Nephrology Flashcards

1
Q

Osmolal gap = measured osms - calculated osms.

Formula for calculated osmoles?

A

(2 x Na) + (glucose / 18) + (BUN/2.8).

An osmolal gap >10 suggests an ingestion (definitely if >20).

Normal serum osmolality is 285-295 mOsm/kg.

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2
Q

Nephrotic range proteinuria = how many grams per day?

A

> 3.5 g per day

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3
Q

Malignancy associated with minimal change disease

A

Hodgkin’s lymphoma

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4
Q

Antibody associated with primary (idiopathic) membranous nephropathy (in 70% of cases):

A

Anti-PLA2R antibodies.

Very high specificity. If positive, no need for renal biopsy

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5
Q

“IV heroin user presents w/ renal failure, nephrotic-range proteinuria; renal biopsy shows amorphous material which is strongly positive on Congo red staining w/ apple green birefringence.” Diagnosis?

(NEJM 4/2020 case report).

A

AA amyloidosis.

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6
Q

“Alcohol intoxication w/ negative ethanol, normal anion gap, elevated osmolal gap”:

A

Isopropyl alcohol.

(Treatment = supportive care).

Remember that methanol and ethylene glycol will have an elevated anion gap.

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7
Q

Alkali therapy can delay the progression of CKD.

At what serum bicarb level (chronically) would you start sodium bicarbonate?

A

<22 mEq/L

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8
Q

Most common cause of nephrotic syndrome in children?

Also causes 10-15% of cases in adults

A

Minimal change glomerulopathy

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9
Q

First line treatment for nephrotic syndrome associated with minimal change disease?

A

High-dose steroids.

Also: diuretics, ACEI/ARB

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10
Q

First line treatment for IgA nephropathy?

A

ACEI or ARB.

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11
Q

Normal ranges!

1) Na
2) K
3) Bicarbonate
4) Chloride

A

1) 135-145 mEq/L
2) 3.5-5.0 mEq/L
3) 23-28 mEq/L
4) 98-106 mEq/L

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12
Q

Anion gap

A

Sodium - (chloride + bicarb)

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13
Q

Goal hourly urine output when treating rhabdomyolysis?

A

200-300 ml/hr

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14
Q

Management of ethylene glycol toxicity (w/ organ toxicity)

A

1) IV fluids
2) Fomepizole
3) Hemodialysis

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15
Q

What can heparin do to potassium?

A

Hyperkalemia.

Mechanism: Heparin causes hypoaldosteronism.

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16
Q

“Chronically ill patient receiving therapeutic dose of acetaminophen on a chronic basis develops confusion, metabolic acidosis”

Diagnosis?

A

Pyroglutamic acidosis.

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17
Q

What happens to sodium during normal pregnancy?

A

Mild hyponatremia.

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18
Q

Primary lipid abnormality of CKD?

MKSAP18

A

Hypertriglyceridemia

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19
Q

“Muscular guy has a creatinine of 1.4”
What lab to get instead to assess renal function?”
(MKSAP18)

A

Cystatin C

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20
Q

Hypocitraturia is seen in:

1) Diet
2) GI issue
3) Meds
4) An RTA

(MKSAP 18)

A

1) High protein
2) Chronic diarrhea
3) Carbonic anhydrase inhibitors (including topiramate)
4) RTA type 1 (hypokalemic distal)

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21
Q

Urine volume to prevent stone recurrence:

MKSAP18

A

2500-3000ml / day

22
Q

Spontaneous remission occurs in what fraction of patients with primary membranous nephropathy?

(MKSAP18)

A

1/3.

Therefore, patients with newly diagnosed primary membranous glomerulopathy are usually observed for 6 to 12 months while on conservative therapy (ACEI/ARB, statin, diuretics).

Also remember, PLA2R antibody testing has almost 100% specificity.

23
Q
Acid base problem:
pH 7.2
Na 138
K 4.4
Cl 112
Bicarb 8
A

Anion gap metabolic acidosis AND normal AG metabolic acidosis

24
Q

Appearance of calcium oxalate stones:

A

Envelope-shaped or dumbbell-shaped

25
Q

Expected metabolic compensation (change in bicarb) in chronic respiratory acidosis?

A

Bicarb should increase by 3.5 for every 10mmHg increase in PCO2

26
Q

What % rise in creatinine is acceptable when starting an ACEI or ARB?

A

25%

27
Q

1) Urine anion gap formula:
2) Urine anion gap indirectly measures what?
3) Negative urine anion gap suggests?
4) Positive urine anion gap suggests?

A

1) Urine sodium + urine potassium - urine chloride
2) Urine ammonium (NH3+)
3) GI losses of bicarb, or an acid load
4) Type 1 or 4 RTA

(Increased acid excretion by the kidney is reflected as an increase in urine ammonium. Chloride is excreted in the urine in equal amounts with the ammonium to maintain electric neutrality. Therefore the amount of chloride in the urine reflects the amount of ammonium present and the urine anion gap can be used as an indicator of the ability of the kidney to excrete acid).

28
Q

Which etiology of nephrotic syndrome is most often associated with thrombosis?

A

Membranous glomerulopathy

Risk is related to the degree of hypoalbuminemia

29
Q

Most common etiology of nephrotic syndrome in black persons:

A

Focal segmental glomerulosclerosis

30
Q

Preeclampsia definition:

New onset HTN plus:

1) Proteinuria
2) Timing during pregnancy

A

1) >300mg/24 or >300mg/g spot protein/Cr
2) After 20 weeks

(Remember that new-onset HTN plus end-organ dysfunction also defines preeclampsia [e.g., elevated transaminases]; also remember that HELLP syndrome requires evidence of hemolysis).

31
Q

1) HTN in pregnancy after 20 weeks, no proteinuria, does not last >12 weeks postpartum
2) HTN in pregnancy before 20 weeks or lasting >12 weeks postpartum

A

1) Gestational HTN

2) Chronic HTN

32
Q

Fabry disease:

1) Inheritance pattern
2) Deficient enzyme
3) Skin findings
4) Eye findings
5) Neuropathic pain? (Y/N)
6) Premature ASCVD? (Y/N)

Should be considered as a cause of CKD of unknown etiology in young adulthood.

A

1) X-linked recessive
2) Alpha-galactosidase A
3) Angiokeratomas, telangiectasias
4) Corneal and lens opacities
5) Yes.
6) Yes.

33
Q

E. coli, Klebsiella, Proteus, and Pseudomonas are all urea-splitting bacteria resulting in a ___ urine pH

A

High (>7.5)

(Remember that an alkaline urine pH can precipitate magnesium ammonium phosphate [struvite] which can create staghorn calculi)

34
Q

1) Struvite stone composition

2) Struvite stone appearance

A

1) Magnesium ammonium phosphate
2) Coffin-lid

(Think alkaline urine pH and urease-producing bacteria)

35
Q

Cystine stone appearance:

A

Hexagonal

36
Q

Top 3 common etiologies of nephrotic syndrome:

Pocket Medicine

A

1) FSGS (40%)
2) Membranous nephropathy (30%)
3) Minimal change disease (20% in adults; however, the most common cause of nephrotic syndrome in children).

37
Q

Viruses and glomerular disease: “classic” associations

1) HCV
2) HBV
3) HIV

A

1) Membranoproliferative glomerulonephritis
2) Membranous nephropathy
3) Focal segmental glomerulosclerosis

38
Q

Adynamic bone disease:

1) Bone turnover (low or high?)
2) PTH and Alk Phos

Osteitis fibrosa cystica:

3) Bone turnover
4) PTH and Alk Phos

A

1) Low
2) Normal

3) High
4) Elevated

39
Q

Iron lab treatment goals for iron therapy in CKD:

A

Transferrin saturation >30%

Ferritin >500ng/mL

40
Q

PAC/PRA ratio suggestive of hyperaldosteronism:

A

> 20

41
Q

Most common cause of normal anion gap metabolic acidosis?

The Curbsiders

A

GI losses of bicarb

42
Q

The three buckets of normal anion gap metabolic acidosis according to Joel Toft, MD:

A

1) GI losses of bicarb – diarrhea, surgical drains, fistulas, ureterosigmoidostomy (rarely done), obstructed ureteroileostomy
2) Chloride intoxication – 0.9% NS, HCl intoxication, early renal failure
3) RTAs

43
Q

1) Barrter syndrome mimics what type of diuretic?

2) Gitelman syndrome?

A

1) Loop diuretics
2) Thiazide diuretics

(These syndromes are associated with metabolic alkalosis; saline-resistant, normotensive).

44
Q

Workup of metabolic alkalosis:

1) Urine chloride <20 mEq/L
2) Urine chloride >20 mEq/L

(Pocket Medicine)

A

1) Saline responsive
- - GI losses (vomiting, NG drainage, villous adenoma)
- - Prior diuretic use, volume depletion
- - Post-hypercapnia (transient excess HCO3 after rapid correction of respiratory acidosis)

2) Saline resistant
- - Hypertensive: think mineralocorticoid excess (primary hyperaldosteronism, secondary hyperaldosteronism from from renovascular disease or renin-secreting tumor, or non-aldo [Cushing’s, Liddle’s, licorice])
- - Normotensive: current diuretics, severe hypokalemia, exogenous alkali, Bartter’s (loop-like), Gitelman’s (thiazide-like)

45
Q

Calcineurin inhibitors’ effect on BP and K:

A

Hypertension and hyperkalemia

Treatment: thiazide diuretics

46
Q

Classes of maintenance meds for kidney transplant:

A

1) Calcineurin inhibitors (tacrolimus or cyclosporine)
2) Antimetabolites (mycophenolate mofetil or azathioprine)
3) Steroids

47
Q

1) FeNa that suggests a prerenal state:

2) FeUrea that suggests a prerenal state:

A

1) <1%

2) <35%

48
Q

3 histologic patterns of RPGM:

A

1) Pauci-immune staining (e.g., ANCA-associated)
2) Linear staining (anti-GBM antibody disease)
3) Granular staining (e.g., lupus nephritis)

(Remember that 1 in 3 patients with anti-GBM disease will have a positive ANCA, usually MPO antibody)

49
Q

“Patient on topiramate develops kidney stones”. What is the stone composition?

A

Calcium phosphate

50
Q

1) Loop diuretics work where?

2) Thiazide diuretics work where?

A

1) Na-K-2Cl cotransporter in the thick ascending limb

2) Na-Cl cotransporter in the early distal tubule