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x Pathoma > 12. Kidney and Urinary Tract Pathology > Flashcards

12. Kidney and Urinary Tract Pathology Flashcards

1
Q

What are a few congenital disorders of the kidneys?

A

horseshoe kidney, renal agenesis, dysplastic kidney, polycystic kidney disease, medullary cystic kidney disease

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2
Q

describe a horseshoe kidney. how did it occur?

A

conjoined kidneys, connected at the lower pole. kidney unit got caught on the inferior mesenteric artery root during ascent from pelvis to abdomen

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3
Q

what is the most common congenital renal abnormality?

A

horseshoe kidney

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4
Q

what does agenesis mean?

A

“without production”

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5
Q

what is renal agenesis?

A

kidneys did not form. may be uni- or bi-lateral

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6
Q

what does unilateral renal agenesis lead to?

A

hypertrophy of the existing kidney

–> hyperfiltration which increases risk of renal failure later in life

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7
Q

what does bilateral renal agenesis lead to?

A

Potter sequence.

oligohydramnios with lung hypoplasia, flat face with low set ears, dev defects of the extremities. incompatible with life

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8
Q

what is Potter sequence?

A

lung hypoplasia, flat face with low set ears, dev defects of the extremities. due to oligohydramnios.

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9
Q

how should I think of the Potter sequence mechanistically?

A

think that due to oligohydramnios, there is not room in the uterus –> flat face and mis-formed extremities. the lung hypoplasia is because there is not room for the lungs to stretch and expand.

memory: Potter because the Pot was too small?

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10
Q

what is oligohydramnios? what causes it?

A

not enough amniotic fluid –> fetal abnormalities. many causes: bilateral renal agenesis is one.

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11
Q

how does bilateral renal agenesis cause oligohydramnios?

A

the amniotic fluid is formed from fetal filtrate (urine). if the fetus cannot make urine, there will be little amniotic fluid.

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12
Q

what is dysplastic kidney?

A

noninherited, congenital malformation of renal parenchyma characterized by cysts and abnl tissue. (one ex: cartilage growing where it should not be)

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13
Q

dysplastic kidney: inherited? uni or bilateral?

A

non-inherited. usually unilateral. if bilateral, must be distinguished from inherited polycystic kidney disease

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14
Q

what is polycystic kidney disease (PKD)?

A

inherited defect, leading to bilateral enlarged kidneys with cysts in the cortex and medulla.

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15
Q

what does polycystic kidney disease look like grossly?

A

kidney with lots of dark shiny bubbles on the surface

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16
Q

PKD: autosomal recessive form generally presents in what population? how does it present?

A

infants. presents as worsening renal failure, hypertension. may present as Potter sequence because so severe it’s as though they have oligohydramnios

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17
Q

PKD: auto dominant form generally presents in what population? how does it present?

A

young adults (ADults). presents as HTN (due to incr renin), hematuria, progressive renal failure

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18
Q

auto recessive form of PKD: associated with what?

A

congenital hepatic fibrosis and hepatic cysts.

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19
Q

auto dom form of PKD: why does it present as it does?

A

presents as HTN, hematuria, progressive renal failure: think about cysts in liver/brain/kidney.

Mutation of APKD1 or APKD2 gene. cysts develop over time.

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20
Q

what gene is responsible for the auto dom form of PKD?

A

mutation in the APKD1 or APKD2 genes (adult polycystic kidney disease genes). cysts develop over time.

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21
Q

auto dom PKD: what is it associated with?

A

berry aneurysm, hepatic cysts, mitral valve prolapse.

22
Q

auto dom PKD: generally, what is the cause of death?

A

berry aneurysm rupture

23
Q

what is medullary cystic kidney disease?

A

inherited defect leading to cysts in the medullary collecting ducts.

24
Q

medullary cystic kidney disease: what type of inheritance?

A

AD

25
Q

medullary cystic kidney disease: presentation? Why?

A

presents as worsening renal failure, due to shrunken kidneys from parenchymal fibrosis

26
Q

what is the most obvious difference between dysplastic kidney and polycystic kidney disease?

A

dysplastic kidney = usually unilateral (but might be BIL on USMLE)

polycystic kidney disease = bilateral. presents with HTN, worsening renal failure.

27
Q

Define Acute Renal Failure.

What are the hallmarks?

A

acute, severe decrease in renal function (occurs over days)

Azotemia (incr BUN, incr Creatinine), often Oliguria

Divided into Pre-renal, Post-renal, Intra-renal types.

28
Q

Pre-renal Azotemia

what is a common cause?

Serum BUN:Cr ratio = ?

FENa = ?

Urine osm = ?

A

Decr blood flow to kidneys (cardiac failure is common cause)

Serum BUN:Cr ratio > 15 (high)

FENa < 1% (tubular function = intact)

Urine osm > 500 (tubules can concentrate urine)

29
Q

NORMAL values are….?

Serum BUN:Cr ratio

FENa

Urine osm

A

Normal Values:

Serum BUN:Cr ratio = 15

FENa < 1% (tubular function intact)

Urine osm > 500 (tubules can concentrate urine)

30
Q

Pre-renal Azotemia

why is Serum BUN:Cr ratio high?

A

low blood flow to kidney due to pre-renal obstruction or overall low volume.

RAAS activated -> aldosterone -> **more Na, water, BUN resorbed. **

Cr is filtered and excreted as usual.

Serum BUN:Cr ratio therefore increases.

31
Q

Postrenal Azotemia, Early stage

Serum BUN:Cr ratio = ?

FENa = ?

Urine Osm = ?

A

Serum BUN:Cr ratio > 15

FENa < 1%

Urine Osm > 500

32
Q

Postrenal Azotemia, Later stage

Serum BUN:Cr ratio = ?

FENa = ?

Urine Osm = ?

A

Serum BUN:Cr ratio < 15

FENa > 2%

Urine Osm < 500

All due to tubular damage

33
Q

Acute Tubular Necrosis: clinical findings?

A
  • Brown granular casts in urine
  • Elevated BUN and creatinine (decr GFR)
  • Hyperkalemia
  • Metabolic acidosis with anion gap
34
Q

Acute Tubular Necrosis: 2 etiologies?

A

Ischemia

Toxicity

35
Q

Acute Tubular Necrosis due to toxicity: what are most common causes?

A

Aminoglycosides (gentamycin, tobramycin, amikacin)

Heavy metals/lead

Myoglobinuria (crush injury)

Ethylene glycol ingestion (kid, accidental)

Radiocontrast dye

Urate due to tumor lysis syndrome

36
Q

If a patient is on chemo for leukemia, what do we give to avoid Tumor Lysis Syndrome/Acute Tubular Necrosis?

A
  • Hydration
  • Allopurinol to decr synthesis of urate.
  • Rasburicase (synthetic urate oxidase) to metabolize uric acid –> Allantoin (more soluble)
37
Q

Ethylene glycol ingestion: high-yield association?

A

kids (accidental ingestion)

Oxalate crystals in urine

38
Q

Acute Tubular Necrosis

why does it take 2-3 weeks to recover from?

A

Tubular cells can regenerate, but they are Stable cells and need time to re-enter the cell cycle.

39
Q

Acute Interstitial Nephritis: cause?

A

drug-induced hypersensitivity

NSAIDs, penicillin, diuretics

40
Q

Acute Interstitial Nephritis: presentation?

A

a few days/weeks after starting a new drug, oliguria, fever, rash

Eosinophils in urine

41
Q

Renal Papillary Necrosis

Presentation? Cause?

A

(a form of intra-renal azotemia)

Presents with gross hematuria, flank pain

Causes: chronic analgesic abuse, diabetes, sickle cell, severe acute pyelonephritis

42
Q

6 causes of nephrotic syndrome?

A

6 causes, grouped in pairs:

minimal change and FSGS

Membranous nephropathy and membranoproliferative glomerulonephritis

diabetes mellitus and amyloidosis

43
Q

Nephrotic syndrome: basic principles?

A

proteinuria

hypoalbuminemia -> pitting edema

hypogammaglobilinemia -> incr risk of infection

hyperlipidemia and hyperchol (due to ‘thin’ blood; liver puts out lipids and chol) -> fatty casts

44
Q

minimal change disease: where is the damage?

what cancer is it associated with?

A

effacement of foot processes

associated with Hodgkin lymphoma (huge production of cytokines by Reed-Sternberg cells)

45
Q

minimal change disease: what proteins are lost?

treatment?

A

albumin but NOT immunoglobulin

responds to steroids

46
Q

Focal Segmental Glomerulosclerosis: associations?

where is the damage?

treatment?

A

associations: HIV, heroin use, sickle cell

effacement of foot processes

no response to steroids -> progresses to renal failure

47
Q

most common cause of death with SLE?

A

renal failure

usually due to diffuse progressive glomerulonephritis - or membranous nephropathy

48
Q

membranous nephropathy

where is the damage?

associations?

appearance on IF?

A

damage = subepithelial deposits of immune complexes

associated with Hep B, Hep C, SLE, solid tumors, NSAIDs

appearance = granular IF, spike and dome

49
Q

membranoproliferative glomerulonephritis

associations

damage

appearance

A

Tram-track appearance! granular IF

associations:

Type I: HBV and HCV

Type II: autoantibody to C3 convertase -> overactivation of complement cascade

50
Q

Diabetes nephrosis

damage?

appearance?

treatment?

A

high glucose -> NEG of vascular basement membrane -> hyaline arteriolosclerosis of efferent vessel

high GFR, hyperfiltration, albumin in urine

Kimmelstiel-Wilson nodules

treatment: ACE inhibitors to counteract the efferent blockage effect

51
Q

systemic amyloidosis

damage?

appearance?

A

amyloid deposits in mesangium

apple-green birefringemce under polarized light w/ Congo red stain

x Pathoma (19 decks)

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