Renal Disorders Flashcards

1
Q

Nephrotic Syndrome

A

● Noninflammatory damage
to the glomerular capillary
wall
● Proteinuria – >3g/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Essentials of Diagnosis of Nephrotic syndrome

A

○ Severe proteinuria (>3g/day)
○ Hypoalbuminemia
○ Edema (legs, lungs, abdomen)
○ Hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common cause of nephrotic
syndrome in children

A

Minimal Change Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Nephrotic syndrome presentation

A

● Weight gain
● Fatigue
● SOB
● Edema
● Frothy urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F Labs cannot be used to distinguish
between forms of nephrotic syndrome

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primary (Idiopathic) Minimal Change Disease

A

● Most common
● Not associated w/ underlying
disease
● ↑ glomerular capillary wall
permeability = foot process
effacement and proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Secondary etiology for Minimal Change Disease

A

● Drugs
○ NSAIDs, Lithium
○ Some antibiotics, including
cephalosporins
● Neoplasms
○ Hodgkin lymphoma
● Infections
○ Viral URI (especially in kids)
○ TB, syphilis, Hepatitis C, Lyme disease.
● Allergy
○ NSAIDs, bee stings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Minimal Change Disease - Presentation

A

● Sudden onset (compared to other causes of
nephrotic syndrome) over days to 1-2 weeks.
● Often following an upper respiratory or
systemic infection
● Microscopic hematuria and AKI (mostly adults)
● Elevated serum creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Minimal Change Disease - Diagnostics

A

● Labs: CBC, CMP, lipid panel, UA, urine
microalbumin/creatinine ratio
○ Can’t be used to distinguish between
forms of nephrotic syndrome
● Kidney biopsy is required for diagnosis
in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Minimal Change Disease - Pathologic Findings

A

● Glomeruli appear normal
● No complement or immunoglobulin deposits
● Effacement of pedicles
○ They fuse and become short and wide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Minimal Change Disease - Management

A

● STEROIDS
○ 1st line is prednisone
○ Up to 16 weeks (and 2 weeks
after remission)
● Infection control
● Treat edema
○ Salt restriction, diuretics
● Prevent blood clots
○ Pt’s mobility should not be restricted
● Maintain adequate protein intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Focal Segmental Glomerulosclerosis -
Epidemiology

A

● More common in adults
● Most common primary glomerular
disease identified in patients with
end-stage kidney disease in the USA
● Higher risk of ESKD in Blacks and males
● Incidence is rising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

FSGS - Etiology/Presentation (Primary)

A

● Circulating permeability factor causes
podocyte dysfunction and pedicle
effacement
● Can also be caused by genetic mutations
● Acute onset nephrotic syndrome (80% of
children and 50% of adults)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Biopsy will show diffuse (≥80 percent)
podocyte foot process effacement with ____

A

Primary FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

FSGS - Etiology/Presentation (Secondary)

A

● Nephrotic syndrome is uncommon
in secondary FSGS (but can still
happen!)
● Slowly increasing proteinuria (often
in non-nephrotic range)
● Almost always serum albumin level
stays normal (no peripheral edema or
hypoalbuminemia)
● Proteinuria w/o hypoalbuminemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Kidney biopsy will show segmental (<80 percent) podocyte foot process effacement with ______

A

FSGS - Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

FSGS - Diagnostics

A

● Labs (are these going to tell you the exact
diagnosis?)
● Genetic testing
● BIOPSY REQUIRED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

FSGS - Management (Primary)

A

● Immunosuppressive medication
○ Corticosteroids, calcineurin inhibitors
○ Only use if nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

FSGS - Management (Secondary)

A

● Treat or remove the underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

FSGS - Management (General)

A

● Sodium and protein
restriction
● BP control
● Minimize proteinuria w/ ACE/ARB
● Statin for hyperlipidemia if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Membranous Nephropathy -
Epidemiology

A

● Most common cause of primary adult
nephrotic syndrome
● Primary MN is more common in White
males over the age of 40 years
● MN in young females should raise the
suspicion of systemic lupus
erythematosus
● Less common in children, but if present
is often associated w/ hepatitis B,
autoimmune, or thyroid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Membranous Nephropathy - Primary Etiology

A

● Autoantibodies against podocyte
antigens
○ phospholipase A2 receptor
PLA2R most common
○ THSD7A or NELL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Membranous Nephropathy - Presentation

A

● Most patients present w/ nephrotic
syndrome
● May just have asymptomatic proteinuria
● Signs of underlying infection or neoplasm
(secondary)
● Caused by gradual subepithelial deposits, so
symptoms develop more slowly than MCD or FSGS
● Proteinuria anywhere from <3.5 to over 20 g/day
● Severe hyperlipidemia (if nephrotic)
● Fatty casts in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Membranous Nephropathy - Diagnostics

A

● Labs: What do you want to order?
● Serologic testing for SLE, syphilis, anviral hepatitis
● Age- and risk-appropriate cancer screening
● PLA2R antibody titer
○ Diagnostic
○ May eliminate need for biopsy
● Kidney biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pathology of Membranous Nephropathy

A

● Thickened glomerular basement
membrane
● “Spike and Dome” pattern -
projections of excess GBM between
the subepithelial immune complex
deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Membranous Nephropathy - Management if high risk

A
  1. Serum creatinine ≥1.5 mg/dL
  2. Progressive decline in kidney function
  3. Severe, disabling, or life-threatening
    nephrotic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Membranous Nephropathy - Management of low risk

A
  1. Normal kidney function
  2. Do not have severe, disabling, or
    life-threatening nephrotic syndrome
28
Q

Hydronephrosis

A

● Hydronephrosis = distention of the
renal calyces and pelvis of one or
both kidneys by urine.
● Most commonly caused by urinary
tract obstruction (UTO)

29
Q

Hydronephrosis - Congenital Etiology

A

● Majority (72%) is in males
● Posterior urethral valves (males only)
● Narrowing of the ureteropelvic or
ureterovesicular junction
● Vesicoureteral reflux

30
Q

______ = blockage at or
below the level of the bladder or urethra

A

Bilateral hydronephrosis

31
Q

_____ = blockage
above the level of the bladder

A

Unilateral hydronephrosis

32
Q

↑ pressure in ureters = ___ nephron function

A

33
Q

Hydronephrosis - Etiology

A

↑ pressure in ureters = ↓ nephron function
● Causes decline in renal blood flow and
GFR
● Damage can become irreversible if
obstruction not corrected
○ Tubular atrophy
○ Nephron loss

34
Q

Hydronephrosis - Presentation

A

● Flank pain (not always)
● Rise in serum creatinine
● New onset or sudden increase in HTN
● Difficulty voiding, polyuria, nocturia
● Fever or dysuria if UTI
● May palpate bladder or abdominal distention, sometimes CVA tenderness, enlarged prostate, or pelvic mass

35
Q

Hydroneprhosis - Diagnostics

A

● Urinalysis
○ Hematuria
○ Pyuria
○ Proteinuria
○ Bacteriuria
○ Sediment normal usually
● Renal function labs
○ GFR, BUN, creatinine
○ Other labs?
● Urodynamic testing if suspecting neurogenic
bladder

36
Q

First line imaging for Hydronephrosis

A

● Diuresis after catheterization
confirms obstruction
● Otherwise US is first line
○ 90% sensitivity and specificity
● Non-contrast CT if suspecting
kidney stone
● MRI if needed
● IV urogram or retrograde pyelogram
● Voiding cystourethrogram
○ Helpful for finding VUR

37
Q

Hydronephrosis - Management in Children

A

● Spontaneous resolution for most neonatal
cases, otherwise regular monitoring
● <1 year old w/ VUR and hx of UTIs are
placed on prophylactic antibiotics
● Sometimes surgical repair

38
Q

Hydronephrosis - Management in adults

A

● Hydronephrosis + infection = Emergency
○ Stents or nephrostomy, antibiotics
● Remove/treat obstruction if possible
○ Kidney stone, tumor, etc
● Surgical drainage
● Dialysis if renal failure

39
Q

Hypertensive Nephrosclerosis

A

● Chronic renal insufficiency
associated with long-standing blood
pressure elevation
● Hypertension can be both the cause and
effect of CKD

40
Q

Hypertensive Nephrosclerosis - Etiology

A
  1. Vascular disease
    ● Intimal thickening and luminal narrowing of the large and small renal arteries and the glomerular arterioles
  2. Glomerulosclerosis
    ● Focal global (involving the entire glomerulus) and focal segmental sclerosis
  3. Interstitial fibrosis and tubular atrophy
41
Q

Hypertensive Nephrosclerosis Presentation

A

● Long history of HTN, which
precedes the following:
● Slowly progressive elevations in
BUN and creatinine
● Mild proteinuria (<1g/day
typically, but can be higher)
● Possible L ventricular
hypertrophy, and/or retinal HTN
changes.

42
Q

Diagnosis of Hypertensive Nephrosclerosis

A

● Inferred from clinical features
and exclusion of other kidney
diseases
● Labs
● Kidney biopsy done only
rarely

43
Q

Management of Hypertensive Nephrosclerosis

A

● BP control
● May still continue to
progress even if BP lowered.

44
Q

Polycystic Kidney Disease -
Epidemiology

A

● Autosomal Dominant (ADPKD) most
common (12 million people worldwide)
● Autosomal recessive (ARPKD) rare,
typically pediatric

45
Q

Renal Vascular Disease

A

● Most common of secondary hypertension
● ↓ renal perfusion causes extensive renin release, activating RAAS → ↑BP
● Risk factors (similar to other vascular diseases): >45 years of age,
atherosclerosis, chronic kidney disease, diabetes, tobacco use

46
Q

Renal Vascular Disease causes

A

● ATHEROSCLEROSIS
● Thrombosis
● Fibromuscular dysplasia (mostly occurs with
young women)
● Injury
● Infection

  1. Renal Artery Stenosis
  2. Renal Artery Aneurysm
  3. Renal Vein Thrombosis
  4. Atheroembolic Renal Disease
47
Q

Renal Vascular Disease Treatment

A

● Blockade of the renin-angiotensin system
● Attainment of goal BPs
● Cessation of tobacco
● Statins
● aspirin
● Renal revascularization is now often reserved for patients failing medical therapy or developing additional complications

48
Q

Renal Artery Stenosis etiology

A

Majority of cases are due to
atherosclerosis, most others are due to
fibromuscular dysplasia (often in young
women. Renal artery narrowing and
subsequent RAAS activation causes
renovascular hypertension

49
Q

Renal Artery Stenosis Treatment

A
  • Treat hypertension with ACE inhibitor/ARB,
    plus diuretic
  • Consider revascularization with stent or
    endarterectomy if there is high chance of
    benefit or high risk of complications
50
Q

Renal Artery Stenosis Diagnosis

A

Renal arteriography is gold standard. Can also use duplex ultrasound, CTA, or MRA

51
Q

Renal Artery Aneurysm

A

● Rare
● Females at higher risk (likely due to higher
incidence of FMD)
● Risk of rupture increased w/ pregnancy
● Majority of patients have HTN

52
Q

Renal Artery Aneurysm presentation

A

● Usually asymptomatic and incidental
finding
● Abdominal/flank pain and hypotension if
ruptured

53
Q

Renal Artery Aneurysm Treatment

A

● Symptomatic or high risk of
rupture = surgical repair
● Asymptomatic and low risk
= observe
● Screen for other aneurysms

54
Q

Renal Vein Thrombosis Etiology

A

Can result from systemic inflammation or prothrombotic state (e.g., nephrotic syndrome, carcinoma, trauma, pregnancy/OCPs), extrinsic compression, trauma

55
Q

Renal Vein Thrombosis treatment

A

● Treat underlying cause
● Consider
thrombolysis/thrombectomy or
anticoagulation based on clinical severity

56
Q

Renal Vein Thrombosis Clinical features

A

Evidence of decreased renal
perfusion (rising Cr, decreased urine output,
hypertension) and renal injury (hematuria,
proteinuria)

57
Q

Diagnosis of Renal Vein Thrombosis

A

Duplex ultrasound, CTA, MRA

58
Q

Atheroembolic Renal Disease

A

● Cholesterol crystal embolism
● More common in older patients w/ diffuse
atherosclerosis
● Portions of plaque break off and embolize,
occludes small arteries or glomerular
arterioles
● May be spontaneous or iatrogenic

59
Q

Presentation of Atheroembolic Renal Disease

A

● Subacute kidney injury several weeks after
inciting event
● Severe hypertension
● Occasionally AKI
● Blue toe syndrome or livedo reticularis
● Other clots. Such as?

60
Q

Atheroembolic Renal Disease Diagnosis (classic triad)

A

● Kidney biopsy is definitive (or skin if lesion present)
OR classic triad
1. A precipitating event (such as
aortic or coronary angiography)
2. Subacute or acute kidney injury
3. Typical skin findings, such as
blue toe syndrome and/or livedo
reticularis

61
Q

Treatment for Atheroembolic Renal Disease

A

● Surgical plaque removal
● Stents
● ASCVD risk reduction
● Poor prognosis. mortality rates
may be as high as 80 percent

62
Q

Renal Fusion

A

● 1:1000 individuals
● “Horseshoe Kidney” is most common type
● Fused kidneys stay low in the pelvis
● Due to abnormal kidney placement and
rotation, ureters are easily compressed
● Hydronephrosis common (which
increases infection risk)
● Frequently associated w/ VUR

63
Q

Renal Fusion presentation

A

● Usually asymptomatic
● Can have GI symptoms, UTO, infections
● Kidney function usually normal

64
Q

Renal Fusion diagnosis

A

● Usually incidental
● X-ray w/ ureteral catheters
● Retrograde urogram
● CT
● US

65
Q

No treatment needed unless
obstruction or infection for _____

A

Renal Fusion