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
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.
Minimal change disease (lipoid nephrosis)
26
LM-segmental sclerosis and hyalinosis EM-effacement of foot process similar to minimal change disease. IF-negative
FSGN
27
LM-diffuse capillary and GBM thickening EM-"spike and dome" appearance with subepithelial deposits. IF-granular.
membranous nephropathy
28
LM-normal glomeruli. EM-foot process effacement IF-negative
MCD
29
LM-Congo red stain shows apple-green birefringence under polarized light.
Amyloidosis
30
Associated with chronic conditions (e.g., multiple myeloma, TB, RA).
Amyloidosis
31
subendothelial IC deposits with granular IF; "tram-track" appearance due to GBM splitting caused by mesangial ingrowth; associated with HBV, HCV.
Type I MPGN
32
intramembranous IC deposits; "dense deposits." C3 nephritic factor.
Type II MPGN
33
Kimmelstiel-Wilson lesion
Diabetic nephropathy
34
Nonenzymatic glycosylation (  EG) of GBM -+ t permeability, thickening. NEG of efferent arterioles -+ inc GFR -+ mesangial expansion.
Diabetic nephropathy
35
LM-mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
Diabetic nephropathy
36
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 (
Nephritic syndrome
37
LM-glomeruli enlarged and hypercellular, neutrophils, "lumpy-bumpy" appearance.
Acute poststreptococcal glomerulonephritis
38
EM-subepithelial immune complex (IC) humps.
Acute poststreptococcal glomerulonephritis
39
IF-granular appearance due to IgG, IgM, and C3 deposition along GBM ancl mesangium.
Acute poststreptococcal glomerulonephritis
40
Most frequently seen in children. Peripheral and periorbital edema, dark urine, and hypertension. Resolves spontaneously.
Acute poststreptococcal glomerulonephritis
41
LM and IF-crescent-moon shape.
Rapidly progressive (crescentic) glomerulonephritis (RPGN)
42
Crescents consist of
FIBRIN and plasma proteins (e.g., C3b) with glomerular parietal cells, monocytes, and macrophages.
43
type II hypersensitivity; antibodies to GBM and alveolar basement membrane -+ linear IF
Goodpasture
44
Goodpasture is a type WHAT hypersensitivity?
Type II
45
Most common cause of death in SLE. | SLE and MPGN can present as nephrotic syndrome and nephritic syndrome concurrently.
Diffuse proliferative glomerulonephritis (DPGN)
46
Due to SLE or MPGN. LM-"wire looping" of capillaries. EM-subendothelial & some intramembranous IgG-based ICs often with C3 deposition. IF- granular.
DPGN
47
Granular IF
Acute post streptococcal GN DPGN Berger's IgA? (there are IgA-based deposits in mesangium)
48
Related to Henoch-Schoinlein purpura. LM-mesangial proliferation. EM-mesangial IC deposits. IF-IgA-basecl IC deposits in mesangium.
Berger's IgA nephropathy
49
Often presents/flares with a U R I or acute gastroenteritis.
Berger's IgA nephropathy
50
Mutation in type IV collagen -+ split basement | membrane. X-linkecl.
Alport syndrome
51
Glomerulonephritis, deafness, and, less commonly, eye problems.
Alport syndrome