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GU Exam 2 > Intrinsic Renal Disease > Flashcards

Intrinsic Renal Disease Flashcards

1
Q

Acute Kidney Injury Presentation – Intrinsic

A

● Often asymptomatic
● Low urine output
● Azotemia – Elevated serum creatinine
and BUN
○ Uremia – Symptomatic azotemia;
nausea, vomiting, fatigue, anorexia,
weight loss, muscle cramps,
pruritus, or changes in mental
status

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2
Q

UA/Urine Micro findings for intrinsic kidney injury

A

○ Volume (oliguric or nonoliguric)
■ Oliguric have worse outcomes
○ Casts
○ Protein
○ Fractional Excretion of Sodium (FENa)
■ <1% – Prerenal disease, GN
■ >1-2% – ATN

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3
Q

Casts seen with Acute Kidney Injury – Intrinsic

A

● “Muddy brown cast;” granular, pigmented =
Acute Tubular Necrosis (ATN)
● “WBC cast;” eosinophils in the urine and blood = Acute Interstitial Nephritis (AIN)
● “RBC cast;” dysmorphic RBC and proteins =
Glomerulonephritis (GN)

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4
Q

Diagnosis of Acute Kidney Injury – Intrinsic

A

● Blood – serum (CMP or BMP)
○ Elevated serum creatinine
○ BUN/Cr ratio
■ >20:1 – Prerenal, post renal, GN
■ <20:1 – ATN, AIN
○ GFR

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5
Q

Acute Kidney Injury complications – Intrinsic

A

● Hyperkalemia → peaked T waves, arrhythmia (prolonged QT)
● Hyperphosphatemia
● Metabolic acidosis
● Anemia
● Platelet dysfunction

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6
Q

Labs for AKI still show evidence AKI without uremia after 1-2 weeks of conservative management, where should we refer?

A

Nephrologist

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7
Q

When to admit for AKI - Intrinsic

A

● Severe hyperkalemia → peaked T waves, arrhythmia (prolonged QT)
● Volume overload
● Uremia
● Anything that may require dialysis or urologic procedure (think post
renal causes)

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8
Q

Acute Kidney Injury Treatment – Intrinsic

A

● Treat underlying cause
● Conservative management of BP and edema
● Remove offending agents
● Uremic → Hospital
○ IV fluids (prerenal causes)
○ Diuresis for edema
○ Electrolyte correction (hyperkalemia,
hyperphosphatemia, metabolic acidosis)
○ Cardiac and mental status monitoring

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9
Q

Acute Tubular Necrosis (ATN)

A

Ischemic or nephrotoxic damage to the tubules of the nephron

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10
Q

Accounts for 85% of acute intrinsic renal injuries

A

Acute Tubular Necrosis (ATN)

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11
Q

Acute Tubular Necrosis Etiology

A

● Ischemia (common → prerenal)
○ Poor perfusion of the kidney
(hypotension, sepsis)
● Nephrotoxins (mediations)
● Many More C Chemotherapy
○ IV Contrast, radiation, rhabdomyolysis, heavy metals, poison, recreational drugs

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12
Q

Acute Tubular Necrosis Presentation

A

● Asymptomatic
● Vague and generalized
● Nausea and vomiting
● Malaise
● Altered mental status

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13
Q

Diagnosis of ATN

A

● Blood
○ Elevated serum creatinine
○ BUN/Cr ratio – <20:1
○ Hyperkalemia
○ Possible elevated phosphate and magnesium, low calcium and sodium
● Urine
○ “Muddy brown,” granular cast
○ FENa – >2%
○ Urine Na – >20 (elevated)

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14
Q

Acute Tubular Necrosis Treatment

A

● Supportive treatment
● Treat infection
● Remove nephrotoxins
● Control fluids
● Treat hyperkalemia and other electrolyte/acid-base disorders

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15
Q

When should you consider dialysis for ATN?

A

● Severely elevated K+
● Uremic complication

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16
Q

Acute Interstitial Nephritis

A

● Interstitial inflammation with edema and possible tubular injury
○ Hypersensitivity reaction where neutrophils and eosinophils are sent to the interstitium

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17
Q

Epidemiology of Acute Interstitial Nephritis

A

● Accounts for 10-15% of acute intrinsic renal injuries
○ 70% due to medications
○ Infectious disease also contributes

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18
Q

Acute Interstitial Nephritis Presentation

A

Classic Triad
● Fever – 80%
● Rash – 25-50%
● Eosinophilia
Others:
● Arthralgia
● Asymptomatic

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19
Q

Acute Interstitial Nephritis Diagnosis

A

● Recent use of causative drug
● Blood
○ Elevated serum creatinine
○ BUN/Cr ratio – <20:1
○ Eosinophilia
● Urine
○ WBC casts, WBCs (95%), RBCs
○ FENa – <1%
○ Proteinuria – variable (more common with NSAIDs)

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20
Q

Acute Interstitial Nephritis Treatment

A

● Dialysis
● Supportive measures
○ IV fluids
○ Renal dosing of meds
Treatment
● Remove the inciting agent or cause (infection, autoimmune)
● Corticosteroids (remember this is an inflammatory issue)

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21
Q

Glomerulonephritis (GN)

A

● Inflammatory damage or injury at the
glomerulus

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22
Q

Glomerulonephritis Pathophysiology

A

○ Antigen/antibody complexes deposited
in glomerular tissue →
attracts macrophages and neutrophils
to the glomeruli → release lysosomal
enzymes damaging the podocytes of
the glomerulus

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23
Q

Presentation of GN

A

● Hypertension
● Edema/fluid retention
● Proteinuria
● Glomerular hematuria

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24
Q

Diagnosis of GN

A

● Blood
○ Elevated serum creatinine
○ BUN/Cr ratio – >20:1
○ GN Serologies
● Urine
○ RBC casts, dysmorphic red cells
○ Proteinuria and hematuria
○ FENa – <1%
● Renal ultrasound
● Renal biopsy to confirm diagnosis

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25
Treatment of GN
● Treatment varies based of kind of GN ● General treatment ○ Monitoring and conservative management of symptoms ○ Correction of hypertension and edema ○ Dialysis if severe complications, uremic signs and symptoms
26
Nephritic Syndrome
● Intraglomerular inflammatory process – inflammatory glomerular damage ● Renal dysfunction = ↑creatinine, ↓GFR ● Proteinuria – 1-3g/day
27
Nephritic Syndrome Essentials of Diagnosis
○ Hematuria/RBC casts ○ Variable proteinuria ○ ↑ serum creatinine ○ HTN ○ Edema (Na+ retention)
28
Nephrotic Syndrome
● Noninflammatory damage to the glomerular capillary wall ● Proteinuria – >3g/day
29
Nephrotic Syndrome Essentials of Diagnosis
○ Severe proteinuria ○ Hypoalbuminemia ○ Edema ○ Hyperlipidemia
30
Nephritic Syndrome Causes
● Infection-Related (Post-Infectious) Glomerulonephritis ● Immunoglobulin A (IgA) Nephropathy ● IgA Vasculitis (IgAV) “Henoch-Schonlein Purpura” ● Rapidly Progressive Glomerulonephritis (RPGN) ● Anti-GBM Antibody Disease “Goodpasture Syndrome” ● Pauci-Immune Glomerulonephritis ● Membranoproliferative Glomerulonephritis/C3 Glomerulopathies ● Lupus Nephritis
31
Post-Infectious Glomerulonephritis Pathophysiology
Microbial antigens bind to the glomerular basement membrane (GBM), activating complement pathways and creating accumulation of antimicrobial antibodies causing glomerular damage
32
Epidemiology of Post-Infectious Glomerulonephritis
● The most common cause of a glomerular disorder in children between 5-15 years ● Rare in children <2 years ● Uncommon in adults >40 years
33
Group A beta-hemolytic Streptococcus is the most common etiology for _____
Post-Infectious Glomerulonephritis
34
Presentation of Post-Infectious Glomerulonephritis
● 7-10 day (may be 1-3 weeks) post infection ● Mild cases ○ Asymptomatic hematuria ● Severe cases ○ Nephritic syndrome
35
Post-Infectious Glomerulonephritis Diagnosis
● Clinical evidence of recent infection ● High ASO titer ● Low complement level ● UA - RBC casts, dysmorphic RBCs, WBCs, renal tubular cells, and proteinuria ● Cultures (urine/blood)
36
Treatment of Post-Infectious Glomerulonephritis
● Treat the underlying condition – Strep ● Supportive ○ If needed – antihypertensives, diuretics ○ If needed – salt, fluid, and/or protein restriction
37
IgA Nephropathy pathophysiology
● IgA deposition in the glomeruli causing dysfunctional filtration and AKI ○ AKA – “Berger disease”
38
Epidemiology of IgA Nephropathy
● Most common type of GN worldwide (>Asia) ● Common among children and young adults ● Male (2-3x) > Female
39
Etiology of IgA Nephropathy
● Heritable condition – Primary ● Cirrhosis, celiacs, HIV – Secondary
40
IgA Nephropathy Presentation
● Episodic gross hematuria with mild proteinuria ○ Seen after “mucosal viral” or upper respiratory infections ○ Sx usually start within 1-2 days of infection Presentation ● Nephritic spectrum labs ○ Asymptomatic to RPGN ○ Reddish-brown “smokey” urine
41
Diagnosis of IgA Nephropathy
● Normal complement levels and serologies ○ Serum creatinine is typically normal ● UA - hematuria, with dysmorphic RBCs ● Clinical Hx – episodic hematuria, 1-2 days post viral illness ● Renal Bx – diffuse mesangial IgA and C3 deposits
42
Treating IgA nephropathy with High BP, decrease GFR, or proteinuria
○ ACEi or ARB therapy to control BP ○ Work to reduce protein to <0.5g/day ○ SGLT-2, hydroxychloroquine (asians)?
43
Immunoglobulin A Vasculitis (IgAV) Pathophysiology
● Systemic small-vessel leukocytoclastic vasculitis ● IgA deposition in small vessels ○ Formerly – “Henoch-Schonlein Purpura”
44
Presentation of Immunoglobulin A Vasculitis (IgAV)
● Palpable purpura in lower extremities and buttock ● Arthralgia ● Abdominal complaints ● Decrease in GFR ● Nephritic urine – hematuria (dysmorphic RBCs), RBC casts
45
Immunoglobulin A Vasculitis (IgAV) Diagnosis
● HPI/presentation →high index of suspicion ● Coagulation studies normal ● Serology mostly normal ● Proteinuria ● Skin biopsy → IgA deposits in the skin
46
Treatment for Immunoglobulin A Vasculitis (IgAV)
● Oral hydration, rest, pain control ○ Most with mild hematuria and proteinuria will fully resolve within a few weeks ● Treat similar to IgA Nephropathy (ACEi/ARB, protein reduction, steroids) ● Nothing has been shown to help severe nephritis
47
Rapidly Progressive Glomerulonephritis pathophysiology
● Rapidly Progressive Glomerulonephritis – “RPGN” ● More severe nephritic syndrome, characterized by addition of uremic signs and symptoms ○ 50% drop in GFR within 3 months ■ ESRD in weeks to months
48
Presentation of Rapidly Progressive Glomerulonephritis
● Uremia ■ N/V, weakness, fatigue, anorexia, muscle cramps, pruritus, mental status change
49
Rapidly Progressive Glomerulonephritis Diagnosis
● Hematuria/RBC casts ● Variable proteinuria ● ↑ serum creatinine ● Uremic ● Complement and serology testing ○ Low complement levels, rising ASO titers ● Renal biopsy – crescentic cellular mass “crescents”
50
Treatment for Rapidly Progressive Glomerulonephritis
● Varies by disease type – treat emergently ● Corticosteroids, and cyclophosphamide or rituximab ● Plasma exchange – rapidly removes free antibody, intact immune complexes, and mediators of inflammation ● May need kidney transplant depending on severity of the renal trauma
51
Pauci-Immune Glomerulonephritis Pathophysiology
● Necrotizing GN following ANCA-associated vasculitis ● Granulomatosis with polyangiitis ○ Inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys
52
Pauci-Immune Glomerulonephritis Presentation
● 90% Granulomatosis with polyangiitis ● Systemic inflammation – fever, malaise ● Vascular involvement ○ Purpura ○ Mononeuritis multiplex (neuropathy of to at least two different peripheral areas) ● Possible lower respiratory tract involvement
53
Pauci-Immune Glomerulonephritis Diagnosis
● Blood ○ Elevated anti-neutrophil cytoplasmic antibodies (ANCA) ■ Serologies can be broken down into further subtypes ○ Complement levels normal ● Bipopsy ○ Necrotizing lesions ○ Crescents – RPGN
54
Anti-GBM Antibody Disease (Goodpasture Syndrome) Pathophysiology
● Circulating anti-glomerular basement membrane (anti-GBM) antibodies ● Basement membrane in the glomerulus and lungs ○ Combination of glomerulonephritis with alveolar hemorrhage
55
Anti-GBM Antibody Disease (Goodpasture Syndrome) Etiology
● Pulmonary infections ● Tobacco use ● Environmental exposures
56
Presentation of Anti-GBM Antibody Disease (Goodpasture Syndrome)
● Often preceded by a respiratory infection ● Dyspnea ● Cough ● Hemoptysis ● Possible respiratory failure ● Sx consistent with RPGN (hematuria, renal failure, uremia)
57
Anti-GBM Antibody Disease (Goodpasture Syndrome) Diagnosis
● Chest x-ray ○ Pulmonary infiltrates from alveolar hemorrhage Anti-GBM Antibody Disease (Goodpasture Syndrome) ● Blood ○ Serum complement levels normal ○ Elevated anti-GBM antibodies ● Biopsy – if needed ○ RPGN – crescents
58
Anti-GBM Antibody Disease (Goodpasture Syndrome) Treatment
● Treat emergently (possibly prior to confirming Dx) ● Plasma exchange (daily up to 2 weeks) ○ Clears anti-GBM antibodies ● Corticosteroids and cyclophosphamide ● Dialysis (for patients with significant renal failure)
59
Pathophysiology of Membranoproliferative Glomerulonephritis (MPGN)
● Immunoglobulin-mediated hypercellularity and thickening of the glomerular basement membrane ○ Proliferation of immune complexes in the basement membrane, activating and depositing complement, damaging the glomerulus
60
Membranoproliferative Glomerulonephritis (MPGN) Presentation
● Nephric features ● May also have Nephrotic features (lots of proteinuria)
61
Membranoproliferative Glomerulonephritis (MPGN) Diagnosis
● Low circulating complement ● Biopsy ○ Thickening of GBM and proliferative changes ○ Various subtypes
62
Membranoproliferative Glomerulonephritis (MPGN) Treatment
● Poor prognosis – usually progressed to ESRD ● ACEi/ARBs ● Corticosteroids for children with nephrotic range proteinuria ● Immunosuppression – controversial
63
C3 Glomerulopathy
● Hypercellularity and thickening of the glomerular basement membrane with C3 but little to no immunoglobulin deposits seen on fluoroscopy ● May be inherited or acquired
64
Lupus Nephritis Pathophysiology
● Lupus autoantibody complexes affecting the glomeruli ○ Complement activation resulting in inflammation and endothelial damage to the kidney
65
Diagnosis of Lupus Nephritis
● Urine ○ High levels of proteinuria ○ Hematuria ● Blood ○ Low complement ○ High ANA ○ Elevated anti-double-stranded (ds) DNA antibody titers
66
Lupus Nephritis classification (via biopsy)
Class I – minimal mesangial lesions Class II – proliferative mesangial lesions Class III – focal proliferative, involving capillaries (< 50% of glomeruli involved) Class IV – diffuse proliferative, involving capillaries (> 50% of glomeruli involved)
67
_____ is continuous with the smooth muscles of the arterioles in the middle (mesi) of the capillaries (angi)
Mesangium
68
Lupus Nephritis treatment - Class I and II
minimal to no treatment ○ Nephritic management (ACEi/ARBs) ○ Steroids for nephrotic range proteinuria
69
Lupus Nephritis Treatment - class III and IV
○ Aggressive immunosuppressive therapy ■ Corticosteroids and cyclophosphamide ○ ACEi/ARBs for HTN or proteinuria

GU Exam 2 (4 decks)

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