Q

Disease: X-linked dominant type IV collagen mutation –> thinning and splitting of GBM; EM: “basket-weave” appearance

A

Alport Syndrome – Nephritic Syndrome; “can’t see (retinopathy, lens dislocation), can’t pee (glomerulonephritis), can’t hear a bee (sensorineural deafness)

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8
Q

Markedly reduced intrauterine urine production leads to ___

A

Potter sequence = Low urine production –> oligohydraminos –> compression –> low-set ears, small receding chin, beak-like nose, abnormally bent lower extremities

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9
Q

Renal hypoplasia definition and frequent association

A

Histologically normal kidney w/ less than 6 lobes; frequently oligomeganephronia (enlarged glomeruli)

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10
Q

Horshoe kidney associated pathologies

A
  1. Renal infection (Pyelonephritis) – ureter obstruction
  2. Renal stones
  3. Hydronephrosis – ureter obstruction
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11
Q

Congenital Disease: Histo: undifferentiated tubules and ducts, mantles of undifferentiated mesenchyme (SmM and cartilage)

A

Renal Dysplasia – aplastic, multicystic, diffuse cystic, obstructive forms

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12
Q

MCC of an abdominal mass in newborns?

A

Unilateral multicystic renal dysplasia = renal enlargement by multiple cysts –> irregular mass

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13
Q

What part of the nephron does it affect?

  • -Adult AD PKD
  • -Autosomal Recessive PKD
A

–AD PKD = Anywhere – Glomerulus, PT, DT, CD

–AR PKD = Collecting Duct

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14
Q

Earliest, most common presentation of AD PKD

A

Hypertension

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15
Q

MCC of Neophrotic syndrome in:

  • -Caucasian Adults
  • -American Blacks
  • -Children
A

Caucasian Adults = Membranous Nephropathy

American Blacks = FGSG

Children = MCD

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16
Q

Disease: EM: “spike and dome” appearance, subepithelial deposits

A

Membranouse Nepropathy = nephrotic presentation of SLE, diffuse capillary and GBM thickening, MCC in Caucasian adults

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17
Q

MCC of 2ndary nephrotic syndrome and end-stage renal disease in US

A

Diabetes –> Diabetic Glomerulonephropathy = Eosinophilic nodular glomerulosclerosis: mesangial expansion, GBM thickening

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18
Q

Disease: Associated w/ Kimmelstiel-Wilson lesions

A

Diabetic Glomerulonephropathy

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19
Q

Disease: Associated w/ effacement of podocyte foot processes in EM, but normal glomerulus in light microscopy and IF studies.

A

Minimal Change Disease – selective proteinuria (albumin)

–Corticosteroids –> remission w/ intermittent relapse

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20
Q

Disease: Associated with VHL tumor suppressor gene deletion on chromosome 3

A

Renal Cell Carcinoma

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21
Q

Disease: Risk factors include Schistosoma haematobium infection (Middle ease), chronic cystitis, smoking, chronic nephrolithiasis

A

SCC of Bladder = chronic irritation –> squamous metaplasia –> dysplasia –> SCC
—Presents with painless hematuria

22
Q

Disease: Associated w/ deletion of WT1 tumor suppressor gene

A

WAGR syndrome = Wilms tumor, Aniridia, Genital abnormalities, mental and motor Retardation

23
Q

Disease: Associated w/ mutations of WT1 tumor suppressor gene

A

Denys-Drash syndrome = Wilms tumor, progressive renal (glomerular) disease, male pseudohermaphroditism

24
Q

Disease: Associated w/ mutations in WT2 gene cluster, particularly IGF-2

A

Beckwith-Wiedmann syndrome = Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (including tongue)

25
Q

Disease: Classically presents w/ painless hematuria, multifocal “field defect” (recurring) tumors, risk factors include: naphthylamine, azo dyes (hair salon), cyclophosphamide or phnacetin

A

Urothelial Carcinoma

26
Q

Characteristics of Flat vs. Papillary pathway of Urothelial Carcinoma

A 
Flat = develops as high grade-flat tumor, early p53 mutations
Papillary = develops as low-grade papillary tumor, progresses to high grade, no early p53 mutations
27
Q

Disease: arises from a urachal remnant, cystitis glandularis, or exstrophy

A

Urinary adenocarcinoma (usually bladder)

  • -Urachal remnant = at dome of bladdre
  • -Cystitis glandularis = columnar metaplasia
  • -Exstrophy = congenital failure failure to form caudal portion of anterior abdominal and bladder walls
28
Q

Disease: Hamartoma of blood vessels, smooth muscle, and adipose tissue

A

Angiomyolipoma – increased frequency in Tuberous Sclerosis

29
Q

Where does Renal Cell Carcinoma arise?

A

Epithelial cells of proximal kidney tubules

30
Q

RCC can cause a varicocele on which side?

A

Left – L spermatic vein leads drains into L renal artery (can be blocked in RCC)

–R spermatic vein drains directly into IVC

31
Q

This type of stone is treated with HCTz

A

Calcium oxalate/phosphate

32
Q

Kidney stones of these 2 substances can form staghorn calculi

A

Ammonium magnesium phosphate = classical staghorn

Cystine

33
Q

Infection w/ urease positive organisms (Proteus, Klebsiella) can lead to this kind of nephrolithiasis

A

Ammonium magnesium phosphate – forms in alkaline urine

34
Q

This kind of kidney stone can’t be seen in X-ray

A

Uric acid

35
Q

Gene products affected in AD PKD vs. AR PKD

A

AD PKD = polycystin 1, 2 = Ca signalling normally inhibiting tubular growth

AR PKD = fibrocystin = regular cell differentiation, proliferation and adhesion in collecting ducts

36
Q

What congenital kidney disease is associated w/ berry aneurysms (family hx of death my aneurysm), hepatic cysts, and mitral valve prolapse?

A

AD PKD

37
Q

Disease: Autosomal dominant defect leading to parenchymal fibrosis and shrunken kidney

A

Medullary Cystic Kidney Disease = cysts in medullary collecting ducts –> worsening renal failure

38
Q

Which 2 parts of the nephron are most susceptible to ischemic damage?

A
  1. Proximal tubule

2. Medullary segment of TAL

39
Q

Acute Tubular Necrosis causes what acid/base change?

A
  1. Increased Anion gap metabolic acidosis (decreased excretion of organic acids (K-H antiport)
  2. Hyperkalemia (decreased renal excretion)
40
Q

Disease: IF microscopy shows linear pattern

A

Goodpasture syndrome (Type 2 hypersensitivity) = anti-basement membrane (type IV collagen) antibody; associated w/ HLA-DRB1

41
Q

What diseases are associated with granular pattern in IF microscopy?

A

PSGN or Diffuse proliferative glomerulonephritis = immune complex deposition

42
Q

In what disease does IgA immune complex deposit in mesangium of glomeruli?

A 
IgA Nephropathy (Berger Disease) = most common nephropathy worldwide
---Childhood presentation of hematuria w/ RBC casts
43
Q

What nephrotic syndrome has good response to steroids?

A

Minimal Change disease (MCD)

—Poor response = FSGS, Membranous nephropathy, MPGN

44
Q

What is the first change in the kidney in Diabetes Mellitus?

A

Nonenzymatic glycosylation of vascular basement membrane –> hyaline arteriolosclerosis (affecting efferents more than afferents) –> hyperfiltration injury –> microalbuminemia

45
Q

What is ‘thyroidization’ of the kidney and when do you see it?

A

Atrophic tubules containing eosinophilic proteinaceous material resembling thyroid follicles

  • –Seen in Chronic Pyelonephritis
  • –May have waxy casts in urine
46
Q

What is the most common cause of acute intrarenal azotemia?

A

Acute Tubular necrosis

47
Q

What kind of acute renal failure?
Urine osm = 500+
FENa = less than 1%
BUN/Cr = 20+

A

Pre-renal azotemia = low renal blood flow –> low GFR

–> more reabsorption of fluid and BUN –> high ratio, low FENa

48
Q

What kind of acute renal failure?
Urine osm = less than 350
FENa = 2%+
BUN/Cr = less than 15

A

Intrinsic renal failure = Usually Acute Tubular Necrosis = patchy necrosis –> debris –> obstruction –> low GFR –> impaired BUN and Na reabsorption;

–classic brown granular/epithelial casts

49
Q

Urine osm, FENa, and BUN/Cr changes in Early vs. Long-standing Post-renal azotemia

A

Post-renal azotemia

  • -Early stage obstruction = decreased outflow –> forces BUN back into blood (high BUN/Cr ratio), normal tubular function (FENa less than 1%, high urine Osm)
  • -Long-standing obstruction = tubular damage –> impaired BUN and Na reabsorption (low BUN/Cr ratio, high FENa), inability to concentrate urine (low Urine osm)
50
Q

When do you see fatty casts (“oval fat bodies”)?

A

Nephrotic syndrome, where lipids are passes along with protein
—“Maltese cross” sign

51
Q

When do you see WBC vs RBC casts?

A

RBC Casts = glomerulonephritis, malignant HTN

WBC Casts = tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

52
Q

3 Types of Urinary Incontinence and their causes

A
  1. Stress Incontinence = urethral hypermobility or intrinsic sphincter deficiency; sneezing, lifting
  2. Urgency Incontinence = overactive bladder; detrusor instability
  3. Overflow Incontinence = incomplete emptying; detrusor underactivity

MQW U5 (8 decks)

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