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GU Exam 2 > Renal Disorders > Flashcards

Renal Disorders Flashcards

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1
Q

Nephrotic Syndrome

A

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

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2
Q

Essentials of Diagnosis of Nephrotic syndrome

A

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

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3
Q

Most common cause of nephrotic
syndrome in children

A

Minimal Change Disease

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4
Q

Nephrotic syndrome presentation

A

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

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5
Q

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

A

T

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6
Q

Primary (Idiopathic) Minimal Change Disease

A

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

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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

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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

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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

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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

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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

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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

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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)

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14
Q

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

A

Primary FSGS

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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

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16
Q

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

A

FSGS - Secondary

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17
Q

FSGS - Diagnostics

A

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

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18
Q

FSGS - Management (Primary)

A

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

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19
Q

FSGS - Management (Secondary)

A

● Treat or remove the underlying cause

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20
Q

FSGS - Management (General)

A

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

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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

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22
Q

Membranous Nephropathy - Primary Etiology

A

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

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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

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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

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25
Pathology of Membranous Nephropathy
● Thickened glomerular basement membrane ● “Spike and Dome” pattern - projections of excess GBM between the subepithelial immune complex deposits
26
Membranous Nephropathy - Management if high risk
1. Serum creatinine ≥1.5 mg/dL 2. Progressive decline in kidney function 3. Severe, disabling, or life-threatening nephrotic syndrome
27
Membranous Nephropathy - Management of low risk
1. Normal kidney function 2. Do not have severe, disabling, or life-threatening nephrotic syndrome
28
Hydronephrosis
● Hydronephrosis = distention of the renal calyces and pelvis of one or both kidneys by urine. ● Most commonly caused by urinary tract obstruction (UTO)
29
Hydronephrosis - Congenital Etiology
● Majority (72%) is in males ● Posterior urethral valves (males only) ● Narrowing of the ureteropelvic or ureterovesicular junction ● Vesicoureteral reflux
30
______ = blockage at or below the level of the bladder or urethra
Bilateral hydronephrosis
31
_____ = blockage above the level of the bladder
Unilateral hydronephrosis
32
↑ pressure in ureters = ___ nephron function
↓
33
Hydronephrosis - Etiology
↑ 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
Hydronephrosis - Presentation
● 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
Hydroneprhosis - Diagnostics
● Urinalysis ○ Hematuria ○ Pyuria ○ Proteinuria ○ Bacteriuria ○ Sediment normal usually ● Renal function labs ○ GFR, BUN, creatinine ○ Other labs? ● Urodynamic testing if suspecting neurogenic bladder
36
First line imaging for Hydronephrosis
● 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
Hydronephrosis - Management in Children
● 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
Hydronephrosis - Management in adults
● Hydronephrosis + infection = Emergency ○ Stents or nephrostomy, antibiotics ● Remove/treat obstruction if possible ○ Kidney stone, tumor, etc ● Surgical drainage ● Dialysis if renal failure
39
Hypertensive Nephrosclerosis
● Chronic renal insufficiency associated with long-standing blood pressure elevation ● Hypertension can be both the cause and effect of CKD
40
Hypertensive Nephrosclerosis - Etiology
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
Hypertensive Nephrosclerosis Presentation
● 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
Diagnosis of Hypertensive Nephrosclerosis
● Inferred from clinical features and exclusion of other kidney diseases ● Labs ● Kidney biopsy done only rarely
43
Management of Hypertensive Nephrosclerosis
● BP control ● May still continue to progress even if BP lowered.
44
Polycystic Kidney Disease - Epidemiology
● Autosomal Dominant (ADPKD) most common (12 million people worldwide) ● Autosomal recessive (ARPKD) rare, typically pediatric
45
Renal Vascular Disease
● 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
Renal Vascular Disease causes
● 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
Renal Vascular Disease Treatment
● 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
Renal Artery Stenosis etiology
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
Renal Artery Stenosis Treatment
- 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
Renal Artery Stenosis Diagnosis
Renal arteriography is gold standard. Can also use duplex ultrasound, CTA, or MRA
51
Renal Artery Aneurysm
● Rare ● Females at higher risk (likely due to higher incidence of FMD) ● Risk of rupture increased w/ pregnancy ● Majority of patients have HTN
52
Renal Artery Aneurysm presentation
● Usually asymptomatic and incidental finding ● Abdominal/flank pain and hypotension if ruptured
53
Renal Artery Aneurysm Treatment
● Symptomatic or high risk of rupture = surgical repair ● Asymptomatic and low risk = observe ● Screen for other aneurysms
54
Renal Vein Thrombosis Etiology
Can result from systemic inflammation or prothrombotic state (e.g., nephrotic syndrome, carcinoma, trauma, pregnancy/OCPs), extrinsic compression, trauma
55
Renal Vein Thrombosis treatment
● Treat underlying cause ● Consider thrombolysis/thrombectomy or anticoagulation based on clinical severity
56
Renal Vein Thrombosis Clinical features
Evidence of decreased renal perfusion (rising Cr, decreased urine output, hypertension) and renal injury (hematuria, proteinuria)
57
Diagnosis of Renal Vein Thrombosis
Duplex ultrasound, CTA, MRA
58
Atheroembolic Renal Disease
● 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
Presentation of Atheroembolic Renal Disease
● Subacute kidney injury several weeks after inciting event ● Severe hypertension ● Occasionally AKI ● Blue toe syndrome or livedo reticularis ● Other clots. Such as?
60
Atheroembolic Renal Disease Diagnosis (classic triad)
● 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
Treatment for Atheroembolic Renal Disease
● Surgical plaque removal ● Stents ● ASCVD risk reduction ● Poor prognosis. mortality rates may be as high as 80 percent
62
Renal Fusion
● 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
Renal Fusion presentation
● Usually asymptomatic ● Can have GI symptoms, UTO, infections ● Kidney function usually normal
64
Renal Fusion diagnosis
● Usually incidental ● X-ray w/ ureteral catheters ● Retrograde urogram ● CT ● US
65
No treatment needed unless obstruction or infection for _____
Renal Fusion

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