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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
Q

Treatment of GN

A

● 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

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26
Q

Nephritic Syndrome

A

● Intraglomerular inflammatory process
– inflammatory glomerular damage
● Renal dysfunction = ↑creatinine, ↓GFR
● Proteinuria – 1-3g/day

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27
Q

Nephritic Syndrome
Essentials of Diagnosis

A

○ Hematuria/RBC casts
○ Variable proteinuria
○ ↑ serum creatinine
○ HTN
○ Edema (Na+ retention)

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28
Q

Nephrotic Syndrome

A

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

29
Q

Nephrotic Syndrome
Essentials of Diagnosis

A

○ Severe proteinuria
○ Hypoalbuminemia
○ Edema
○ Hyperlipidemia

30
Q

Nephritic Syndrome Causes

A

● 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
Q

Post-Infectious Glomerulonephritis Pathophysiology

A

Microbial antigens bind to the glomerular basement
membrane (GBM), activating complement pathways and
creating accumulation of antimicrobial antibodies
causing glomerular damage

32
Q

Epidemiology of Post-Infectious Glomerulonephritis

A

● 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
Q

Group A beta-hemolytic Streptococcus is the most common etiology for _____

A

Post-Infectious Glomerulonephritis

34
Q

Presentation of Post-Infectious Glomerulonephritis

A

● 7-10 day (may be 1-3 weeks) post infection
● Mild cases
○ Asymptomatic hematuria
● Severe cases
○ Nephritic syndrome

35
Q

Post-Infectious Glomerulonephritis Diagnosis

A

● 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
Q

Treatment of Post-Infectious Glomerulonephritis

A

● Treat the underlying condition – Strep
● Supportive
○ If needed – antihypertensives, diuretics
○ If needed – salt, fluid, and/or protein restriction

37
Q

IgA Nephropathy pathophysiology

A

● IgA deposition in the glomeruli causing dysfunctional
filtration and AKI
○ AKA – “Berger disease”

38
Q

Epidemiology of IgA Nephropathy

A

● Most common type of GN worldwide (>Asia)
● Common among children and young adults
● Male (2-3x) > Female

39
Q

Etiology of IgA Nephropathy

A

● Heritable condition – Primary
● Cirrhosis, celiacs, HIV – Secondary

40
Q

IgA Nephropathy Presentation

A

● 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
Q

Diagnosis of IgA Nephropathy

A

● 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
Q

Treating IgA nephropathy with High BP, decrease GFR, or proteinuria

A

○ ACEi or ARB therapy to control BP
○ Work to reduce protein to <0.5g/day
○ SGLT-2, hydroxychloroquine (asians)?

43
Q

Immunoglobulin A Vasculitis
(IgAV) Pathophysiology

A

● Systemic small-vessel leukocytoclastic vasculitis
● IgA deposition in small vessels
○ Formerly – “Henoch-Schonlein Purpura”

44
Q

Presentation of Immunoglobulin A Vasculitis (IgAV)

A

● Palpable purpura in lower extremities and buttock
● Arthralgia
● Abdominal complaints
● Decrease in GFR
● Nephritic urine – hematuria
(dysmorphic RBCs), RBC casts

45
Q

Immunoglobulin A Vasculitis
(IgAV) Diagnosis

A

● HPI/presentation →high index of suspicion
● Coagulation studies normal
● Serology mostly normal
● Proteinuria
● Skin biopsy → IgA deposits in the skin

46
Q

Treatment for Immunoglobulin A Vasculitis
(IgAV)

A

● 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
Q

Rapidly Progressive Glomerulonephritis pathophysiology

A

● 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
Q

Presentation of Rapidly Progressive Glomerulonephritis

A

● Uremia
■ N/V, weakness, fatigue, anorexia,
muscle cramps, pruritus, mental status
change

49
Q

Rapidly Progressive Glomerulonephritis Diagnosis

A

● 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
Q

Treatment for Rapidly Progressive Glomerulonephritis

A

● 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
Q

Pauci-Immune Glomerulonephritis Pathophysiology

A

● Necrotizing GN following ANCA-associated vasculitis
● Granulomatosis with polyangiitis
○ Inflammation of the blood vessels in your nose, sinuses,
throat, lungs and kidneys

52
Q

Pauci-Immune Glomerulonephritis Presentation

A

● 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
Q

Pauci-Immune Glomerulonephritis Diagnosis

A

● Blood
○ Elevated anti-neutrophil cytoplasmic antibodies (ANCA)
■ Serologies can be broken down into further subtypes
○ Complement levels normal
● Bipopsy
○ Necrotizing lesions
○ Crescents – RPGN

54
Q

Anti-GBM Antibody Disease
(Goodpasture Syndrome) Pathophysiology

A

● Circulating anti-glomerular basement membrane (anti-GBM) antibodies
● Basement membrane in the glomerulus and lungs
○ Combination of glomerulonephritis with alveolar hemorrhage

55
Q

Anti-GBM Antibody Disease
(Goodpasture Syndrome) Etiology

A

● Pulmonary infections
● Tobacco use
● Environmental exposures

56
Q

Presentation of Anti-GBM Antibody Disease
(Goodpasture Syndrome)

A

● Often preceded by a respiratory infection
● Dyspnea
● Cough
● Hemoptysis
● Possible respiratory failure
● Sx consistent with RPGN (hematuria, renal failure, uremia)

57
Q

Anti-GBM Antibody Disease
(Goodpasture Syndrome) Diagnosis

A

● 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
Q

Anti-GBM Antibody Disease
(Goodpasture Syndrome) Treatment

A

● 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
Q

Pathophysiology of Membranoproliferative Glomerulonephritis (MPGN)

A

● 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
Q

Membranoproliferative Glomerulonephritis (MPGN) Presentation

A

● Nephric features
● May also have Nephrotic features (lots of proteinuria)

61
Q

Membranoproliferative Glomerulonephritis (MPGN) Diagnosis

A

● Low circulating complement
● Biopsy
○ Thickening of GBM and proliferative changes
○ Various subtypes

62
Q

Membranoproliferative Glomerulonephritis (MPGN) Treatment

A

● Poor prognosis – usually progressed to ESRD
● ACEi/ARBs
● Corticosteroids for children with nephrotic range proteinuria
● Immunosuppression – controversial

63
Q

C3 Glomerulopathy

A

● 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
Q

Lupus Nephritis Pathophysiology

A

● Lupus autoantibody complexes affecting the glomeruli
○ Complement activation resulting in
inflammation and endothelial damage to
the kidney

65
Q

Diagnosis of Lupus Nephritis

A

● Urine
○ High levels of proteinuria
○ Hematuria
● Blood
○ Low complement
○ High ANA
○ Elevated anti-double-stranded (ds) DNA
antibody titers

66
Q

Lupus Nephritis classification (via biopsy)

A

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
Q

_____ is continuous with the
smooth muscles of the arterioles in the
middle (mesi) of the capillaries (angi)

A

Mesangium

68
Q

Lupus Nephritis treatment - Class I and II

A

minimal to no treatment
○ Nephritic management (ACEi/ARBs)
○ Steroids for nephrotic range proteinuria

69
Q

Lupus Nephritis Treatment - class III and IV

A

○ Aggressive immunosuppressive therapy
■ Corticosteroids and cyclophosphamide
○ ACEi/ARBs for HTN or proteinuria

GU Exam 2 (4 decks)

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