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Internal Medicine: PGY-1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Name a few causes of low vs. high BUN

A

High
- high protein diet
- antianabolic meds (steroids, tetracyclines)
- catabolic process (fever, infection)
- low effective arterial blood volume
- UGIB

Low
- low protein diet
- malnutrition
- impaired hepatic function

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2
Q

What is the expected rise in serum creatinine in 24h-period in average patient with anuric AKI? When can it be expected to be worse?

A
  • 88-176mmol/L per day
  • extreme catabolic state, rhabdo
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3
Q

Risk factors for developing AKI?

A
  • prior CKD
  • age
  • diabetes
  • black race
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4
Q

What are the symptoms of AKI?

A
  • Asymptomatic
  • Decreased urine output
  • Peripheral edema
  • Gross hematuria
  • SOB
  • Uremia symptoms: fatigue, weak, N/V, low appetite, pruritus, asterixis, paresthesia, anemia, pericarditis
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5
Q

When should you consider RRT in patients with AKI?

A
  • anuria >6h
  • severe oliguria (<200ml x12h)
  • severe hyperK (>6.5)
  • severe metabolic acidosis (pH<7.2 with normal PaCO2)
  • hypervolemia (esp. if pulm. edema present)
  • severe azotemia
  • uremia sequelae (eg., pericarditis)
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6
Q

Definition of CKD?

A
  • presence of kidney damage (albuminuria), or
  • decreased kidney function (GFR <60) >3 months
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7
Q

Structures affected in AKI:
1. prerenal
2. intrarenal
3. postrenal

A
  • structures: up to and including afferent arterioles
  • renal parenchyma: glomeruli, interstitium, tubules, blood vessels
  • any: process obstructing urine flow
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8
Q

Biocemical lab to suggest prerenal AKI? Intrarenal?

A

BUN:creat
- pre: >20:1 (caused by increased urea reabsorption in PCT 2/2 low effective arterial blood volume
- intra: <15:1

FENa
- pre: <1% or <35% (if on diuretics)
- intra: >1-2% or >35%

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9
Q

Urine sediments:
- prerenal
- intrarenal
- postrenal

A

Prerenal
- Bland, hyaline casts

Intrarenal
- ATN: granular, “muddy”, pigmented; tubular epithelial cells
- AIN: WBC casts
- GN: RBC casts
- Nephrotic: Fatty casts

Postrenal
- Hematuria (stones, bladder Ca, clots)
- Absent (neurogenic bladder)

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10
Q

How does hyperCa2+ cause AKI?

A

Causes:
- a reduction in glomerular filtration related to afferent arteriolar contriction
- renal salt wasting –> hypovolemia

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11
Q

HRS 1 vs 2: main difference?

A

HRS 1
- Rapid, doubling creatinine in <2wks
- commonly associated with MOF
- Oliguria more common

HRS 2
- Indolent
- Stable course often associated with refractory ascites

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12
Q

What are the general categories of intrarenal AKI?

A
  • Vascular
  • GN
  • ATN
  • AIN
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13
Q

Which type of vasculitis can involve the renal artery? Associated with intrarenal AKI?

A

Renal Artery
- Medium: PAN, Kawasaki
- Large: GCA, Takaysu

Intrarenal AKI
- Small: GPA, eGPA, Churg-Strauss Syndrome, microscopic polyangiitis, HSP (often cause GN)

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14
Q

What are the lab features of atheroembolic renal disease? (intrarenal AKI)

A
  • peripheral + urinary eosinophilia
  • serum hypocomplementation
  • other labs can indicate other organ involvement: hepatocellular injury (etc.)
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15
Q

What is the mechanism of AKI in ATN?

A

Tubular dysfunction 2/2 tubular epithelial cell injury (ischemic vs. toxic)

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16
Q

What is the timing + prognosis of contrast-induced nephropathy?

A
  • CIN develops 24-48h after contrast exposure
  • Recovery usually within 7-10 days
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17
Q

Common meds associated with ATN?

A
  • NSAIDS
  • Vancomycin
  • Aminoglycosides
  • Polymyxins
  • Pentamidine
  • Ampho B
  • Foscarnet
  • Tenofovir
  • Cisplatin
  • MTX
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18
Q

Why pigment and contrast-induced nephropathies can sometimes be associated with FENa <1%?

A

In addition to toxicity of renal tubules, they can induce afferent arteriole constriction = prerenal physiology

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19
Q

What is AIN? Classic triad?

A
  • Inflammation + edema within renal interstitium
  • Triad: fever, maculopapular rash, peripheral eosinophilia (all 3 present only 10-15% of cases)
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20
Q

Meds associated with AIN?

A

Most common:
- NSAID + antibiotics
- PCN, cephalosporins, cipro, rifampin, sulfa, vanco

Others:
- Allopurinol, acyclovir, famotidine, lasix, PPI, phenytoin

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21
Q

When does AIN usually develop in relation to exposure to medication?

A
  • 7-10 days
  • sooner possible, especially if repeat exposure to culprit drug
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22
Q

AIN etiology typically meds, infection, autoimmune, and tubulointerstitial nephritis uveitis (rare). Which infection more commonly associated with AIN? Autoimmune? Which population typically affected by TINU?

A

Infection
- bacterial: brucella, campylobacter, e. coli, legionella, salmonella, strep, staphy, yersinia
- viral: CMV, EBV, HIV, hantavirus

Autoimmune
- SLE, sarcoidosis, sjorgren

TINU
- young women
- S&S: uveitis, TIN, constitutional symptoms

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23
Q

Which malignancies are typically associated with renal obstruction?

A
  • RCC
  • bladder
  • prostate
  • TCC of collecting system
  • MM
  • mets
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24
Q

Most common primary cause of glomerular disease?

A

IgA Nephropathy

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25
Nephrotic vs Nephritic syndromes: urinary findings
Nephrotic - proteinuria >3.5g/d - fatty casts: frothy urine - microscopic hematuria - sediment: bland Nephritic - sediment: dysmorphic RBC, RBC casts +/- WBC - varying proteinuria <3.5g/d - hematuria - sterile pyuria
26
DDx: Nephrotic vs. Nephritic; BONUS - most common causes of nephritic-nephrotic syndrome?
Nephrotic - MCD - FSGS - Membranous nephropathy - Diabetes - Amyloi light chain, amyloidosis, light chain deposition - Lupus nephritis Nephritic - PSGN - IgA nephropathy (Berger) - GPA, eGPA (Wegener) - Goodpasture - Alport - RPGN - Lupus nephritis Nephritic-nephrotic syndrome - Membranoproliferative GN - Diffuse proliferative GN
27
Nephrotic syndrome: what are the [1] symptoms, [2] exam findings?
Symptoms - swelling, weight gain (nephrotic) - fatigue - dyspnea - foamy urine Exam - HTN - peripheral edema - ascites - pleural effusions - less common: Muehrcke's lines [nails], eruptive xanthoma, xanthelesma
28
General lab features of nephrotic syndrome?
- proteinuria >3.5g/d - albumin <2.5g/dL - hyperlipidemia - creatinine variable
29
Common sites of theombosis in nephrotic syndrome?
- renal veins - lower extremity veins
30
Agents available to treat nephrotic syndrome?
ACEi
31
Which primary cause of nephrotic syndrome associated with thromboembolism more?
membranous nephropathy
32
Meds associated with nephrotic syndrome?
- NSAIDs - lithium - gold - penicillamine - captopril - tamoxifen
33
What infections are associated with nephrotic syndrome?
- Bacterial: IE, vDRL - Viral: HIVm HBV, HCV - Protozoal: malaria, toxoplasmosis - Helminthic: schistosomiasis, filariasis
34
Most common malignancies associated with nephrotic syndrome?
- MM - lymphoma - lung - RCC
35
In addition to amyloidosis as secondary cause of nephrotic syndrome, what other disease associated with fibrillar deposits in mesangium or GBM?
- fibrillary GN (more common) - immunotactoid glomerulopathy
36
Nephritic syndrome: symptoms and exam findings?
Symptoms - hematuria, oliguria (AKI) - CP, dyspnea (uremic pericarditis) - peripheral edema (low albumin) - headache (HTN) Exam - HTN - Skin: palpable purpura (small-vessel vasculitis) - pericardial friction rub (uremic pericarditis)
37
What type of dysmorphic RBC is most specific for GN?
Acanthocytes, ring-shaped RBCs with vesicle-shaped protrusions ("mickey Mouse ears")
38
What are the subcategories of GN based on serology?
- ANCA+ - Anti-GBM+ - Low C3/4 - Other
39
What does "ANCA" refer to?
Antineutrophil cytoplasmic antibodies: group of antibodies against proteins found in the cytoplasm of neutrophils (eg., PR3, MPO)
40
When patients are ANCA positive, what are the 2 distinct patterns seen on immunofluorescence microscopy?
- c-ANCA: antibodies to PR3 - p-ANCA: antibodies to MPO
41
What causes of GN are associated with low complement levels?
- PSGN (low c3, normal c4) - Membranoproliferative GN (low c3, normal c4) - SLE (both low, but C3
42
DDx of renal injury in the setting of IE?
- renal infarction 2/2 septic emboli - AIN 2/2 meds - ATN 2/2 septicemia or abx
43
Typical clinical features of IgA nephropathy? % of which will progress to ESRD?
Typically 2nd/3rd decades More common white/asian men **2 presentations**: 1. macroscopic hematuria usually ~5 days s/p URTI (more common in <40yo), or 2. asymptomatic with abn urine sediment + proteinuria (more common in older) ***40%!!!***
44
What 2 causes of GN are histologically the same? How are the differentiated?
- HSP and IgA nephropathy - Extrarenal manifestations: palpable purpura is universally present in HSP
45
Symptoms of hyperK+?
- cardiac arrhythmia, palpitations - weakness, paralysis, paresthesia - N/V, diarrhea - reduced DTR
46
ECG changes of hyperK+?
47
What [1] conduction abnormalities and [2] dysrhythmias are assocaited with hyperK+?
Conduction - BBB - bifascicular block - AV block Dysrhythmia - sinus brady - asystole - idioventricular rhythms (VT, VF)
48
DDx: Hematuria (4 main categories)
1) Pigments - beets, myoglobin, hemoglobin, porphyrin, rifampin, food colouring 2) Transient: - menstruation, UTI, fever, exercise, trauma, endometriosis, renal vein thrombosis 3) Glomerular - nephritic: MPGN II, RPGN, IgA - hereditary: Alport's, thin BM disease, Loin pain hematuria syndrome 4) Extra-glomerular - tumor: kidneys, ureter, bladder, urethra - stones - cystic kidney disease: PCKD, medullary cystic kidney disease, medullary sponge kidney
49
Hematuria: glomerular vs. extra-glomerular
Glomerular - cola urine - proteinuria - dysmorphic RBC (acanthocytes) - RBC casts - no clots Extra-glomerular - bright red urine - no proteinuria - no dysmorphic RBC, clots, RBC casts
50
DDx: Proteinuria (4 main categories)
1) Functional [<1g/d] - infection, fever, exercise, orthostatic 2) Tubular [0.5-1g/d] - interstitial nephritis, ATN 3) Glomerular [1-3g/d, usually >3g/d] - nephrotic/nephritic syndrome, early diabetes 4) Overflow [any amount, usually >1g/d] - MM
51
Proteinuria: test which detects all proteins?
Sulfosalicylic acid test
52
Which medication can cause "pseudo-renal failure"?
Cimetidine, trimethoprim - can reduce tubular secretion of creatinine causing small but significant increase in creat w/o change in GFR
53
Contrast-Induced Nephropathy: - Timing: onset, peak, recovery - Risk factors - Prevention
Timing - immediately after exposure - peaks: 48-72h - recovery: same as ATN Risk Factors - CKD, MM, Dm, HTN, volume deplete, HF, nephrotoxins, procedures (dye load) Prevention - use low-dose dye (if possible) - IVF: 1. NS0.45% 1ml/kg/h 12h before/after dye, or 2. NS or NaHCO3 at 3ml/kg/h 1h prior/6h post dye, or 3. NAC 150mg/kg in 500mL NS 30min before contrast then 50mg/kg 4h after
54
GN terms: - Focal - Diffuse - Segmental - Global
Area of glomerulus affected: - Focal: <50% - Diffuse: >50% - Segmental: segment of glomerulus - Global: entire glomerulus
55
GN: proliferative vs. non-proliferative
Non-proliferative - lack of cell proliferation in glomerulus, usually nephrotic Proliferative - increased cells # in glomerulus; usually nephritic
56
DDx: non-proliferative vs. proliferative GN
Non-Proliferative (nephrotic) - MCD - FSGS - Membranous - Other (amyloidosis/MGRS, Dm) Proliferative (nephritic) - MPGN - ANCA: GPA, eGPA - RPGN (linear, immune, pauci immune)
57
Causes (primary/secondary) of Nephrotic syndromes?
1) MCD - Cancer: T-cell lymphoma/**Hodgkins**, leukemias - Drugs: **NSAIDs**, Li, COX2i - Infx (rare): HIV, EBV, TB 2) FSGS (more severe form of MCD) - Drugs: Li, heroin, pamidronate, 'roids - Hyperfiltration: **obesity**, single kidney, reflux nephropathy, HTN, SCD - Infx: **HIV**, parvo, EBV 3) Membranous - **SLE** - Cancer: **solid tumors**, CLL - Drugs: gold, penacillamine, **NSAID**, **anti-TNFs** - Infx: HBV, HCV, HIV, syphilis
58
DDx + Tx: RPGN: 1) linear 2) immune 3) pauci immune
1) Linear - **anti-GBM disease** (syndrome if lung involved) - Tx: PLEX + pulse steroids + Cyclo; if no improvement at 3 months, taper off 2) Immune - **SLE**: low C3/4; hydroxychloroquine + steroids - **PSGN**: low C3; resolves 3-4 weeks - **IgA**: normal C3/4; ACEi + steroids + Cyclo/Azathio - **MPGN**: low C3/4 - HCV, cryo, CLL) ; steroids + Cyclo 3) Pauci Immune - **ANCA**: GPA/Wegener (c-anca), microscopic polyangiitis, eGPA (p-anca), churg-strauss; steroids + Cyclo (if RPGS, if not, use Ritux)
59
DDx - CKD
- any causes of acute AKI - renovascular: atherosclerosis, HTN, glomerulosclerosis (with age) - diabetes - GNs - PCKD - MM - nephrotoxins
60
Risk factors for progression of CKD?
- hypertension - age - proteinuria - dyslipidemia - high protein diet (unclear)
61
S&S Uremia
- Constitutional: tired, weak - Neuro: poor concentration, slow speech, myotonic jerks, altered taste/smell, restless leg - GI: N/V, anorexia - Heme: anemia, platelets dysfunction - MSK: bone disorders, cramps - Derm: pruritus - Sex: amenorrhea, sex dysfunction
62
CKD-MBD - targets for PO4, Ca2+, PTH?
- Ca2+: normal - PO4: <1.5mmol/L - PTH: <2-3x normal
63
Criteria for dialysis in CKD?
- any acute (AEIOU) indications - GFR <10 - albumin <35 - uremic symptoms
64
How do ACEi help in CKD? Should be started in which patients? When should it be discontinued?
Benefits - ACEi cause efferent arteriole vasodilation > decrease intraglomerular pressure > decreased long term remodeling/stress > slow progression of CKD - lowers BP, proteinuria, and mediators of glomerular tubule hypertrophy/fibrosis Should **START** - in all CKD +/- HTN +/- proteinuria Shoudl **STOP** - if >30% rise in creatinine after starting
65
RTA type I, II, IV (III extremely rare) - Patho - Serum K+ - Serum HCO3 - Urine pH - Urine AG (urine net charge; UNC) - Tx

Internal Medicine: PGY-1 (17 decks)

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