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Medicine Boards > Nephrology > Flashcards

Nephrology Flashcards

1
Q

When to start sodium bicarb in a patient with CKD? how does it help outcomes?

A

when bicarb chronically < 22

slow progression of CKD

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2
Q

Treatment of minimal change dz (glomerulonephropathy)

A

1st line - Glucocorticoids a
+
standard treatment of the nephrotic syndrome (ACEi or ARB, diuretics for edema, and cholesterol-lowering medication if total cholesterol >200

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3
Q

Which drugs to use in CKD + T2DM to reduce risk of CKD progression/CV events (or both) ?

A
  • SGLT2 inhibitor (empagliflozin)

- GLP1 receptor agonist (liraglutide).

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4
Q

What are the causes of euvolemic hyponatremia with Ur Na >20 and Uosm >300 ? what if Uosm 50-100?

A
  1. SIADH, Hypothyroidism, adrenal insufficiency (addison disease), cerebral salt wasting
  2. compulsive water drinking
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5
Q

whats a normal plasma osm? what is the equation? what is osmolar gap?

A

285-295

serum osm = 2{Na+] + gluc/18 + BUN/28

osm gap is measured - calculated osm, normal is <10, if elevated think of methanol, ethylene glycol, propylene glycol, and isopropyl alcohol poisoning

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6
Q

How to calculate free water deficit?

A

[(Na - 140)/140] x TBW

TBW = 0.5 x weight (kg)

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7
Q

in SIADH what is urine sodium? what is urine osm? what else do you have to rule out?

A

UNa >20 mEq/L
UOsm >300 mOsm/L
r/o hypothyroidsm, adrenal insufficiency (low cortisol), and cerebral salt wasting

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8
Q

How to differentiate renal vs. extra renal phosphate wasting?

A

24-hr phos collection or calculate FEPO4

If 24hr Phos >100mg/d OR FEPO4 >5% = renal phos wasting

FEPO4 = (Ur PO4 x Serum Cr x 100)/(Serum PO4 x Ur Cr)

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9
Q

How much should PCO2 correct for metabolic acidosis? (acute vs chronic)

A

Should decrease by…
ACUTE = (1.5 x HCO3) + 8 +/- 2
CHRONIC = HCO3 + 15

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10
Q

How much should HCO3 correct for respiratory acidosis? (acute vs chronic)

A

Should increase by …
ACUTE = 1 mEq/L for every 10mmHg of PaCO2
CHRONIC = 3.5 mEq/L for each 10mmHg of PaCO2

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11
Q

How much should PCO2 correct for metabolic alkalosis?

A

should increase by …

ACUTE = 0.7 mmHg for each 1 mEq/L

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12
Q

How much should HCO3 correct for respiratory alkalosis? (acute vs chronic)

A

should decrease by…
ACUTE = 2mEq/L for each 10mmHg of PaCO2
CHRONIC = 4mEq/L for each 10mmHg PaCO2

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13
Q

Anion gap equation?

A

Na - (Cl + HCO3) = 8-12

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14
Q

IF AG is reduced <4, what does that suggest?

A

Multiple myeloma or Hypoalbuminemia

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15
Q

Urine anion gap equation? what should it be with normal AG metabolic acidosis? what is it with impaired urine acidification (ie. type 1 RTA)?

A

(Ur Na + Ur K) - Ur Cl

  1. negative, -20 - -25
  2. positive, 20 - 40
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16
Q

What is Delta-delta equation? what does it tell you?

A
  1. (norm AG - measured AG) / (normal HCO3 - measured HCO3) – basically change in AG over change in HCO3, should be 1-2
  2. Used in METABOLIC ACIDOSIS –
    - – If delta delta is <1 = concurrent normal AG acidosis
    - – If delta delta is >2 = concurrent metab alkalosis
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17
Q

What is Balkan Endemic Nephropathy (BEN)?

A
  • gross hematuria (non glomerular)
  • CKD 2/2 tubulointerstitial injury
  • slowly progressive tubulointerstitial disease linked to aristolochic acid (nephrotoxic alkaloid from the plant Aristolochia clematitis)
  • high prevalence rate in southeastern Europe (Serbia, Bulgaria, Romania, Bosnia and Herzegovina, and Croatia) and is the cause of kidney disease in up to 70% of patients receiving dialysis in some of the most heavily affected regions
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18
Q

When/how does HCTZ help with recurrent nephrolithiasis?

A

Ca-oxylate or Ca-phosphate stones who have HYPERCALCIRUIA as urine Ca can be decreased by HCTZ by inducing mild hypovolemia, triggering increased proximal sodium reabsorption and passive calcium reabsorption. Can augment this affect by low sodium diet.

Other tx - potassium citrate or bicarb (but if urine citrate is normal this won’t make a difference)

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19
Q

Treatment of primary (75%) Membranous Glomerulonephropathy.

A
  1. observe for 6-12 months on conservative therapy - ACEi, statin, diuretic (edema management) 30% have spontaneous remission in 1-2yrs
  2. If remain nephrotic –> immunosupression
    - - (1) Glucocorticoids + alkylating agents (75-85% remission in 1 yr)
    - - (2) Calcineurin inhib (cyclosporine or tacrolimus)
    - - (3) Rituximab (noninferior in inducing remission but superior in maintaining remission than cyclosporine)
20
Q

What are causes of secondary (25%) membranous glomerulonephropathy

A

malignancy (solid tumors, lymphoma), infection (Hep B, Hep C, malaria, syphillis), SLE, drugs (NSAIDS)

**high propensity for renal vein thrombosis

21
Q

What antibody is found in primary membranous glomerulonephropathy

A

Anti-PLA2R in 75% of primary cases (rarely in secondary) – podocyte antigen that elicits immune complex formation with circulating autoantibodies

22
Q

Name 4-5 main nephrotic syndromes

A
  1. MCD (young)
  2. FSGS (black, HIV, APOL1 gene, common, obesity, premature birth, solitary kidney – all leads to adaptive podocyte injury)
  3. Membranous Glomerulonephropathy (white, malignancy, Hep C, Hep B, associated renal artery thrombosis)
  4. Diabetic Nephropathy
  5. Membranoproliferative GN (also nephritic, assoc Hep C)

Others… amyloidosis, monoclonal immunoglobulin deposition disease

23
Q

Name nephritic syndromes

A
  1. Anti GBM (goodpastures)
  2. Pauciimmune (norm complement, necrotizing GN)
    - - GPA - c-ANCA/PR-3
    - - MPA - p-ANCA/MPO
    - - EGPA
    - - renal limited ANCA (anca positive but no other involvement)

3A. Immune deposition (low complement)
– post infectious (strep, staph, *IE) - 1-6 weeks post illness
– Lupus nephritis
– membranoproliferative GN
– cryoglobulinemia (HCV, Low C4)
3B. Immune deposition (normal complement)
– IgA nephropathy
– IgA vasculitis - can be 2 days post flu illness

24
Q

pathophys of hypercoag in nephrotic syndrome?

A
  • hypoalbuminemia (esp<2.8) –> hepatic overproduction of proteins –> inc levels of procoagulants (factor V, factor VIII, fibrinogen)
  • Urinary loss of albumin in high volume + urinary losses of LMW anticoagulants (AT III, protein S) + fibrinolytics (plasminogen).
25
Q

Define preeclampsia vs. eclampsia

A
  1. Preeclampsia = new HTN (after 20wks) + proteinuria (>300mg/g) + new end organ damage (elevated LFT, Cr, pulm edema, thrombocytopenia, cerebral or visual sx)
  2. Eclampsia - above + tonic-clonic seizure
26
Q

What is Fabry disease?

A
  • Xlinked recessive inborn error of glycosphingolipid metabolism caused by deficiency of a-galactosidase A
  • Abnormalities in SKIN, EYE, KIDNEY, HEART, BRAIN, PERIPHERAL NERVOUS SYSTEM (from defective storage of sphingolipid)
  • Sx: childhood pain and burning in hands + feet after exercise/fever/fatigue/stress + angiokeratomas + decreased perspiration + corneal and lense opacities
  • consider when see CKD in young adult
  • DX via biopsy OR measure leukocyte enzymatic activity + genetic confirmation
  • TX enzyme replacement with human recombinant a-galactosidase A
27
Q

Before starting EPO what levels should TF sat % and ferritin be? goal hb in CKD?

A

transferrin sat >30%
ferritin >500 ng/mL

Goal 10-11 (not above11.5)

28
Q

What is IgG4 related disease?

A

tubulointerstitial nephritis

  • middle aged men
  • pyuria, proteinuria
  • elevated IgG + IgE
  • peripheral eos
  • enlarged kidneys or renal masses (cortical nodules)
  • Elevated ANA
  • Low complements

DX - Bx showing infiltrate w/ IgG4 + plasma cells

TX - steroids

(other assoc - autoimmune pancreatitis, allergic rhinitis, submandibular gland swelling)

29
Q

Treatment of symptomatic hypermagnesemia in patients with CKD

A

IV NS - Mg diuresis
Furosemide
IV calcium - antagonize Mg

30
Q

Differential Dx for RPGN based on (3) Histologic Patterns on immunofluoresscence

A

(1) Pauci-immune (ie. ANCA assoc GN)
(2) Linear (ie. anti-GBM)
(3) Granular (ie. Lupus Nephritis)

31
Q

What drugs increase serum Cr?

A
  • cimetidine
  • trimethoprim
  • cobicistat
  • dolutegravir

MOA - reduce proximal tubule secretion of creatinine - resulting increases in serum Cr, despite stable GFR.

Management: recheck Cr in 1 week to confirm no further rise

32
Q

What is Lead nephropathy? clinical presentation?

A
  • tubular dysfunction and CTIN
  • occupational exposure - welding, smelting, battery, mining (or drinking moonshine)
  • toxicity after years of exposure to lead in water, soil, plant, food
  • present - HTN + gout + progressive kidney disease
  • Gout common b/c lead reduces urine excretion of uric acid therefore get hyperuricemia
33
Q

Which immunosuppressive therapy is safe in pregnancy?

A

Tacrolimus
Cyclosporine
Azathioprine

NOT MMF or sirolimus or everolimus

34
Q

What kind of acid base disturbance does salicylate toxicity create

A
  1. respiratory alkalosis 2/2 central hyperventilation from salicylate
  2. AG metabolic acidosis 2/2 salicylate tox
  3. metabolic alkalosis from vomiting
35
Q

Ethylene glycol ingestion

  • how did patient ingest?
  • lab abnormalities
  • clinical appearance
  • treatment
A
  • anti-freeze, solvents, cosmetics
  • AG metabolic acidosis, bicarb <10, osmolal gap >10, calcium oxalate precipitation in renal tubules and crystals in urine, AKI
  • NEUROTOX/inebriation, flank pain, hypocalcemic symptoms, CVD collapse, pulm edema
  • IV hydration, FOMEPIZOLE, HD (if indicated), Pyridoxine and Thiamine, Sodium Bicarb
36
Q

Methanol ingestion

  • how did patient ingest?
  • lab abnormalities
  • clinical appearance
  • treatment
A
  • window washer fluid, solvents, paints
  • AG metabolic acidosis, bicarb <10, osmolal gap >10
  • CNS damage, optic nerve/EYE DAMAGE(blindness), papilledema, mydriasis, afferent pupillary defect, abd pain, pancreatitis
  • FOMEPIZOLE, HD (if indicated), Folic acid, sodium bicarb
37
Q

Propylene Glycol injection

  • how did patient ingest?
  • lab abnormalities
  • clinical appearance
  • treatment
A
  • solvent in IV meds (lorazepam)
  • AG metabolic acidosis, osmolal gap >10, AKI
  • tx - d/c IV infusion + HD
38
Q

What is Pyroglutamic acidosis? Tx?

A

AG metab acidosis from chronic Tylenol ingestion, (80% female) usually in critically ill/malnutrition/liver disease/CKD/vegetarian –> impaired mental status/confusion –> urine testing for organic anions shows elevated urine pyroglutamate (5-oxoproline).

Tx - d/c tylenol, consider NAC to regenterate depleted glutathione stores

39
Q

When would you measure a serum cystatin C level?

A

to assess kidney function in people with higher muscle mass 0 will give a more accurate GFR b/c less dependent on muscle mass.

40
Q

What metabolic disturbance do RTAs cause?

A

Non-AG metabolic Acidosis

41
Q

Difference between Type 1,2 and 4 RTA

A

Type 1 (distal) RTA - (+) urine anion gap, low K, ur pH>5.5 [defect in H+ secretion] (most commonly assoc with Sjogren syndrome, can also get ca phos kidney stones due to prox resorption of citrate (hypocitraturia) from potassium wasting)

Type 2 (prox) RTA - (-) urine anion gap, low K. [defect in bicarb reabs]

Type 4 (distal) RTA - (+) urine anion gap, high K, ur pH<5.5 [aldosterone deficiency or resistance]

42
Q

how to calculate urine anion gap?

A

urine AG (uNa+uK) - uCl

43
Q

What surrogate do we use to measure “acid in the urine”?

A 
Urine Chloride (if<15 = low) 
b/c can't measure ammonium (how we excrete H+), but ammonium binds to Cl, therefore we measure Cl
44
Q

3 most common causes of low urine Cl (<15) and metabolic alkalosis?

A

vomiting
nasogastric suction
diuretic use

(also called “saline responsive metabolic alkalosis”)

45
Q

Indications for Kidney Biopsy?

A
  • increase Cr without explanation
  • Proteinuria >500mg/24hr
  • Active urine sediment (casts, dysmorphic erythrocytes)
46
Q

What metabolic abnormality would you see with laxative abuse?

A

Non-gapped metabolic acidosis 2/2 GI loss of bicarb. negative Ur anion gap 2/2 excretion of Cl (acid) ~compensatory

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