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Renal Flashcards

1
Q

Although only a transient structure, what is the first functional unit of the kidney to appear?

A

Mesonephros

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2
Q

What adult structures of the kidney are derived from the mesonephric duct?

A

Collecting ducts, calyces, renal pelvises, and ureters. All of these derive from the ureteric bud which is an EXTENSION of the mesonephros

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3
Q

What’s the 60-40-20 rule for remembering body fluid?

A

60% of total body weight is water
of that 40 would be ICF and 20 would be ECF (i.e. 2/3 is intracellular, 1/3 is extracellular)

Of the extracellular fluid, only 1/4 is plasma

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4
Q

What compartment is highest in Mg2+?

A

Intracellularly

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5
Q

What is the molecular pathogenesis of diabetic nephropathy?

A

Microalbuminuria results from non-enzymatic glycosylation of the basement membrane eliminating the normal negative charge barrier.

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6
Q

What will you see on glomerular histology in diabetic patients?

A

Kimmelstiel-Wilson nodules, ovoid or spherical lamellated eosinophilic nodules located in the peripheral mesangium. They also stain PAS+.

Aka nodular glomerulosclerosis

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7
Q

How would diabetic nephropathy be described on histology/path?

A

Glomerular basement membrane thickening
Increased mesangial matrix deposition
Kimmelstiel-Wilson nodules

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8
Q

What is the equation for clearance?

A

Cx = UxV/Px

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9
Q

The perfect estimate of GFR is _____, but instead we use _____.

A

Inulin

Creatinine, even though creatinine slightly overestimates GFR.

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10
Q

What is PAH used to estimate?

A

RPF

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11
Q

Kidneys receive ___% of CO at rest.

A

25%

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12
Q

Renal blood flow is approximately ___x the RPF. Why?

A

2x

because almost or nearly 50% of the blood flow is red cells which does not pass the glomerular BM

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13
Q

What is the typical filtration fraction? GFR/RPF?

A

Roughly 20%

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14
Q

Which diuretic is a carbonic anhydrase inhibitor? Where does it act and what does it do?

A

Acetazolamide used in the treatment of acute angle-closure glaucoma and altitude sickness

Inhibits carbonic anhydrase in the PCT preventing NaHCO3 reabsorption -> HCO3- wasting -> metabolic acidosis and alkaline urine

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15
Q

Which diuretic class is contraindicated in patients prone to forming kidney stones?

A

Loop diuretics (e.g. furosemide) due to increase Ca2+ concentrations in the urine

In these patients thiazides are a better choice

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16
Q

Triamterene and amiloride are K____ diuretics that act on the ____ channel in the _____.

A

K-sparing

Inhibit ENaC in the principal cells of the collecting tubule

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17
Q

What is Fanconi Syndrome?

A

Failure of reabsorption in the PCT -> loss of glucose and AA, HCO3-, and phosphate reabsorption most affected

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18
Q

What is Bartter syndrome?

A

Failure of reabsorption in the TAL -> hypokalemia and metabolic acidosis (like loop diuretics)

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19
Q

Liddle’s syndrome, which is autosomal ____ leads to increased activity of _____.

A

Autosomal dominant

Overactive sodium channels in the collecting duct

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20
Q

Why does alkalosis cause hypokalemia?

A

There is a K+/H+ exchanger that will push K+ into cells in order to get H+ out into the bloodstream in an effort to correct pH.

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21
Q

What is the mnemonic for remembering renal tubule disorders (in order from proximal tubule to collecting duct!)?

A

FABulous Glittering LiquidS

FAnconi - PCT
Bartter - TAL (NKCC)

Gitelman - DCT (NaCC co-transporter)
Liddle - increased ENaC
Syndrome of apparent mineralocorticoid excess (i.e. 11betahydroxy def.)

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22
Q

How do you calculate the anion gap? What is a normal range?

A

Na - (Cl + HCO3-)

Normal range = 8-12

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23
Q

What is the mnemonic for high anion gap metabolic acidosis?

A

MUDPILES

Methanol
Uremia
DKA
Propylene glycol
Iron tablets
Lactic acidosis
Ethylene glycol
Salicylates (late)
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24
Q

What is the mnemonic for normal anion gap acidosis?

A

HARDASS

Hyperalimentation
Addison disease
Renal tubule acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
25
Q

What are the various shapes of kidney stones/crystals?

A

Hexagonal - cystine
Coffin - struvite/magnesium ammonium phosphate
Pyramid or dumbbell - calcium oxalate
Rectangular, diamond, or rhombus - uric acid
Elongated/wedge shaped or rosette - Calcium phosphate

26
Q

What effect do ACE inhibitors have on bradykinin?

A

Increase, this is thought to be responsible for the ACE inhibitor-induced cough

(ACE normally breaks down bradykinin)

27
Q

Abrupt onset gross hematuria in an otherwise healthy patient with sickle trait = ?

A

Renal papillary necrosis

Sickled cells cause obstruction of small kidney vessels -> ischemia

28
Q

What is the pathogenesis of minimal change disease?

A

Systemic T cell dysfunction leads to the production of glomerular permeability via podocyte foot process fusion -> decreased negative charge -> selective albuminuria

(albumin is small enough to pass through slits normally and relies on the negative charge to avoid filtration)

29
Q

What is the a good diuretic treatment for acute ICP or cerebral edema? What is a possible side effect?

A

Manitol (osmotic diuretic)

Can cause pulmonary edema, dilutional hyponatremia, metabolic acidosis, and hyperkalemia.

30
Q

Which stones precipitate in alkaline urine? in acidic?

A

Alkaline urine =
Calcium oxalate
Calcium phosphate
Magnesium ammonium phosphate/struvite

Acidic urine =
Uric acid
Cystine

31
Q

What are the first 2 lab tests in the work up of metabolic alkalosis?

A

Urine chloride and volume status

(differential can be initially separate on low vs high chloride and then for high chloride low vs high volume.

32
Q

Poisoning with what substance can precipitate calcium oxalate stones?

A

Ethylene glycol

33
Q

What effect does urea ADH/vasopressin have on urea reabsorption?

A

Activates urea transporters in the medullary collecting duct, increasing urea reabsorption.

34
Q

What effect do beta blockers have on renin secretion?

A

Beta blockers block beta 1 receptors in the juxtaglomerular cells, which stimulate the release of renin.

35
Q

Nephritic syndrome is marked by damage to the _____, while nephrotic damage is marked by damage to ____. What is the protein cut off ?

A 
Nephritic = GBM
Nephrotic = podocytes

> 3.5 gm lost per day = nephrotic

36
Q

Which is an inflammatory condition: nephritic or nephrotic disease?

A

Nephritic, so with those you’ll see fever and other signs of an inflammatory state

37
Q

Will minimal change disease show any defects on LM?

A

No!

38
Q

“spike and dome appearance” with subepithelial deposits = ?

A

Membranous nephropathy

39
Q

Increased pH = calcium ____ stones

Decreased pH = calcium ____ stones

A 
inc = phosphate
dec = oxalate
40
Q

What is the treatment for calcium oxalate and phosphate stones (other than more fluids!)?

A

Thiazides or citrate

41
Q

Which of the kidney stones is radiolucent (i.e. can’t be visualized on xray)?

A

Uric acid

42
Q

How does PSGN look on immunofluorescence? On EM?

A

lumpy bumpy on immuno

subepithelial humps on EM

43
Q

Which nephritic syndrome looks like “wire looping” on LM/EM?

A

Diffuse proliferative glomerulonephritis (due to SLE or MPGN)

44
Q

What are the main deposits in RPGN?

A

Fibrin and macrophages

45
Q

What type of nephritis/nephrosis is seen in Wegener’s kidney manifestations?

A

RPGN (crescentic nephritis)

46
Q

What is IgA nephropathy/how does it present?

A

Most common cause of glomerulonephritis
Often affects older children/young adults
Painless hematuria 5-7 day after URI -> often subsides but returns with subsequent URIs

Mesangial hypercellularity
Mesangial IgA deposits

47
Q

What are the symptoms of the 3 phases of ATN?

A

Initiation: ischemic injury to renal tubules precipitated by hemorrhage, acute MI, sepsis, surgery, etc.

Maintenance: decreased urine output, fluid overload, increasing creatinine/BUN, hyperkalemia, metabolic acidosis (retention of hydrogen and anions)

Recovery: Gradual inc in urine output -> high vol diuresis. Hypokalemia, Hypomagnesia, hypophosphatemia, and hypocalcemia due to slowly recovering tubular function

48
Q

Where do JG cells reside?

A

In the wall of the afferent arteriole. JG cells themselves are actually modified smooth muscle cells.

49
Q

What two buffers seen in the urine are used to excrete acid?

A

NH4+ (due to extra NH3 production)

H2PO4- (due to extra HPO4)

50
Q

If urine osmolarity is >500, what kind of AKI do you have?

A

Prerenal

Osmolarity will be decreased (<350) in intrarenal and postrenal AKI

51
Q

High BUN/Cr ratio (i.e. >20) = ___renal AKI

A

prerenal

52
Q

BUN/Cr ratio <15 = ___renal AKI

A

intrarenal

53
Q

What is AIN/how does it present?

A

Hypersensitivity reaction to drug (usually 1-2 weeks after starting it) -> interstitial inflammation

Marked by pyuria + eosinophils!

Diuretics, penicillins, sulfonylureas, rifampin, NSAIDs, are all especially common offenders

54
Q

Patients in the maintenance phase of ATN have oliguria and are thus at risk for what metabolic abnormalities?

A

Hyperkalemia

Metabolic acidosis

55
Q

Which diuretic can cause calcium wasting?

A

Loop diuretics (e.g. furosemide)

56
Q

What cell type becomes malignant in renal (clear) cell carcinoma?

A

Epithelia of proximal convoluted tubules

57
Q

What complications can result from BPH?

A

UTI
Bladder hypertrophy
Hydronephrosis
CKD

58
Q

Recurrent pyelonephritis can lead to _____.

A

Renal scarring

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