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Renal > Nephritic? Nephrotic? > Flashcards

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
Q

Diabetic Nephropathy

A

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
Q

Lupus NephrOpathy

A

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
Q

Amyloidosis Nephrotic Syndrome

A

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
Q

Nephritic Syndrome - Diagnostic Features

A 
Reduced GFR (elevated serum creatinine) 
Hematuria + RBC casts
Hypertension 
Edema
Proteinuria (sub-nephrotic)
29
Q

Mechanism of edema formation - Nephritic vs. Nephrotic

A

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
Q

Post-infectious glomerulonephritis - Pathogenesis and Presentation

A

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
Q

Post-infectious GN - Lab findings

A

Elevated levels of antibodies to streptococcal antigens (ASO titer)

Decrased levels of complement C3 with normal levels of C4 (alternate pathway)

32
Q

Post-infectious GN - Pathology

A

Light microscopy shows infiltration of neutrophils and monocytes

IF shows granular deposits of IgG and C3 in the subendothelial, mesangial, and subepithelial spaces

33
Q

Post-infectious GN - Treatment/Prognosis

A

Self-limited disease; 95% of patients recover spontaneously

34
Q

IgA Nephropathy - Epidemiology

A

Most common type of acute glomerulonephritis; usually presents in young men

35
Q

IgA Nephropathy - Pathogenesis

A

Associated with deposition of abnormal IgA immune complexes in the mesangium with activation and proliferation of mesangial cells

36
Q

IgA Nephropathy - Pathology

A

Light microscopy shows mesangial cell and ECM proliferation

IF shows IgA, IgG, and C3 deposition in the mesangium

37
Q

IgA Nephropathy - Presentation, Treatment, and Prognosis

A

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
Q

Henoch-Schonlein purpura

A

IgA deposits in the skin of patients with IgA Nephropathy

39
Q

Goodpasture’s Syndrome

A

Pulmonary hemorrhage, iron deficiency anemia, and glomerulonephritis associated with circulating antibody to GBM

40
Q

anti-GBM - Pathogenesis and Pathology

A

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
Q

anti-GBM disease - Treatment & Prognosis

A

Aggressive treatment with steroids, immunosuppressive agents, and plasma exchange

42
Q

Pauci-immune renal vasculitis - Definition

A

Small vessel vasculitis of the kidneys NOT caused by immune-complex deposition

43
Q

Pauci-immune renal vasculitis - Pathogenesis and Pathology

A

90% of patients have anti-neutrophil cytoplasmic antibodies (ANCA)

Glomuerli demonstrate fibrinoid necrosis and crescents

44
Q

Pauci-immune renal vasculitis - Treatment

A

Steroids + cyclophosphamide or rituximab

45
Q

Lupus Nephritis - Pathogenesis and Pathology

A

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
Q

Cryoglobulinemia - Definition and Epidemiology

A

Precipitation of immune complexes within the small vessels of the kidney, causing vasculitis

Often associated with HCV infection

47
Q

Cryoglobulinemia - Pathology

A

Membranoproliferative pattern of injury with subendothelial immune complex deposition

48
Q

Cryoglobulinemia - Clinical presentation

A

Most patients with symptomatic disease present with palpable purpura, arthralgias, and weakness; patients typically have low C4 levels

49
Q

Cryoglobulinemia - Treatment & Prognosis

A

Treatment of underlying HCV (peginterferon, ribavirin) or B cell depleting therapies (rituximab)

Plasmapheresis to remove the cryoglobulins

50
Q

Rapidly Progressive Glomerulonephritis (RPGN)

A

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
Q

Glomerular diseases caused by immune complex deposition

A

IgA Nephropathy / Henoch-Schonlein Purpura
Post-infectious glomerulonephropathy
Anti-GBM disease
Lupis Nephritis

52
Q

Alport’s disease

A

Triad of nephritis, deafness, and ocular lesions; due to an X-linked mutation in collagen IV

53
Q

3 main primary causes of Nephrotic Syndrome

A

MCD
FSGS
MN

54
Q

What pattern of kidney disease is associated with HIV?

A

FSGS with a Nephrotic presentation

Renal (13 decks)

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