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USMLE 1 > Renal- Phatology > Flashcards

Renal- Phatology Flashcards

1
Q

Casts in urine

  • WBC casts
  • Fatty casts (“oval fat bodies”)
  • RBC casts
A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.

Nephrotic syndrome. Associated with “Maltese cross” sign.

Glomerulonephritis, hypertensive emergency

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2
Q

Casts in urine

  • Granular (“muddy brown”) casts
  • Waxy casts
  • Hyaline casts
A

Acute tubular necrosis (ATN)

End-stage renal disease/chronic renal failure

Nonspecific, can be a normal finding, often seen in concentrated urine samples

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3
Q

Nomenclature of glomerular disorders

  • Focal
  • Diffuse
A

< 50% of glomeruli are involved

> 50% of glomeruli are involved

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4
Q

Nomenclature of glomerular disorders

  • Proliferative
  • Membranous
A

Hypercellular glomeruli

Thickening of glomerular basement membrane (GBM)

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5
Q

Nephritic syndrome

- Types

A
  • Acute poststreptococcal glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • IgA nephropathy (Berger disease)
  • Alport syndrome
  • Membranoproliferative glomerulonephritis
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6
Q

Nephrotic syndrome

- Types

A
  • Focal segmental glomerulosclerosis (1° or 2°)
  • Minimal change disease (1° or 2°)
  • Membranous nephropathy (1° or 2°)
  • Amyloidosis (2°)
  • Diabetic glomerulonephropathy (2°)
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7
Q

Minimal change disease (lipoid nephrosis)

  • Epidemiology
  • Etiology
  • Electromicroscopy
A

Most common cause in children.

1° (idiopathic) and may be triggered by recent infection, immunization, immune stimulus.

EM—effacement of podocyte foot processes

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8
Q

Focal segmental glomerulosclerosis

  • Epidemiology
  • Etiology
A

Most common cause in African-Americans and Hispanics.

Can be 1° (idiopathic) or 2° (eg, HIV infection, sickle cell disease, heroin abuse, massive obesity, interferon treatment, or congenital malformations).

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9
Q

Focal segmental glomerulosclerosis

  • Light microscopy
  • Inmunofluorecence microscopy
  • Electronic microscopy
A

ƒƒ LM—segmental sclerosis and hyalinosis
ƒƒ IF—often ⊝ but may be ⊕ for nonspecific focal deposits of IgM, C3, C1
ƒƒ EM—effacement of foot processes similar to minimal change disease

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10
Q

Membranous nephropathy (membranous GN)

  • Etiology
  • LM, IF, EM
A

1° (eg, antibodies to phospholipase A2 receptor) or 2° to drugs (eg, NSAIDs, penicillamine, gold), infections (eg, HBV, HCV, syphilis), SLE, or solid tumors.

ƒƒ LM—diffuse capillary and GBM thickening
ƒƒ IF—granular due to IC deposition
ƒƒ EM—“Spike and dome” appearance of subepithelial deposits

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11
Q

Amyloidosis

- Light microscopy

A

LM—Congo red stain shows apple-green birefringence under polarized light due to amyloid deposition in the mesangium

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12
Q

Diabetic glomerulonephropathy

- Light microscopy

A

ƒƒ LM—Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)

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13
Q

Mogensen classification of diabetic nephropathy

A

1: Increased GFR, renal hypertrophy
2: Onset of histological changes
3: Early clinical nephropathy
4: Overt nephropathy
5: Renal failure

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14
Q

Acute poststreptococcal glomerulonephritis

  • Epidemiology
  • Presentation
A

in children. ~ 2–4 weeks after group A streptococcal infection of pharynx or skin

Presents with peripheral and periorbital edema, cola-colored urine, HTN. ⊕ strep titers/serologies, low complement levels (C3) due to consumption.

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15
Q

Acute poststreptococcal glomerulonephritis

  • Light microscopy
  • Inmunofluorecence microscopy
  • Electronic microscopy
A

ƒƒ LM—glomeruli enlarged and hypercellular

ƒƒ IF—(“starry sky”) granular appearance (“lumpy bumpy”) due to IgG, IgM, and C3 deposition along GBM and mesangium

ƒƒ EM—subepithelial immune complex (IC) humps

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16
Q 
Rapidly progressive (crescentic) glomerulonephritis
- LM
A

ƒƒ LM—crescent moon shape. Crescents consist of fibrin and plasma proteins (eg, C3b) with glomerular parietal cells, monocytes, macrophages

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17
Q

Rapidly progressive (crescentic) glomerulonephritis

  • Linear IF due to antibodies to GBM and alveolar basement membrane:
  • Negative IF/Pauci-immune (no Ig/C3 deposition):
  • Granular IF:
A

Goodpasture syndrome—hematuria/hemoptysis; type II hypersensitivity reaction; Treatment: plasmapheresis

Granulomatosis with polyangiitis (Wegener)—PR3 ANCA/c-ANCA or Microscopic polyangiitis—MPO ANCA/p-ANCA

PSGN or DPGN

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18
Q

Diffuse proliferative glomerulonephritis

- Etiology

A

Often due to SLE (think “wire lupus”).

*DPGN and MPGN often present as nephrotic syndrome and nephritic syndrome concurrently.

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19
Q

Diffuse proliferative glomerulonephritis

  • Light microscopy
  • Inmunofluorecence microscopy
  • Electronic microscopy
A

LM—“wire looping” of capillaries

IF—granular;

EM—subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition

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20
Q

IgA nephropathy (Berger disease)

  • Etiology
  • LM, IF, EM
A

Episodic hematuria that occurs concurrently with respiratory or GI tract infections

ƒƒ LM—mesangial proliferation
ƒƒ IF—IgA-based IC deposits in mesangium;
ƒƒ EM—mesangial IC deposition

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21
Q

Alport syndrome

  • Mutation
  • Clinical findings
  • EM
A

Mutation in type IV collagen. XD

Eye problems (eg, retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness

ƒƒ EM—“Basket-weave”

22
Q

Membranoproliferative glomerulonephritis

- Type I

A

Type I 2° to hepatitis B or C or idiopathic.

ƒƒ Subendothelial IC deposits with granular IF

23
Q

Membranoproliferative glomerulonephritis

- Type II

A

associated with C3 nephritic factor

ƒƒ Intramembranous deposits, also called dense deposit disease

24
Q

Membranoproliferative glomerulonephritis

- Both types

A

In both types, mesangial ingrowth Ž GBM splitting Ž “tram-track” appearance on H&E and PAS stains.

25
Q

Kidney

stones

A

Pag. 582

26
Q

Renal cell carcinoma

  • Histology
  • Clinical manifestations
A

Polygonal clear cells filled with accumulated lipids and carbohydrate. Often golden-yellow

Manifests with hematuria, palpable masses, 2° polycythemia, flank pain, fever, weight loss.

27
Q

Renal cell carcinoma

  • Epidemiology
  • Paraneoplastic syndromes
  • Mutation
A

Most common in men 50–70 years old.

Associated with paraneoplastic syndromes: PTHrP, Ectopic EPO, ACTH, Renin

Associated with gene deletion on chromosome 3

28
Q

Renal oncocytoma

  • Histology
  • Clinical presentation
A

Benign epithelial cell tumor arising from collecting ducts. Large eosinophilic cells with abundant
mitochondria without perinuclear clearing

Presents with painless hematuria, flank pain, abdominal mass

29
Q

Nephroblastoma (Wilms tumor)

  • Epidemiology
  • Histology
  • Presentation
A

Most common renal malignancy of early childhood (ages 2–4).

Contains embryonic glomerular structures.

Presents with large, palpable, unilateral flank mass and/or hematuria. WT1 or WT2 on chromosome 11.

30
Q

ƒƒWAGR complex

A

Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental Retardation/intellectual disability (WT1 deletion).

31
Q

ƒƒ Denys-Drash syndrome

A

Wilms tumor, Diffuse mesangial sclerosis (early-onset nephrotic syndrome), Dysgenesis of gonads (male pseudohermaphroditism), WT1 mutation

32
Q

ƒƒ Beckwith-Wiedemann syndrome

A

Wilms tumor, macroglossia, organomegaly,

hemihyperplasia (WT2 mutation)

33
Q

Transitional cell carcinoma (urothelial carcinoma)

  • Epidemiology
  • Presentation
  • Associations
A

Most common tumor of urinary tract system (renal calyces, renal pelvis, ureters, and bladder)

Can be suggested by painless hematuria (no casts).

Associated with problems in your Pee SAC:
Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide.

34
Q

Squamous cell carcinoma of the bladder

- Risk factors include

A

Chronic irritation of urinary bladder Ž squamous metaplasia Ž dysplasia and squamous cell carcinoma

Schistosoma haematobium infection (Middle East), chronic cystitis, smoking, chronic nephrolithiasis. Presents with painless hematuria.

35
Q

Urinary incontinence

A

Pag. 584

36
Q

Urinary tract infection (acute bacterial cystitis)

  • Clinical presentation
  • Etiology
A

Presents as suprapubic pain, dysuria, urinary frequency, urgency. Systemic signs (eg, high fever, chills) are usually absent.

Causes:
ƒƒ E coli (most common).
ƒƒ Staphylococcus saprophyticus—seen in sexually active young women.
ƒƒ Klebsiella.
ƒƒ Proteus mirabilis—urine has ammonia scent

37
Q

Urinary tract infection (acute bacterial cystitis)

- Lab findings

A

Lab findings: ⊕ leukocyte esterase. ⊕ nitrites (indicate gram ⊝ organisms).

Sterile pyuria and ⊝ urine cultures suggest urethritis by Neisseria gonorrhoeae or Chlamydia trachomatis

38
Q

Acute pyelonephritis

  • Clinical presentation
  • Labs
A

Presents with fevers, flank pain (costovertebral angle tenderness), nausea/vomiting, chills.

Presents with WBCs in urine +/− WBC casts. CT would show striated parenchymal enhancement

39
Q

Chronic pyelonephritis

  • Phatophysiology
  • Findings
A

result of recurrent episodes of acute pyelonephritis

Coarse, asymmetric corticomedullary scarring, blunted calyx. Tubules can contain eosinophilic casts resembling thyroid tissue

40
Q

Xanthogranulomatous pyelonephritis

- Phatophysiology

A

rare; grossly orange nodules that can mimic tumor
nodules; characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages.

Associated with Proteus infection

41
Q

Consequences of renal failure

A

ƒƒMetabolic Acidosis
ƒƒDyslipidemia (especially  triglycerides)
ƒƒHyperkalemia
ƒƒUremia—clinical syndrome marked by:
ƒƒNa+/H2O retention (HF, pulmonary edema,
hypertension)
ƒƒGrowth retardation and developmental delay
ƒƒ Erythropoietin failure (anemia)
ƒƒ Renal osteodystrophy

42
Q

Renal osteodystrophy

A

Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease Ž 2° hyperparathyroidism.

Causes subperiosteal thinning of bones.

43
Q

Acute interstitial nephritis (tubulointerstitial nephritis)

  • Etiology
  • Clinical findings
A 
Remember these P’s:
ƒƒ Pee (diuretics)
ƒƒ Pain-free (NSAIDs)
ƒƒ Penicillins and cephalosporins
ƒƒ Proton pump inhibitors
ƒƒ RifamPin

Associated with fever, rash, hematuria, pyuria, and costovertebral angle tenderness

44
Q

Acute tubular necrosis

- Stages

A
  1. Inciting event
  2. Maintenance phase—oliguric; lasts 1–3 weeks; risk of hyperkalemia, metabolic acidosis, uremia
  3. Recovery phase—polyuric;

*Key finding: granular (“muddy brown”) casts

45
Q

Renal papillary necrosis

  • Phatophysiology
  • Associations
A

Sloughing of necrotic renal papillae Ž gross hematuria and proteinuria. May be triggered by recent infection or immune stimulus

SAAD papa with papillary necrosis:
Sickle cell disease or trait
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus
46
Q

Autosomal dominant polycystic kidney disease

  • Clinical presentation
  • Mutations
  • Associations
A

Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure in ~ 50%

Mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4).

Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis.

47
Q

Autosomal recessive polycystic kidney disease

- Clinical features

A

Often presents in infancy. Associated with congenital
hepatic fibrosis. Significant oliguric renal failure in utero can lead to Potter sequence.

Systemic hypertension, progressive renal insufficiency, and portal hypertension from congenital hepatic fibrosis.

48
Q

Autosomal dominant tubulointerstitial kidney disease (medullary cystic kidney disease)
- Phatophysiology

A

tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine.

Medullary cysts usually not visualized; smaller kidneys on ultrasound. Poor prognosis

49
Q

Simple cysts

A

Are filled with ultrafiltrate (anechoic on ultrasound).

Very common and account for majority of all renal masses. Found incidentally and typically asymptomatic.

50
Q

Complex cysts

A

including those that are septated, enhanced, or have solid components on imaging

Require follow-up or removal due to risk of renal cell carcinoma.

USMLE 1 (73 decks)

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