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Step 1 > Renal Random Facts > Flashcards

Renal Random Facts Flashcards

1
Q

What does the mesonephros become?

A

Men- Wolffian ducts (ductus deferens and epidydimus); Women- vestigal Gartner’s duct

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2
Q

What is a multi cystic dysplastic kidney

A

Due to abnormal interaction between ureteric bud and metanephric mesenchyme. Leads to a nonfunctional kidney consisting of cysts and connective tissue

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3
Q

Relationship to ureter to ductus deferens

A

Ureters pass under the ductus deferens

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4
Q

What do the uterine vessels travel in?

A

Cardinal ligament

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5
Q

What is the 60-40-20 rule?

A

60% total body water: 40% intracellular, 20% ECF

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6
Q

How do you measure plasma volume and extracellular volume?

A

Plasma volume measured by radio labeled albumin, extracellular volume measured by inulin

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7
Q

Equation for renal blood flow

A

RBF=RPF/(1-Hct); RPF is the clearance of PAH

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8
Q

How does changing the plasma protein concentration change the GFR, RPF, and FF?

A

Increased plasma protein concentration decreases the GFR, doesn’t affect the RPF, and therefore decreases the FF (GFR/RPF)

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9
Q

Hartnup disease

A

Autosomal recessive, deficiency of neutral amino acid transporters in proximal renal tubular cells and on enterocytes, causes a neutral aminoaciduria and decreased absorption from the gut

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10
Q

What is Fanconi syndrome

A

Generalized reabsorptive defect in PCT, associated with increased excretion of nearly all amino acids, glucose, HCO3-, and PO4(3-). May result in metabolic acidosis (proximal renal tubular acidosis)

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11
Q

Bartter syndrome

A

AR, affects Na/K/2Cl transporter, results in hypokalemia and metabolic alkalosis with hypercalciuria

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12
Q

Gitelman syndrome

A

AR, reabsorptive defect of NaCl in DCT. Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

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13
Q

Liddle syndrome

A

AD, Gain of function mutation causing increased Na reabsorption in collecting tubules (increased activity of epithelial Na channel). Results in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone. Tx: amiloride

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14
Q

Syndrome of apparent mineralocorticoid excess

A

Hereditary deficiency of 11-beta-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralocorticoid receptor containing cells before cortisol can act on the mineralocorticoid receptors. Causes hypertension, hypokalemia, metabolic alkalosis. Low serum aldosterone levels.

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15
Q

Actions of angiotensin II (6)

A
  1. acts at ATII receptors on vascular SM to cause vasoconstriction, 2. Constricts effect arteriole of glomerulus, 3. Increases aldosterone, 4. Stimulates ADH leading to H2O reabsorption, 5. Increases PCT Na/H activity, 6. Stimulates the hypothalamus (thirst)
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16
Q

How does the macula densa work?

A

Senses decreased NaCl deliver to DCT causes adenosine release, causes vasoconstriction

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17
Q

Where does Epo come from?

A

Interstitial cells in peritubular capillary bed

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18
Q

Where is vitamin D converted to its active form?

A

By the PCT cells

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19
Q

What do ADH and aldosterone regulate?

A

ADH regulates osmolarity, aldosterone regulares ECF volume and Na content

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20
Q

Effect of ANP

A

Causes increased GFR and increased Na filtration with NO compensatory Na reabsorption in distal nephron. Net effect: Na loss and volume loss

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21
Q

What causes K to shift out of cells?

A

Digitalis, hyperosmolarity, lysis of cells, acidosis, beta-blocker, high blood sugar (insulin deficiency) [DO LABS}

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22
Q

How do you monitor for too much magnesium?

A

DTRS (hypermagnesemia decreases DTRs), also causes lethargy, bradycardia, hypotension, cardiac arrest, and hypocalcemia

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23
Q

Respiratory compensation for metabolic acidosis

A

Winters formula. Pco2= 1.5[HCO3-] +8 +/-2

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24
Q

What can cause a metabolic alkalosis?

A

Loop/thiazide diuretics, vomiting, antacid use, hyperaldosteronism

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25
Q

What causes an anion gap metabolic acidosis?

A

MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, iron tablets/isoniazid, lactic acidosis, ethylene glycol (oxalic acid), salicylates

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26
Q

What causes a normal anion gap metabolic acidosis?

A

HARD-ASS: hyperalimentation, addison disease, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion

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27
Q

Type 1 renal tubular acidosis

A

Distal, urine pH >5.5, defect in ability of alpha-intercalated cells to secrete H+ -> no new HCO3- is generated -> metabolic acidosis. Associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover)

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28
Q

Type 2 RTA

A

Proximal, urine pH

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29
Q

Causes of type 2 RTA

A

Fanconi syndrome and carbonic anhydrase inhibitors

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30
Q

Causes of type 1 RTA

A

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

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31
Q

Type IV RTA

A

Hyperkalemic, urine pH

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32
Q

What causes type IV RTA?

A

Decreased aldosterone production (e.g. diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency), or aldosterone resistance (e.g. K-sparing diuretics, nephropathy due to obstruction, TMP/SMX)

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33
Q

When do you see waxy casts?

A

End-stage renal disease/chronic renal failure

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34
Q

“Starry sky” granular appearance on light microscopy, “lumpy bumpy”

A

Acute poststreptococcal glomerulonephritis

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35
Q

Where are the immune complex deposits in APGN?

A

Subepithelial

36
Q

Most impt prognostic factor for APGN?

A

Age

37
Q

What do the crescents in RPGN consist of?

A

Fibrin and plasma proteins (ex. C3b) with glomerular parietal cells, monocytes, and macrophages

38
Q

What diseases can lead to RPGN and what do you see with each of them?

A

Goodpasture- type II hypersensitivity, Ab to GBM, linear immunofluorescence; Granulomatosis with polyangiitis (Wegener)- PR3-ANC/c-ANCA; microscopic polyangiitis- MPO-ANCA, p-ANCA

39
Q

What causes diffuse proliferative glomerulonephritis?

A

SLE or membranoproliferative glomerulonephritis

40
Q

“Wire looping” of capillaries

A

DPGN

41
Q

Where are the immune complex deposits in DPGN?

A

Subendothelial

42
Q

What do you see in IgA nephropathy?

A

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

43
Q

What causes Alport syndrome?

A

Mutation in type IV collagen, causes thinning and splitting of glomerular basement membrane. Most commonly X-linked

44
Q

“Basket weave” appearance on EM

A

Alport Syndrome

45
Q

Sx of Alport syndrome

A

Eye problems, glomerulonephritis, sensorineural deafness

46
Q

Where are the immune complex deposits in type I membranoproliferative glomerulonephritis?

A

Supendothelial

47
Q

“Tram track” appearance on PAS and H&E stain

A

MPGN; Due to GBM splitting by mesangial ingrowth

48
Q

Where are the immune complexes in type II MPGN?

A

Intramembranous

49
Q

What are type I and type II MPGN associated with?

A

Type I may be 2/2 hepatitis B or C infection. Type II is associated with C3 nephritis factor (stabilizes C3 convertase causing decreased serum C3 levels)

50
Q

Fatty casts

A

Nephrotic syndrome

51
Q

Most common cause of nephrotic syndrome in AA and hispanics

A

FSGS

52
Q

Most common cause of nephrotic syndrome in Caucasians

A

Membranous nephropathy

53
Q

Where are the deposits in Membranous nephropathy?

A

Subepithelial

54
Q

EM of membranous nephropathy

A

“Spike and dome” appearance with subepithelial deposits

55
Q

Nephrotic presentation of SLE

A

Membranous nephropathy

56
Q

LM of membranous nephropathy

A

granular

57
Q

Diabetic glomerulonephropathy on LM

A

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

58
Q

How does diabetes cause kidney problems

A

Non-enzymatic glycosylation of GBM causes increased permeability and thickening; non-enzymatic glycosylation of efferent arterioles causes increased GFR causes mesangial expansion

59
Q

Envelope shaped kidney stone

A

Calcium oxalate

60
Q

Coffin lid shaped kidney stone

A

Ammonium magnesium phosphate (aka struvite)

61
Q

Rhomboid or rosette shaped kidney stone

A

Uric acid

62
Q

Hexagonal kidney stone

A

Cysteine

63
Q

What is the test for cysteine stones?

A

Sodium cyanide nitroprusside test

64
Q

Where does renal cell carcinoma arise from?

A

PCT cells

65
Q

What paraneoplastic syndromes is RCC associated with?

A

Ectopic EPO, ACTH, PTHrP

66
Q

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

A

Renal oncocytoma, benign epithelial cell tumor

67
Q

Cause of Wilms tumor

A

“Loss of function” mutation of tumor suppressor genes WT1 or WT2 on chromosome 11

68
Q

What is Wilms tumor associated with?

A

Beckwith-Wiedmann: Wilms tumor, macroglossia, organomegaly, hemihypertrophy; WAGR: Wilms, aniridia, genitourinary malformation, mental retardation

69
Q

CT findings in acute pyelonephritis

A

Striated parenchymal enhancement

70
Q

Thyroidization of the kidney

A

Chronic pyelonephritis

71
Q

Bone changes with renal osteodystrophy

A

Subperiosteal thinning of bones

72
Q

What is ARPCD associated with?

A

Hepatic fibrosis

73
Q

What is medullary cystic disease?

A

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidney on ultrasound. Poor prognosis

74
Q

When is mannitol contraindicated?

A

Anuria, HF

75
Q

Clinical uses for acetazolamide

A

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri

76
Q

Toxicity of acetazolamide

A

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

77
Q

Toxicity of loop diuretics

A

Ototoxicity, hypokalemia, dehydration, allergy (sulfa), interstitial nephritis, gout

78
Q

Which loop diuretic can be used in patients with a sulfa allergy?

A

Ethacrynic acid

79
Q

Toxicity of thiazides

A

HYPER problems: hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia; HYPO problems: hypokalemia, hypotension

80
Q

What are the K sparing diuretics

A

Spironolactone and eplerenone; triamterene, and amiloride

81
Q

MOA of spironolactone and eplerenone

A

Aldosterone receptor antagonists in cortical collecting tubule

82
Q

MOA of triamterene and amiloride

A

Block Na channels in the cortical collecting tubule

83
Q

Toxicity of ACE inhibitors

A

Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), increased Creatinine, Hyperkalemia, and Hypotension (especially watch for first dose hypotension)

84
Q

Which drug is a direct renin inhibitor?

A

Aliskiren

85
Q

When is Aliskiren contraindicated

A

In diabetics taking ACE inhibitors or ARBs

86
Q

Which diuretics lead to acidemia and how?

A

Carbonic anhydrase inhibitors: decrease HCO3 reabsorption; K sparing: aldosterone blockade prevents K secretion and H secretion. Additionally, hyperkalemia leads to K entering all cells (via H/K exchanger) in exchange for H exiting cells

87
Q

Which diuretics lead to alkalemia and how

A

Loop diuretic and thiazides. Volume contraction increases AT II, increases Na/H exchange in PCT, increased HCO3 reabsorption. K loss leads to K exiting all cells (in exchange for H entering cells). In low K state, H (rather than K) is exchanged for Na in cortical collecting tubule causing alkalosis and “paradoxical aciduria”

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