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Nephritic? Nephrotic? Flashcards

1
Q

Normal urinary albumin excretion

A

< 20 mg/day

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2
Q

Microalbuminuria

A

Urinary albumin excretion 30-300mg/day

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3
Q

Nephrotic Syndrome - pathogenesis

A

An excessive leak of protein through the glomerular capillary wall into the urinary space

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4
Q

Nephritic Syndrome - pathogenesis

A

Active inflammation within the glomerulus leads to damage of the glomerulus with subsequently decreased GFR

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5
Q

Nephrotic syndrome - Diagnostic criteria

A 
Proteinuria > 3.5 g/day
Hypoalbuminemia <3.0 g/dL
Edema
Hyperlipidemia 
Lipiduria
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6
Q

Clinical risks associated with nephrotic syndrome

A

Infection - due to urinary loss of IgG and complement

Thrombosis - due to increased synthesis of coagulation factors by the liver and urinary loss of AT3

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7
Q

Clinical features of nephritic syndrome

A 
Microhematuria 
RBC casts 
Non-nephrotic proteinuria 
Decreased GFR 
Hypertension 
Edema
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8
Q

Idiopathic nephrotic syndrome - 4 main patterns

A

Nephrotic syndrome due to primary disease of the glomerulus; differentiated on the basis of 4 major histologic patterns

  1. Minimal change disease (MCD)
  2. Focal segmental glomerulosclerosis (FSGS)
  3. Membranous nephropathy (MN)
  4. Membranoproliferative Glomerulonephropathy (MPGN)
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9
Q

Secondary causes of nephrotic syndrome - 4

A

Diabetes
Lupus
Light chain deposition
Amyloidosis

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10
Q

Minimal Change Disease - Histological findings

A

Glomeruli appear normal by light microscopy

Immunofluoresence shows no Ig or complement deposition

Electron microscopy shows foot process fusion only

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11
Q

Minimal Change Disease - Pathogenesis

A

May involve a T-cell derived circulating factor that acts directly on the glomerulus to damage the podocyte and cause destruction of the permeability barrier

Associated with expression of CD80 antigen on podocytes with shedding of CD80 in the urine

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12
Q

Minimal Change Disease - Clinical Presentation & Treatment

A

Children present with edema and normal renal function

First-line treatment is prednisone (+ cyclophosphamide for relapsing cases); prognosis is good

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13
Q

Focal Segmental Glomerulosclerosis (FSGS) - Epidemiology & Pathogenesis

A

Most common cause of nephrotic syndrome in adults; often associated with HIV

May be caused by a circulating factor soluble urokinase-type plasminogen activator receptor (suPAR) that damages glomerular epithelial cells

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14
Q

FSGS - Histological findings

A

Light microscopy shows segmental scarring (sclerosis) in some (focal) glomeruli

Immunofluorescence is usually negative

Electron Microscopy shows foot process fusion

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15
Q

FSGS - Clinical Presentation & Treatment

A

More likely to present with HTN than MCD

Treatment - steroid therapy results in partial or complete remission in 1/2 of patients; relapse is common and progression to renal failure is common

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16
Q

Membranous Nephropathy - Pathogenesis

A

Auto-immune mediated glomerular disease; caused by antibody to the phospholipase A2 receptor (anti-PLA2R) on the podocyte; the immune complex activates complement which injures the podocyte and the immune complex is trapped in the subepithelial space

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17
Q

MN - Histological Findings

A

Light microscopy shows thickening of the GBM with extensions of new basement membrane material between immune complex deposits (“spikes)

Immunofluorescence shows granular deposition of immunoglobulin, C3, and C5b-9

Electron microscopy shows subepithelial immune complex deposition

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18
Q

Membranous Nephropathy - Epidemiology & Associations

A

Most common cause of idiopathic nephrotic syndrome in older adults; associated with Hepatitis B, lupus, cancer, and drugs (gold, penicillamine)

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19
Q

MN - Treatment and prognosis

A

Patients can be followed conservatively; patients who progress (increasingly severe proteinuria, impaired renal function) are treated with steroids and cyclophosphamide

50% progress to end stage renal failure, 25% remain unchanged, 25% remit

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20
Q

Membranoproliferative glomerulonephropathy (MPGN) - General definition & Types

A

Histologic pattern is defined by mesangial proliferation + thickening of the GB

Type I: associated with immune complex deposits
Type II: associated with complement activation in the capillary wall without immune complex deposition

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21
Q

MPGN Histologic Findings - Type I vs. Type 2

A

Light microscopy shows thickening of the basement membrane and mesangial cell proliferation (Types I and 2)

Type 1: IF shows deposition of C3 and IgG
Type 2: IF shows deposition of C3 only; no IgG

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22
Q

MPGN Type I Pathogenesis & Lab Findings

A

MPGN Type 1 is due to subendothelial trapping of immune complexes followed by activation of the classical complement pathway

Low C3 and C4 levels are observed

23
Q

MPGN Type 2 Pathogenesis & Lab Findings

A

MPGN Type 2 is associated with a cirgulating IgG (Nephritic Factor, C3Nef) that can spontaneously activate the alternative complement pathway

Low C3, normal C4

24
Q

MPGN Clinical Presentation & Treatment

A

Most patients present with nephrotic syndrome but some present with acute nephritis (mixed nephrotic/nephritic); MPGN 1 is associated with HCV

Treatment: steroids; prognosis is poor and many progress to end stage renal disease

25
Diabetic Nephropathy
Diabetes is the most common cause of nephrotic syndrome in adults Clinical presentation: Reinopathy, neuropathy, nephrotic proteinuria Biopsy shows nodular glomerulosclerosis with thickening of the GBM Treatment: glucose control, BP control, ACEIs
26
Lupus NephrOpathy
SLE usually manifests as a nephritic presentation; occasionally, it can present with a membranous histologic pattern in which renal function is normal or only slightly depressed These patients may have lower ANA titers than usual for nephritic SLE patients
27
Amyloidosis Nephrotic Syndrome
More common in older individuals; may occur as a manifestation of multiple myeloma Diagnostic features: presence of monoclonal light chains on serum/urine protein electrophoresis; positive Congo Red staining
28
Nephritic Syndrome - Diagnostic Features
``` Reduced GFR (elevated serum creatinine) Hematuria + RBC casts Hypertension Edema Proteinuria (sub-nephrotic) ```
29
Mechanism of edema formation - Nephritic vs. Nephrotic
Nephrotic syndrome - edema results from loss of oncotic pressure of the capillary system due to massive proteinuria Nephritic syndrome - edema results from increased tubular reabsorption of salt and water due to reduced glomerular perfusion
30
Post-infectious glomerulonephritis - Pathogenesis and Presentation
Typically occurs 14-21 days following GAS infection; caused by deposition of anti-GAS complexes within the glomerulus Presents as edema, hematuria, HTN, and proteinuria with decreased GFR
31
Post-infectious GN - Lab findings
Elevated levels of antibodies to streptococcal antigens (ASO titer) Decrased levels of complement C3 with normal levels of C4 (alternate pathway)
32
Post-infectious GN - Pathology
Light microscopy shows infiltration of neutrophils and monocytes IF shows granular deposits of IgG and C3 in the subendothelial, mesangial, and subepithelial spaces
33
Post-infectious GN - Treatment/Prognosis
Self-limited disease; 95% of patients recover spontaneously
34
IgA Nephropathy - Epidemiology
Most common type of acute glomerulonephritis; usually presents in young men
35
IgA Nephropathy - Pathogenesis
Associated with deposition of abnormal IgA immune complexes in the mesangium with activation and proliferation of mesangial cells
36
IgA Nephropathy - Pathology
Light microscopy shows mesangial cell and ECM proliferation IF shows IgA, IgG, and C3 deposition in the mesangium
37
IgA Nephropathy - Presentation, Treatment, and Prognosis
Most patients present with asymptomatic microhematuria, mild proteinuria, and normal or only mildly reduced renal function 25-50% of patients progress to renal failure Treatment: Steroids, ACEIs
38
Henoch-Schonlein purpura
IgA deposits in the skin of patients with IgA Nephropathy
39
Goodpasture's Syndrome
Pulmonary hemorrhage, iron deficiency anemia, and glomerulonephritis associated with circulating antibody to GBM
40
anti-GBM - Pathogenesis and Pathology
Caused by circulating antibody to antigens in type IV collagen within the GBM IF shows linear IgG deposits, complement activation, neutrophil infiltration, and crescent formation
41
anti-GBM disease - Treatment & Prognosis
Aggressive treatment with steroids, immunosuppressive agents, and plasma exchange
42
Pauci-immune renal vasculitis - Definition
Small vessel vasculitis of the kidneys NOT caused by immune-complex deposition
43
Pauci-immune renal vasculitis - Pathogenesis and Pathology
90% of patients have anti-neutrophil cytoplasmic antibodies (ANCA) Glomuerli demonstrate fibrinoid necrosis and crescents
44
Pauci-immune renal vasculitis - Treatment
Steroids + cyclophosphamide or rituximab
45
Lupus Nephritis - Pathogenesis and Pathology
Caused by deposition of auto-immune immune complexes; IF shows C3, IgG, IgM, IgA, and C1q ("full house") deposition within the mesangium, subendothelial, and supepithelial spaces
46
Cryoglobulinemia - Definition and Epidemiology
Precipitation of immune complexes within the small vessels of the kidney, causing vasculitis Often associated with HCV infection
47
Cryoglobulinemia - Pathology
Membranoproliferative pattern of injury with subendothelial immune complex deposition
48
Cryoglobulinemia - Clinical presentation
Most patients with symptomatic disease present with palpable purpura, arthralgias, and weakness; patients typically have low C4 levels
49
Cryoglobulinemia - Treatment & Prognosis
Treatment of underlying HCV (peginterferon, ribavirin) or B cell depleting therapies (rituximab) Plasmapheresis to remove the cryoglobulins
50
Rapidly Progressive Glomerulonephritis (RPGN)
Serum creatinine doubles or GFR falls by 50% within a few days to 3 months Usually associated with anti-GBM disease, ANCA vasculitis, and Lupus Treatment: high dose steroids, cytotoxic drugs, plasma exchange
51
Glomerular diseases caused by immune complex deposition
IgA Nephropathy / Henoch-Schonlein Purpura Post-infectious glomerulonephropathy Anti-GBM disease Lupis Nephritis
52
Alport's disease
Triad of nephritis, deafness, and ocular lesions; due to an X-linked mutation in collagen IV
53
3 main primary causes of Nephrotic Syndrome
MCD FSGS MN
54
What pattern of kidney disease is associated with HIV?
FSGS with a Nephrotic presentation

Renal (13 decks)

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