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nephrology Flashcards

1
Q

alternative marker for GFR thats not affected by age or muscle mass

A

serum cystatin c

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2
Q

what can cause an overestimation of GFR

A

falsely low Cr from loss of muscle mass because of advanced age, liver failure, or malnutrition

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3
Q

what is the only protein detected on a UA

A

albumin

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4
Q

what test thats not widely use can detect albumin with other proteins

A

sulfosalicylic acid (SSA) test

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5
Q

urine protein of >150 mg/g but <200 mg/g can indicate while protein >3500 indicates

A

tubulointerstitial disease or glomerular disease

vs glomerular disease

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6
Q

Proteinuria is a marker of and cand indicate

A

l parenchymal and glomerular disease and an independent predictor of progressive kidney disease,
cardiovascular disease, and peripheral vascular disease.

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7
Q

how to diagnose orthostatic/positional proteinuria

A

by obtaining split daytime

(standing) and nighttime (supine) urine collections.

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8
Q

coexisiting protein and hematuria can indicate what subtype of disease

A

glomerular causes of hematuria, even in the absence of casts.

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9
Q

Hematuria with preserved erythrocyte morphology in the urine, often without proteinuria or casts, is consistent with

A

extraglomerular bleeding (GU cancer, kidney stones, trauma, infection, and medications)

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10
Q

work up for hematuria

A
  • urinalysis or urine culture to exclude infection, and if normal…
  • noncontrast helical CT to detect calculi and contrast CT to detect renal cell carcinoma, and if normal…

• urine cytology, then stop evaluation if normal and patient is at low risk for malignancy (age <35 years, female sex, no other
risk factors), otherwise…

• cystoscopy for patients with positive urine cytology, aged >35 years, male, or if risk factors for malignancy are present
(cigarette smoking, analgesic abuse, benzene exposure, or voiding abnormalities)

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11
Q

leukocytes in urine indicate

A

glomerular or tubulointerstitial inflammation, infection, or an allergic reaction.

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12
Q

sterile pyuria (pyuria and a negative urine culture) suggests

A

Mycobacterium tuberculosis, interstitial cystitis, or

interstitial nephritis.

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13
Q

Eosinophiluria indicates

A

AIN, postinfectious GN, atheroembolic disease of the kidney, septic emboli, or small-vessel vasculitis but abscence doesn’t rule out any of these either

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14
Q

causes for for blood on dipstick urinalysis in the absence of intact erythrocytes on urine microscopy

A

dialysis and rhabdo

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15
Q

Urine lipids and fat are almost always associated with

A

heavy proteinuria or the nephrotic syndrome.

These may appear as free lipid droplets, round or oval fat bodies, or fatty casts.

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16
Q

what are kidney us used for

A

nephrolithiasis
• kidney size and cortical thickness (increased echogenicity implies parenchymal disease)
• renal cysts and tumors
• obstruction and hydronephrosis
• bladder size, postvoid residual, and the prostate in bladder outlet obstruction

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17
Q

what are kidney CT used for

A

nephrolithiasis (noncontrast abdominal helical CT)
• renal tumors and cysts (contrast abdominal CT)
• causes of unexplained urologic/nonglomerular hematuria (CT urography)

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18
Q

what are kidney MRI used for

A
  • when radiocontrast agents must be avoided (risk of nephrogenic systemic fibrosis in patients with CKD)
  • to characterize renal masses, cysts, and renal vein thrombosis
  • to look for renal artery stenosis using MRA with gadolinium contrast
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19
Q

indications for kidney biopsy

A

glomerular hematuria
• severely increased albuminuria
• acute or CKD of unclear origin
• kidney transplant dysfunction

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20
Q

contraindications for kidney biopsy

A

bleeding diatheses, severe anemia, UTI, hydronephrosis, uncontrolled
hypertension, renal tumor, and atrophic kidneys.

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21
Q

hypertonic hyperosmolar causes of hyponatremia

A
  • glucose (most common)
  • BUN
  • alcohols
  • mannitol
  • sorbitol
  • glycine (bladder irrigation during urological procedures)
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22
Q

lab studies consistent with hypovolemic hypoosmolar hyponatremia

A

Spot urine sodium <20 mEq/L

BUN/creatinine >20:1

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23
Q

causes of hypovolemic hyponatremia

A

GI or kidney sodium losses, mineralocorticoid

insufficiency

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24
Q

hypervolemic hyponatremia lab findings

A

Spot urine sodium <20 mEq/L (HF and cirrhosis
in absence of diuretic therapy)
Spot urine sodium >20 mEq/L (acute and
chronic kidney failure)

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25
Q

causes of hypervolemic hyponatremia

A

HF, cirrhosis, kidney failure

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26
Q

euvolemic lab finding possibilities

A

Spot urine sodium >20 mEq/L

Urine osmolality usually >300 mOsm/L
vs
Urine osmolality 50 to 100 mOsm/L

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27
Q

euvolemic hyponatremia with spot sodium <20 and osm >300 causes

A

SIADH, hypothyroidism, adrenal insufficiency
(Addison disease), cerebral salt wasting syndrome
Euvolemia (normal volume)

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28
Q

euvolemic hyponatremia with spot sodium <20 and osm 50-100 causes

A

Compulsive water drinking

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29
Q

illness that cause siadh

A

malignancy (SCLC); intracranial pathology; and pulmonary diseases, especially those that increase
intrathoracic pressure and decrease venous return to the heart

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30
Q

MEDS that cause siadh

A

thiazides, SSRIs,

tricyclic antidepressants, narcotics, phenothiazines, and carbamazepine.

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31
Q

what can happen with overcorrecting hyponatremia

A

Central pontine myelinolysis (osmotic demyelination syndrome) may occur if hyponatremia is corrected too rapidly.

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32
Q

tx for siadh hyponatremia

A

1st water restriction
2nd option loop diuretic with salt
3rd Demeclocycline

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33
Q

causes of hypernatremia

A

inadequate access to water (older patients in nursing homes), a kidney concentrating defect (DI, most commonly caused by lithium),
and/or impaired pituitary secretion of ADH (e.g., sarcoidosis). Most commonly, hypernatremia results from loss of hypotonic
fluids (GI, kidney, skin) with inadequate water replacement

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34
Q

causes of hyperkalemia

A

• hyporeninemic hypoaldosteronism (Type 4 RTA; commonly seen among patients with diabetes)
• acute and chronic kidney failure
• low urine flow states
• medications (ACE inhibitors, ARBs, potassium-sparing diuretics, pentamidine, trimethoprim-sulfamethoxazole, and
cyclosporine)
• potassium shifts (rhabdomyolysis, hemolysis, hyperosmolality, insulin deficiency, β-adrenergic blockade, and metabolic

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35
Q

ekg changes in hyperkalemia

A

peaking of the T waves and shortening of the QT interval. As hyperkalemia progresses, the PR interval is prolonged, a loss of P waves occurs, and eventual widening of the QRS complexes is seen with a “sinewave” pattern that can precede asystole.

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36
Q

significant hyperkalemia but no ecg changes likely means

A

pseudohyperkalemia

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37
Q

what matters more of severity of hyperkalemia serum amount or ekg changes

A

ekg

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38
Q

If hypomagnesemia is suspected, look for

A

neuromuscular irritability, hypocalcemia, and hypokalemia

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39
Q

causes of hypomagnesemia

A
  • GI losses (diarrhea, steatorrhea, intestinal bypass, pancreatitis)
  • kidney losses (loop and thiazide diuretics, alcohol-induced)
  • medictxations (cisplatin, aminoglycosides, amphotericin B, cyclosporine)
  • hungry bone syndrome following parathyroidectomy
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40
Q

tx for magnesium deficiency

A

Administer oral slow-release magnesium and IV magnesium sulfate to achieve a serum magnesium level >1 mg/dL

41
Q

anion gap equation

A

e anion gap = [Na+] − ([Cl–] + [HCO3–])

42
Q

causes of high anion gap metabolic acidosis

A

DKA
• CKD
• lactic acidosis (usually because of tissue hypoperfusion)
• aspirin toxicity
• alcoholic ketoacidosis
• methanol and ethylene glycol poisoning (also typically associated with an osmolar gap)

43
Q

cause of normal anion gap metabolic acidosis

A

• GI HCO3
– loss (diarrhea)
• kidney HCO3
– loss (ileal bladder, proximal RTA)
• reduced kidney H+ secretion (distal RTA, type IV RTA)
• Fanconi syndrome (phosphaturia, glucosuria, uricosuria, aminoaciduria)
• carbonic anhydrase inhibitor use (acetazolamide and topiramate)

44
Q

Urine anion gap for normal AG metabolic acidosis to differentiate RTA from extrarenal losses ie diarrhea

A

extrarenal bicarb loss - a markedly negative (-20 to -25 mEq/L) UAG.

RTA type 1 (urine bicarb/cl is impaired) - UAG being markedly positive (20-40 mEq/L).

45
Q

Type 1 RTA metabolic findings

A 
Normal anion gap metabolic acidosis
hypokalemia
 positive UAG, urine pH >5.5 (only in
the setting of systemic acidosis)
serum [HCO3] ≅ 10 mEq/L
46
Q

Type 1 RTA associated findings

A 
Nephrolithiasis and nephrocalcinosis,
autoimmune disorders (SLE, Sjögren syndrome),
amphotericin B use, urinary obstruction
47
Q

Type 2 RTA metabolic findgs

A 
Normal anion gap metabolic acidosis,
 normal or negative UAG, 
hypokalemia, 
urine pH <5.5, serum
[HCO3] ≅ 16-18 mEq/L
48
Q

Type 2 RTA associated findings

A

Glycosuria, phosphaturia, uricosuria,
aminoaciduria, and tubular proteinuria (Fanconi
syndrome)

49
Q

Type 4 RTA metabolic findings

A

Normal anion gap metabolic acidosis,
hyperkalemia,
positive UAG,
urine pH <5.5

50
Q

Type 4 RTA associated findings

A

Diabetes mellitus, urinary tract obstruction

51
Q

treatment of Type 1 RTA

A

A, administration of bicarbonate

52
Q

treatment for type 2 RTA

A

The addition of a thiazide diuretic may help by inducing volume depletion, lowering the GFR, and thereby decreasing the filtered load of bicarbonate.

53
Q

treatment for type 4 RTA

A

a, which will treat the acid-base disturbance. These
patients, often with early CKD and diabetes, may develop severe hyperkalemia following treatment with ACE inhibitors or
ARBs.

54
Q

how to treat etoh ketoacidosis

A

IV normal saline, glucose, and thiamine

55
Q

• If (Δ anion gap/Δ [HCO3]) is <1, consider concurrent normal anion gap acidosis.

A

concurrent normal anion gap acidosis.

56
Q

• If (Δ anion gap/Δ [HCO3]) is >2

A

concurrent metabolic alkalosis

57
Q

what does it mean when you have an increased osmolar gap

A

gap> 10 can suggest alcohol poisoning
Ethanol is the most common cause of alcohol poisoning. Methanol, isopropyl alcohol, and ethylene glycol can also
increase the osmolal gap.

58
Q

major findings in ethanol poisoning and tx

A

CNS depression, oliguria, flank pain and hematuria
No anion gap but increased osmolar gap
Tx- supportive

59
Q

major findings in isopropyl alcohol and tx

A

CNS depression, ↑ Ketones
No anion gap but increased osmolar gap
Tx- supportive

60
Q

major findings in methonol and tx

A

windshield wiper fluid
CNS depression, Vision loss
increased anion gap and osmolar gap
Tx- Fomepizole, Dialysis (severe) and Folic acid

61
Q

major findings in ethylene glycol and tx

A

anti-freeze
-CNS depression, Acute kidney injury, Calcium oxalate crystals in the urine
increased anion gap and osmolar gap
Tx- Fomepizole, Dialysis (severe)

62
Q

types of nephropathy

A

Focal segmental glomerulosclerosis
membranous
minimal change and DM

63
Q

Focal segmental

glomerulosclerosis associations

A

Most common cause of nephrotic syndrome in blacks
“Collapsing” variety associated with HIV
Associated with morbid obesity

64
Q

Membranous

glomerulopathy Associations

A

Most common cause of nephropathy in whites
Positive antibody against phospholipase A2 receptor
Secondary causes include: infection (hepatitis B and C, malaria,
syphilis); SLE; drugs (NSAIDs); cancer (solid tumors, lymphoma)
High propensity for thrombosis, especially renal vein
thrombosis

65
Q

Minimal change

glomerulopathy

A

Most common cause of primary nephrotic syndrome in children

10% of nephrotic syndrome in adults

66
Q

Diabetic

nephropathy

A

Most common secondary cause of the nephrotic syndrome and the most common overall cause in adults
Annual measurement of albumin-creatinine ratio measured beginning 5 years after diagnosis of type 1 diabetes and at time of diagnosis of type 2 diabetes

67
Q

hallmark sign of nephritis

A

dysmorphic erythrocytes and erythrocyte casts

68
Q

types Pauci-immune GN (necrotizing GN with few immune

deposits, normal complement)

A

Granulomatosis with polyangiitis
Microscopic polyangiitis
Eosinophilic granulomatosis with polyangiitis

69
Q

type of gns with Immune complex deposition (low complement with
exception of IgA nephropathy)

A

IgA nephropathy
IgA vasculitis (Henoch-Schönlein purpura)
LN
Infection-related GN
Membranoproliferative GN
Cryoglobulinemia (see Monoclonal Gammopathies and Cryoglobulinemia)

70
Q

what is anti–Glomerular Basement Membrane Antibody Disease and what is it if pulmonary capillaries are involved

A

autoimmune disease caused by antibodies directed against type IV collagen.
it causes pulmonary hemorrhage (Goodpasture syndrome).

71
Q

lab and biopsy finding in anti-glomberular basement membrane antibody disease

A

normal complement levels and elevated levels of anti-GBM antibodies. Kidney biopsy shows proliferative GN
with linear deposition of immunoglobulin.

72
Q

tx for anti–Glomerular Basement Membrane Antibody Disease

A

cyclophosphamide and glucocorticoids, combined with daily plasmapheresis.

73
Q

granulomatosis with polyangiitis anca association

A

c-anca RP-3

74
Q

MPA is associated with anca

A

p-anca mpo

75
Q

labs and biopsy in pauci immune gn

A

Complement levels are normal. Kidney biopsy shows absent or minimal staining with immunoglobulin

76
Q

tx for pauci immune gn (MPO, GPA)

A

glucocorticoids and cyclophosphamide (or rituximab) with or without plasmapheresis.

77
Q

most common presentations of IGA nephropathy

A

asymptomatic microscopic hematuria (with or without proteinuria) or episodic gross hematuria
coincident with a URI (synpharyngitic nephritis).

78
Q

compliment level and biopsy in iga nephropathy

A

Kidney biopsy shows glomerular IgA deposits on immunofluorescence. Complement levels are normal.

79
Q

tx for iga nephropathy

A

benign course without treatment; patients with proteinuria and risk factors for progression may benefit from ACE inhibitors or ARBs

80
Q

IgA vasculitis (HSP) diagnosis

A

Diagnosis is confirmed either by finding an IgA-dominant leukocytoclastic vasculitis or by kidney biopsy, which shows lesions
similar to IgA nephropathy. Complement levels are normal

81
Q

labortory findings of LN

A

ANA and anti–double-stranded antibodies are positive, and C3 and C4 complement levels are depressed

82
Q

tx for LN based on class

A

Class I and II (minimal or proliferative mesangial) lesions require no specific therapy.

  • Classes III and IV (focal and diffuse glomerular lesions) are treated with high-dose glucocorticoids and either IV cyclophosphamide or mycophenolate mofetil.
  • Class V (membranous) LN has a course similar to idiopathic membranous glomerulopathy
83
Q

post-strep/staph GN occurs when

A

poststreptococcal GN typically occur after a latent period of 1 to 6 weeks

84
Q

diagnosis of Post-infectious GN

A

Diagnosis is clinical in nephritic patients who have an ongoing or preceding infection. Complement levels are low

85
Q

membranoproliferative GN is associated with which illness/demographic

A

children or young adults as proteinuria or the nephrotic syndrome. It is associated with
immune complex disease (SLE), infections (hepatitis C), and monoclonal gammopathy

86
Q

Causes of Glomerular Diseases Associated with Low Complement Levels

A
  • postinfectious GN (e.g., endocarditis, Group A streptococcal infection)
  • SLE
  • cryoglobulinemia
  • membranoproliferative GN
  • atheroembolic disease
87
Q

diagnosis criteria for ADPKD

A
  • ≥2 cysts (unilateral or bilateral) for ages 15 to 29 years
  • ≥2 cysts in each kidney for ages 30 to 59 years
  • ≥4 cysts in each kidney for ages >60 years
88
Q

when do you gene analysis test for ADPKD

A

if imagining is equivical

89
Q

symptoms of ADPKD

A

Hypertension is a common presentation. More than 50% of patients develop recurrent flank or back pain from kidney stones,
cyst rupture or hemorrhage, or infection.

90
Q

urgent uro referral is needed for kidney stones in what settings

A 
pyelonephritis or urosepsis
• AKI
• large stones requiring surgical removal
• bilateral obstruction
• obstruction of a solitary kidney
91
Q

most severe extra renal complication of adpkd

A

ruptured aneurysm

92
Q

treatment for adpkd

A

treat symptoms: HTN and pyelo/cyst infection

consider screening for aneurysm for people with adpkd esp if they have fam history

93
Q

what is hereditary nephritis

A

rare end stage renal disease Xlinked also known as alport syndrome

94
Q

symptoms of hereditary nephritis

A

sensorineural hearing loss and characteristic ocular findings such as lenticonus. Proteinuria, hypertension, and CKD usually develop over time.

95
Q

Tx for hereditary nephritis

A

none, patients get end stage renal disease by teenage to 4th decade of life

96
Q 
Pre-renal AKI:
 BUN-Creatinine 
Urine Osmolality (mEq/L)
 Urine Sodium 
FENa 
Urinalysis and Microscopy Ratio
A 
>20:1
>500
<20
<1%
Specific gravity >1.020; normal or hyaline casts
97
Q 
ATN:
 BUN-Creatinine 
Urine Osmolality (mEq/L)
 Urine Sodium 
FENa 
Urinalysis and Microscopy Ratio
A 
10:1 
~300
 >40 
>2% (can be low in contrast nephropathy)
Specific gravity ~1.010; muddy brown casts and
tubular epithelial cells
98
Q

post renal BUN: creatinine ratio

A

20:1

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