Renal Flashcards

1
Q

Balkan Endemic Nephropathy

A

Tubulointerstitial disease (fibrous) 2/2 aristocholic acid (endemic to Balkans, also in wt loss supplements). Increased risk transitional cell carcinoma of renal pelvis, ureter, bladder

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2
Q

Type 4 RTA etiologies

A

Aldosterone deficiency or resistance
Mild-mod CKD 2/2 diabetic nephropathy
Chronic interstitial nephritis: SLE or AIDS
Acute GN
Meds: NSAIDS, calcinuerin inhibs, ACE inhibitors, heparin, trimethoprim

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3
Q

Type 4 RTA presentation

A

Hyperkalemia
Normal serum AG
Impaired urine acidification (=positive urine AG)
Urine pH

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4
Q

Type 4 RTA w/u

A

Plasma renin activity
Serum aldosterone
Serum cortisol

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5
Q

Type 1 RTA presentation

A

Hypokalemia
Normal serum AG
Impaired urine acidification (=positive urine AG)
Urine pH >5.5

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6
Q

Type 2 RTA presentation

A

Hypokalemia (secondary hyperaldosteronism)
Glycosuria (w normal plasma glucose)
Low molecular weight proteinuria
Phosphaturia
Normal=negative urine AG since urine able to appropriately excrete acid

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7
Q

Thin glomerular basement membrane disease

A

persistent hematuria, normal kidney function, and positive family history of hematuria without kidney failure

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8
Q

Low C3

A
Post strep GN
Membranoproliferative GN
SLE
Infection related GN
Cryoglobulinemic vasculitis (C4 often low too)
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9
Q

Normal C3

A
IgA nephropathy
IgA vasculitis (aka Henoch Schonlein purpura)
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10
Q

Age to start doing cystoscopy for hematuria

A

35yo, unless smoker, exposure to cyclophosphamide or analine dye

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11
Q

Cutoff for treatment of hypertension based on ambulatory BP monitoring

A

135/85 awake, 125/75 asleep

Use average BP

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12
Q

When to start combo anti-HTN

A

20/10 above goal BP

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13
Q

Aminoglycoside nephrotoxicity features

A

Onset w/in 5-10d
Non-oliguric
Granular casts in the urine

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14
Q

Gitelman mimics

A

thiazide diuretic

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15
Q

oncogenic osteomalacia

A

2/2 benign soft tissue tumor -> overexpression of FGF-23
bone pain/increased alk phos/osteomalacia/fractures, hypophosphatemia, renal phosphorus wasting, low 1,25-dihydroxy VitD w normal 25-hydroxy Vit D

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16
Q

trimethoprim Cr effect

A

can raise Cr by 0.5 based on change in secretion, not decrease in GFR

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17
Q

FeNa/FeUrea cutoffs for pre-renal

A

FeNa 2% likely ATN

FeUrea

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18
Q

Treatment class IV SLE nephritis

A

IV steroids plus IV MMF or IV cyclophosphamide

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19
Q

Orlistat renal effects

A

Increased intestinal uptake of oxalate -> oxalate nephropathy

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20
Q

Acquired cystic kidney disease

A

increases with time in ESRD/on HD. large number of small bilateral kidney cysts, reduced kidney size, and a markedly increased (30x) risk for developing renal cell carcinoma

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21
Q

5 types of cardiorenal syndrome

A

1) acute heart failure leading to acute kidney injury (AKI) (CRS1), 2) chronic heart failure leading to chronic kidney disease (CKD), 3) AKI leading to acute heart failure, 4) CKD leading to cardiac dysfunction (heart failure, coronary artery disease, arrhythmias), and 5) systemic conditions leading to simultaneous heart and kidney dysfunction (such as sepsis)

22
Q

HTN prior to 20th week of pregnancy?

A

Chronic HTN

23
Q

Gestational HTN

A

Begins after 20th wk of pregnancy and must resolve w/in 12wks postpartum

24
Q

Reset osmostat

A

stable, mild hypo-osmolar hyponatremia 2/2 downward setting of the level at which sensors of plasma osmolality trigger the release of antidiuretic hormone and is associated with quadriplegia, tuberculosis, advanced age, pregnancy, psychiatric disorders, and chronic malnutrition

25
Q

Metabolic compensation for respiratory acidosis

A

Increase bicarb by 1-2 for every 10mmHg increase in pCO2. After 24-48hrs, increase bicarb by 3-4 for every 10mmHg increase in pCO2

26
Q

Causes FSGS

A

chronic hypertension, diabetes mellitus, progressive kidney disease, obesity, sickle cell disease, reflux nephropathy, or after nephrectomy, drugs (pamidronate, interferon), HIV

27
Q

When to screen for intracranial aneurysms in ADPKD

A
  1. family history of aneurysm or subarachnoid hemorrhage
  2. previous rupture
  3. high-risk occupations in which a rupture would affect the lives of others.
28
Q

Type 1 RTA associated conditions

A

genetic causes, autoimmune disorders (Sjogren’s, AA hepatitis, primary biliary cirrhosis, SLE, RA), nephrocalcinosis/hypercalciuria, dysproteinemias, drugs/toxins (ifosamide, amphotericin B, lithium, ibuprofen), and tubulointerstitial disease

29
Q

Henoch Schonlein purpura AKA

A

IgA vasculitis

30
Q

Bartter syndrome mimics

A

Loop diuretic

metabolic alkalosis, hypokalemia, and normal to low blood pressure with mild volume depletion

31
Q

Tx calcium oxalate stones

A

maintain UOP >2L/d and adequate calcium intake
cholestyramine to bind oxalate in the gut to decrease absorption
if low urine citrate -> alkalinize with potassium citrate

32
Q

Compensation for respiratory alkalosis

A

Acute: Decrease HCO3 by 2 for every 10mmHg decrease in pCO2

Chronic (after 24-48hrs): Decrease HCO3 by 4-5 for every 10mmHg decrease in pCO2

33
Q

Delta delta ratio

A

delta AG/ delta HCO3
delta AG = AG - 12 (=normal AG)
delta HCO3 = 25 - HCO3
if delta delta ratio less than 1 likely combo of anion gap metabolic acidosis plus non anion gap metabolic acidosis
if delta delta ratio >2 -> combo of anion gap metabolic acidosis plus metabolic alkalosis

34
Q

Hypophosphatemia symptoms

A

weakness, myalgia, rhabdomyolysis, arrhythmias, heart failure, respiratory failure (diaphragmatic weakness), seizures, coma, and hemolysis

35
Q

Sx of D lactic acidosis

A

intermittent confusion, slurred speech, ataxia, and an increased anion gap metabolic acidosis with a normal plasma lactate level

36
Q

Assessment of volume status in metabolic alkalosis

A

Urine Cl
>15: saline-responsive metabolic alkalosis causes include vomiting, remote use of diuretics, and post-hypercapnic metabolic alkalosis

37
Q

Tumor lysis electrolyte findings

A

Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia

38
Q

Primary vs secondary FSGS

A

Primary: hypoalbuminemia, extensive foot process effacement on biopsy -> consider immunosuppression
Secondary: enlarged glomeruli, minimal edema, rarely full picture of nephrotic syndrome -> ACE/ARB plus treatment of underlying condition

39
Q

Cholesterol embolization AKI

A

peripheral eosinophilia, hypocomplementemia, inflammation/eosinophiliuria, digital ischemia/infarction, can have livedo reticularis

40
Q

Osmolal gap

A

Difference between measured osms and calculated osms. If high gap, think methanol, ethylene glycol, sorbitol, mannitol, significantly elevated lipids, paraproteins
Calculated osms = 2xNa + urea + glucose + ethanol (optional)

41
Q

Treatment suspected ethylene glycol intoxication

A
  1. fomepizole (competitively inhibits alcohol dehydrogenase)

2. bicarb if pH

42
Q

Acquired hypokalemic periodic paralysis associated condition

A

Thyrotoxicosis, esp in men of Asian or Mexican descent

Can also be hertiable

43
Q

Hypokalemic periodic paralysis precipitants

A

Exercise
Carbohydrate rich meal
-> sudden intracellular shift of potatssium

44
Q

Goal BP chronic HTN in pregnancy

A

More liberal: 120-160/80-105 mm Hg

different than in pre ecclampsia

45
Q

Water restriction test

A

Use: confirm DI, differentiate central vs nephrogenic
Procedure: restrict water, measure hourly urine volume, urine osmolality, and plasma sodium concentration
Interpretation: if serum Osms don’t increase to >600 -> DI
Then give desmopression. If central -> serum Osms will increase. If nephrogenic -> serums Osms will not increase

46
Q

Goal HCO3 in CKD

A

23-29 (reduces risk of progression of CKD)

47
Q

Proteinuria equivalents for pre ecclampsia

A

thrombocytopenia (platelet count 1.1 or a doubling of the serum creatinine concentration in the absence of other kidney disease)
impaired liver function (elevated blood concentrations of liver aminotransferases to twice the normal concentration)
pulmonary edema
cerebral or visual symptoms

48
Q

Iron study goals ESRD

A

Transferrin sat >30%
Ferritin >500
(KDIGO recommends IV iron)

49
Q

Differentiate primary vs secondary membranous glomerulopathy

A

antibody to the phospholipase A2 receptor (PLA2R)
if positive: more likely primary
secondary causes: malignancies (solid organ cancers, especially lung, colon, and breast), autoimmune diseases (such as lupus or mixed connective tissue disease), infections (hepatitis B and C), and medications (penicillamine, gold, and NSAIDs)

50
Q

Treatment calcium-based nephrolithiasis

A

HCTZ

51
Q

Treatment uric acid nephrolithiasis

A

maintain UOP >2L/d
alkalinize urine w K citrate
allopurinol if refractory