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Renal > Renal First Aid Pathology I > Flashcards

Renal First Aid Pathology I Flashcards

1
Q

Defect in collecting tubule’s ability to excrete H+; urine pH > 5.5;
hypOkalemia.

A

Type I RTA (distal)

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2
Q

As a result of increased urine pH and bone resorption, Type I RTA increases the risk of

A

calcium phosphate stones

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3
Q

Defect in PCT HCO3- reabsorption.
May be seen with Fanconi’s syndrome.
Urine ph < 5.5.
HypOkalemia

A

Type 2 RTA (proximal)

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4
Q

Hypoaldosteronism or lack of collecting tubule response to aldosterone. HypERkalemia impairs ammoniagenesis in PCT –> decreased buffering capacity and decreased urine pH.

A

Type 4 (hyperkalemic)

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5
Q

What does the presence of casts in the urine tell you?

A

Hematuria is of renal (vs. bladder) origin

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6
Q

RBC casts

A

Glomerulonephritis, ischemia, or malignant HTN

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7
Q

WBC casts

A

Tubulointersitial inflammation,
Acute pyelonephritis,
Transplant rejection

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8
Q

Fatty casts (“oval fat bodies”)

A

Nephrotic syndrome

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9
Q

Granular muddy brown casts

A

Acute tubular necrosis

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10
Q

waxy casts

A

advanced renal disease/chronic renal failure

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11
Q

hyaline casts

A

nonspecific, can be a normal finding

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12
Q

hematuria with no RBC casts

A

bladder cancer, kidney stones

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13
Q

pyuria with no casts

A

acute cystitis

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14
Q

Involves only glomeruli, thus a primary disease

of the kidney

A

1° glomerular disease (MCD)

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15
Q

Involves glomeruli and other organs, thus a disease of another organ system, or a systemic disease that has impact on the kidney

A

2° glomerular disease (SLE, diabetic nephropathy)

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16
Q

< 50% of glomeruli are involved

A

Focal (eg FSGN)

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17
Q

> 50% of glomeruli are involved

A

Diffuse (eg DPGN)

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18
Q

Hypercellular glomeruli

A

Proliferative (eg mesangial proliferative)

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19
Q

Thickening of glomerular basement membrane

A

Membranous (eg membranous nephropathy)

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20
Q

4 pure nephritic syndromes

A

Acute post streptococcal GN
Rapidly progressive GN
Berger’s IgA glomerulonephropathy
Alport syndrome

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21
Q

5 pure nephrotic syndromes

A 
MCD
Focal segmental glomerulosclerosis 
Membranous nephropathy
Diabetic nephropathy
Amyloidosis
22
Q

2 mixed nephrotic/nephritic

A

Diffuse proliferative GN

Membranoproliferative GN

23
Q

Associated with HIV infection, heroin abuse, massive obesity, interferon treatment, and chronic kidney disease due to congenital absence or surgical removal. Most common cause of nephrotic syndrome in adults.

A

Focal segmental glomerulosclerosis

24
Q

SLE’s nephrotic presentation. Can be

idiopathic or caused by drugs, infections, SLE, solid tumors.

A

Membranous nephropathy

25
Q

Selective loss of albumin, not globulins, caused
by GBM polyanion loss. May be triggered by a recent infection or an immune stimulus. Most common in children. Responds to corticosteroids.

A

Minimal change disease (lipoid nephrosis)

26
Q

LM-segmental sclerosis and hyalinosis
EM-effacement of foot process similar to
minimal change disease.
IF-negative

A

FSGN

27
Q

LM-diffuse capillary and GBM thickening
EM-“spike and dome” appearance with subepithelial deposits.
IF-granular.

A

membranous nephropathy

28
Q

LM-normal glomeruli.
EM-foot process effacement
IF-negative

A

MCD

29
Q

LM-Congo red stain shows apple-green birefringence under polarized light.

A

Amyloidosis

30
Q

Associated with chronic conditions (e.g., multiple myeloma, TB, RA).

A

Amyloidosis

31
Q

subendothelial IC deposits with granular IF;
“tram-track” appearance due to GBM splitting caused by mesangial ingrowth;
associated with HBV, HCV.

A

Type I MPGN

32
Q

intramembranous IC deposits;
“dense deposits.”
C3 nephritic factor.

A

Type II MPGN

33
Q

Kimmelstiel-Wilson lesion

A

Diabetic nephropathy

34
Q

Nonenzymatic glycosylation (  EG) of GBM -+ t permeability, thickening. NEG of efferent arterioles -+ inc GFR -+ mesangial expansion.

A

Diabetic nephropathy

35
Q

LM-mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

A

Diabetic nephropathy

36
Q

Inflammatory process. When it involves glomeruli, it leads to hematuria and RBC casts in urine. Associated with azotemia, oliguria, hypertension (due to salt retention), and proteinuria (

A

Nephritic syndrome

37
Q

LM-glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy” appearance.

A

Acute poststreptococcal glomerulonephritis

38
Q

EM-subepithelial immune complex (IC) humps.

A

Acute poststreptococcal glomerulonephritis

39
Q

IF-granular appearance due to IgG, IgM, and C3 deposition along GBM ancl mesangium.

A

Acute poststreptococcal glomerulonephritis

40
Q

Most frequently seen in children. Peripheral and periorbital edema, dark urine, and hypertension. Resolves spontaneously.

A

Acute poststreptococcal glomerulonephritis

41
Q

LM and IF-crescent-moon shape.

A

Rapidly progressive (crescentic) glomerulonephritis (RPGN)

42
Q

Crescents consist of

A

FIBRIN and plasma proteins (e.g., C3b) with glomerular parietal cells, monocytes, and macrophages.

43
Q

type II hypersensitivity; antibodies to GBM and alveolar basement membrane -+ linear IF

A

Goodpasture

44
Q

Goodpasture is a type WHAT hypersensitivity?

A

Type II

45
Q

Most common cause of death in SLE.

SLE and MPGN can present as nephrotic syndrome and nephritic syndrome concurrently.

A

Diffuse proliferative glomerulonephritis (DPGN)

46
Q

Due to SLE or MPGN.
LM-“wire looping” of capillaries.
EM-subendothelial & some intramembranous IgG-based ICs often with C3 deposition.
IF- granular.

A

DPGN

47
Q

Granular IF

A

Acute post streptococcal GN
DPGN
Berger’s IgA? (there are IgA-based deposits in mesangium)

48
Q

Related to Henoch-Schoinlein purpura.
LM-mesangial proliferation.
EM-mesangial IC deposits.
IF-IgA-basecl IC deposits in mesangium.

A

Berger’s IgA nephropathy

49
Q

Often presents/flares with a U R I or acute gastroenteritis.

A

Berger’s IgA nephropathy

50
Q

Mutation in type IV collagen -+ split basement

membrane. X-linkecl.

A

Alport syndrome

51
Q

Glomerulonephritis, deafness, and, less commonly, eye problems.

A

Alport syndrome

Renal (22 decks)

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