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FA note cards > Renal > Flashcards

Renal Flashcards

1
Q

most common site of obstruction

A

Ureteropelvic junction

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2
Q

Potter sequence (syndrome) sx

A

Oligohydramnios → compression of developing fetus → limb deformities, facial anomalies (low-set ears, retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs pulmonary hypoplasia (cause of death)

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3
Q

Causes of Potter sequence

A

ARPKD, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency

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4
Q

On what vessel does a horseshoe kidney get trapped?

A

Under IMA and remain low in the abdomen

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5
Q

What do you have increased risk of in duplex collecting system?

A

UTIs

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6
Q

Course of ureters

A

Pass under uterine artery or under vas deferens (retroperitoneal)

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7
Q

Best estimate of GFR

A

Creatinine clearance

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8
Q

Best estimate of RPF

A

PAH clearance

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9
Q

Equation for filtration fraction

A

FF = GFR/RPF

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10
Q

Normal FF?

A

20%

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11
Q

Where is glucose reabsorbed?

A

In the proximal convoluted tubule (PCT) by Na+/glucose cotransport

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12
Q

Plasma glucose threshold for glucosuria? When are all transports saturated?

A

∼ 200 mg/dL

∼ 375 mg/min

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13
Q

What is absorbed in the early PCT?

A

all glucose and amino acids and most HCO3, Na, Cl, PO43, K, H2O, and uric acid

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14
Q

Effect of PTH at the PCT?

A

inhibits Na/PO43 cotransport → PO43 excretion

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15
Q

Effect of ATII at the PCT?

A

Stimulates Na/H exchange → ↑ Na, H2O, and HCO reabsorption (permitting contraction alkalosis)

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16
Q

Tonicity of filtrate leaving the PCT?

A

Isotonic

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17
Q

What occurs in the thin descending loop of Henle?

A

Passive reabsorbtion of H2O via medullary hypertonicity (impermeable to Na+) Concentrating segment. Makes urine hypertonic

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18
Q

Which section of the kidney is the “concentrating segment”

A

thin descending loop of Henle

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19
Q

What occurs in the thick ascending loop of Henle?

A

Reabsorbs Na, K, and Cl

Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through ⊕ lumen potential

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20
Q

What happens to the concentration of urine in the TAL?

A

Makes urine less concentrated as it ascends; impermeable to H2O

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21
Q

What happens to the concentration of urine in the DCT?

A

Makes urine fully dilute (hypotonic)

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22
Q

PTH effect on DCT?

A

↑ Ca2/Na exchange: Ca2+ reabsorption

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23
Q

Aldosterone regulation in the collecting tubule?

A

reabsorbs Na+ in exchange for secreting K+ and H+

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24
Q

ADH effect in collecting tubule?

A

acts at V2 receptor to ↑ aquaporins on apical side

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25
Q

Order of Na reabsorption

A

Early PCT > TAL > DCT > CD

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26
Q

Fanconi syndrome

A

Generalized reabsorptive defect in PCT

↑ excretion of all amino acids, glucose, HCO3, and PO4; leads to metabolic acidosis

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27
Q

Causes of Fanconi Syndrome

A 
hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease, cystinosis), ischemia, multiple myeloma, nephrotoxins/drug, lead poisoning
(Fanconi is First dx in renal tubule)
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28
Q

Bartter syndrome

A

AR reabsorptive defect in thick ascending loop of Henle
Affects Na/K/2Cl cotransporter → hypokalemia and metabolic alkalosis with hypercalciuria
Presents like loop diuretic use

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29
Q

Gitelman syndrome

A

AR reabsorptive defect of NaCl in DCT
HypoK, hypoMg, metabolic alkalosis, hypocalciuria
Presents like thiazide use

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30
Q

Liddle syndrome

A

GoF: ↑ Na+ reabsorption in collecting tubules d/t ↑ Na channel activity
HTN, hyperK, metabolic alkalosis, ↓ aldosterone
Looks like hyperaldosteronism except aldosterone is zero
Treat w/ amiloride

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31
Q

Syndrome of Apparent Mineralocorticoid Excess

A

Hereditary deficiency of 11β-hydroxysteroid dehydrogenase: converts cortisol to cortisone in cells with MC-r
↑ MC activity: HTN, hypoK, metabolic alkalosis
Can happen w/ too much licorice
Treat with corticosteroids

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32
Q

Distal renal tubular acidosis

A

Type 1; pH > 5.5
Defect in ability of α intercalated cells to secrete H → no new HCO3 → metabolic acidosis
Hypokalemia, Ca phosphate stones

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33
Q

Causes of Type 1 RTA

A

Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract

34
Q

Proximal renal tubular acidosis

A

Type 2
Defect in PCT HCO reab
Hypokalemia, hypophosphatemic stones

35
Q

Causes of type 2 RTA

A

Fanconi syndrome and carbonic anhydrase inhibitors

36
Q

Hyperkalemic renal tubular acidosis

A

Type 4
D/t Hypoaldosteronism
Hyperkalemia

37
Q

Casts in urine

A

Indicates glomerular or renal tubular

ie. not bladder cancer or infection or kidney stones

38
Q

RBC casts

A

Glomerulonephritis, malignant hypertension

39
Q

WBC casts

A

Tubulointerstitial in ammation, acute pyelonephritis, transplant rejection

40
Q

Fatty casts (“oval fat bodies”)

A

Nephrotic syndrome. Associated with “Maltese cross” sign

41
Q

Granular (“muddy brown”) casts

A

Acute tubular necrosis

42
Q

Waxy casts

A

End-stage renal disease/chronic renal failure

43
Q

Hyaline casts

A

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

44
Q

PSGN on LM, IF and EM

A

LM: glomeruli enlarged and hypercellular
IF: starry sky; granular
EM: subepithelial immune complex humps

45
Q

RPGN on LM and IF

A

Crescent moon shape; crescents consist of brin and plasma proteins with glomerular parietal cells, monocytes, macrophages

46
Q

Diffuse proliferative glomerulonephritis on LM, EM and IF

A 
LM—“wire looping” of capillaries
EM—subendothelial and sometimes
intramembranous IgG-based ICs with
C3 deposition
IF—granular
47
Q

Dz associated with diffuse proliferative glomerulonephritis

A

SLE

48
Q

IgA nephropathy on LM, EM and IF

A

LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA-based IC deposits in mesangium

49
Q

Alport syndrome

A

Type IV collagen; Xlinked
“Basket-weave” on EM
Lens dislocations, glomerulonephritis, sensorineural deafness

50
Q

Membrano- proliferative glomerulonephritis

A

Type I: subendothelial immune complex with granular IF; “tram-track”; GBM splitting
Type II: DDD

51
Q

Cause of type I Membrano- proliferative glomerulonephritis

A

2° to hepatitis B or C infection or idiopathic

52
Q

Cause of type II Membrano- proliferative glomerulonephritis

A

C3 nephritic factor (IgG antibody that stabilizes C3 convertase)

53
Q

FSGS on LM, IM and EM

A

LM: segmental sclerosis and hyalinosis
IF: ⊝, but may be ⊕ for nonspecific focal
deposits of IgM, C3, C1
EM: effacement of foot process like MCD

54
Q

Most common cause of nephrotic syndrome in African Americans and Hispanics

A

FSGS

55
Q

Membranous nephropathy on LM, IF, and EM

A

LM: diffuse capillary and GBM thickening
IF: granular d/t immune complex deposition; nephrotic presentation of SLE
EM: “spike and dome” appearance with subepithelial deposits.

56
Q

Most common cause of 1° nephrotic syndrome in Caucasian adults

A

Membranous nephropathy

57
Q

Diabetic glomerulo- nephropathy on LM

A

Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

58
Q

Most common cause of end-stage renal disease in the United States

A

Diabetic glomerulo- nephropathy

59
Q

Ammonium magnesium phosphate stone

A

↑ pH; Radiopaque
Coffin lid shaped
Urease ⊕ bugs
Form staghorn calculi

60
Q

Uric acid stone

A

↓ pH; Radiolucent
Rhomboid or rosettes
Gout and ↑ cell turnover (leukemia)

61
Q

Cystine stone

A

↓ pH; Radiolucent
Hexagonal
Hereditary: lost function of cystine reabsorbing PCT transporter
Sodium cyanide nitroprusside test ⊕

62
Q

Calcium stone

A

Most common; Radiopaqu
oxalate > phosphate
↓ pH

63
Q

Hydronephrosis

A

Distention/dilation of renal pelvis and calyces

64
Q

Renal cell carcinoma

A

From PCT cells: polygonal clear cells filled with lipids and carbohydrates (golden-yellow)
Most common 1° renal malignancy

65
Q

RCC spread

A

Invades renal vein (may develop varicocele if left sided) then IVC and spreads hematogenously; metastasizes to lung and bone

66
Q

Renal oncocytoma

A

Benign epithelial cell tumor from collecting ducts

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

67
Q

Nephroblastoma

A

Wilms tumor
Contains embryonic glomerular structures
LoF of WT1 or WT2 on 11
WAGR complex

68
Q

Denys-Drash

A

Wilms tumor, early-onset nephrotic syndrome, male pseudohermaphroditism (WT1 mutation)

69
Q

Beckwith-Wiedemann

A

Wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)

70
Q

Transitional cell carcinoma

A 
Painless hematuria (no casts)
Most common tumor of urinary tract system
71
Q

Squamous cell carcinoma of the bladder

A

Squamous metaplasia → dysplasia and squamous cell carcinoma
Risk: Schistosoma infection (Middle East), chronic cystitis, smoking, cx nephrolithiasis
Painless hematuria

72
Q

Stress incontinence

A

Urethral hypermobility or intrinsic sphincteric defciency
Leak w/ ↑ intra-abdominal pressure
⊕ bladder stress test

73
Q

Urgency incontinence

A

Overactive bladder (detrusor instability): leak with urge to void immediately

74
Q

Over flow incontinence

A

Incomplete emptying (detrusor underactivity or outlet obstruction): leak with overfilling

75
Q

Acute pyelonephritis histology

A

Neutrophils in ltrate renal interstitium; WBCs in urine +/− WBC casts
Affects cortex with relative sparing of glomeruli/vessels

76
Q

Acute pyelonephritis presentation

A

Fevers, flank pain, nausea/vomiting, chills

77
Q

Chronic pyelonephritis appearance

A

Coarse, asymmetric corticomedullary scarring, blunted calyx

Tubules can contain eosinophilic casts resembling thyroid tissue

78
Q

Chronic pyelonephritis risks

A

Predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones

79
Q

Xanthogranulomatous pyelonephritis

A

Rare; grossly orange nodules; mimic tumor nodules; widespread kidney damage due to granulomatous tissue containing foamy macrophages

80
Q

Diffuse cortical necrosis

A

Acute generalized cortical infarction of both kidneys
D/t vasospasm or DIC
Strong association w/ obs problems

81
Q

Acute tubular necrosis

A

Seen in hospitalized patients
Granular (“muddy brown”) casts
Spontaneously resolves

82
Q

Renal papillary necrosis

A

Sloughing of necrotic renal papillae; gross hematuria and proteinuria

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