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RENAL II, Test 2 > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

two things that can be treated w/ plasmaphoresis?

A

TTP and Good Pasture Sx

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2
Q

non pitting vs pitting edema

A
  • Non-pitting edema: swollen cells due to increased ICF volume – does NOT respond to diuretics
  • Pitting edema: increased ISF volume – nephrotic syndrome, CHF, pregnancy, cirrhosis
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3
Q

what are major transport mechanisms along the nephron?

A
  1. PCT: glucose, AA’s, phosphate, Cl-, Na+ all taken into cell - driven by Na/K ATPase pump
  2. DCT: Sodium brings Cl- in as well as Ca2+
  3. Principal cells: sodium comes in K+ moves out (driven by sodium ATPase pump)
    - under ADH stimulation aquaporins are inserted here
  4. Alpha intercalated cells: potassium in, H+ out
    Beta intercalated cells: Cl- in, HCO3- out
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4
Q

diuresis

A

“well hydrated”

  • CD impermeable to water
  • dilute urine
  • Low ADH
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5
Q

antidiuresis

A

“dehyrdration”

  • CD highly water-permeable
  • low volume concentrated urine
  • high ADH

ADH increases H20 permeability of late distal tubule/collecting duct

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6
Q

anion gap acidosis

A

: E. Elm Park: Ethanol, Ethylene glycol, Lactic acid, Methanol, Paraldehyde, Aspirin, Renal failure, Ketone bodies

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7
Q

azotemia

A

elevation of blood urea nitrogen (BUN) and Creatine levels, largely related to decreased glomerular filtration rate (GFR)
• Pre-renal azotemia: due to hypoperfusion of kidneys (i.e. hemorrhage, shock, volume depletion, CHF), impairs renal fn. in the absence of parenchymal damage (BUN:Cr >20:1)
• Postrenal azotemia: urine flow obstructed beyond the level of kidney

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8
Q

Uremia

A

when azotemia is associated with other sx and clinical signs: failure of renal excretory function but also host metabolic and endocrine alterations resulting from renal damage.

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9
Q

AKI

A

dominated by oliguria or anuria, and recent onset of azotemia (elevated BUN). Can result from glomerular, interstitial, or vascular injury or acute tubular injury
• rapid decline in GFR
• frequently reversible, though can progress to CKD
• severe forms have oliguria and anuria

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10
Q

CKD

A

Chronic Kidney disease (CKD): prolonged signs of uremia, ending in chronic renal parenchymal diseases
• GFR is less than 20-25% of normal.
• (<60 ml/min for 3 mos) or persisitent albuminuria
• milder, often clinically silent
• kidneys can’t regulate volume and solute composition → edema, metabolic acidosis, hyperkalemia
• CKD is generally irreversible

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11
Q

ESRD

A

End-Stage renal disease:

• GFR is less than 5% of normal – terminal stage of uremia

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12
Q

Renal tubular defects characterized by what?

A

Renal tubular defects: dominated by polyuria, nocturia, electrolyte disorders. Result from diseases that directly affect tubular structure (medullary cystic disease) or cuase defects in specific tubular functions

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13
Q

UTI’s dominated by what?

A

Urinary tract infections: see bacteriuria and pyuria (bacteria and leukocytes in urine) – may effect the kidney “pyelonephritis” or the bladder “cystitis”

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14
Q

Nephrolithiasis - see what?

A

Nephrolithiasis: renal stones – see severe spasms of pain (renal colic) and hematuria

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15
Q

nephritic syndrome

A 
due to glomerular disease and glomerular inflammatory response. Decreased GFR 
•	hematuria
•	hypertension
•	azotemia
•	oliguria
•	edema
•	mild/moderate proteinuria

ex. APSGN
RPGN

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16
Q

RPGN - basics

A

Rapidly progressive glomerulonephritis: “Crescentic Glomerulonephritis”
• nephritic syndrome with rapid decline in GFR (hours to days)
• acute nephritis, proteinuria, acute renal failure

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17
Q

Nephrotic syndrome

A

due to glomerular disease, not inflammatory reaction, minimal changes in GFR
• severe proteinuria (>3.5 g/day)
• hypoalbuminemia (<3.0 gm/dL)
• hyperlipidemia/lipiduria (due to increased lipoprotein synth in liver)
• generalized edema, periorbital edema

ex: MG, MCD, FSGS

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18
Q

chronic renal failure

A

azotemia –> uremia

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19
Q

mixed glomerulopathies?

A

MPGN, IgA nephropathy, Alport Syndrome, Thin BM disease

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20
Q

Hereditary glomerulopathies?

A
  1. Alport syndrome
  2. Thin basement membrane disease
  3. Fabry disease
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21
Q

what are parts of glomerulus?

A

mesangial cells in center, endothelium (in inside surrounding RBCs), BM in middle, viscerial epithelium (urinary space), parietal epithelium

  • glomerular basement membrane: made of collagen Type IV, laminin, enactin
  • visceral epithelial cells (podocytes): filtration slits: nephrin molecules and podocin
  • mesangial cells lie b/w the capillaries and are for contractile, phagocytic and proliferative purposes

Glomerulus characteristics:

  • high permeability to water, small solutes, cationic ions
  • larger and more anionic, the less permeable – exclusion of albumin
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22
Q

what are crescents?

A

accumulations of cells composed of proliferating parietal epithelial cells and infiltrating leukocytes.

i. occurs following immune/inflamm. injury
ii. fibrin leaks into urinary space often through ruptured membranes

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23
Q

Hyalinosis and Sclerosis?

A

a. Hyalinosis = accumulation of material that is homogenous and eosinophilic by light microscopy. results in endothelial or capillary wall injury and glomerular damage
b. Sclerosis = accumulations of extracellular collagenous matrix

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24
Q

Diffuse, global, focal, segmental

A 
Diffuse = involving all glomeruli
Global = involving the entire glomerulus
Focal= involving only a portion of the glomeruli
Segmental = affecting a part of each glomerulus
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25
Q

Subepithelial humps?

A

APGN (nephritic)

IF: see granular IgG and C3 in GBM and mesangium
LM: diffuse proliferation of leukocytes

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26
Q

GBM dirsuption of fibrin, crescents?

A

Anti-GBM Ab (Goodpastures syndrome) = nephritic

IF: see linear IgG and C3;
LM: fibrin in crescents

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27
Q

subepithelial deposits?

A

membranous glomerulopathy (nephrotic)

IF: see diffuse granular IgG and C3

LM: diffuse capillary wall thickening

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28
Q

just fusion of foot processes?

A

MCD (nephrotic)

no unusual IF or LM

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29
Q

fusion of foot processes and sclerosis?

A

FSGS (nephrotic)

IF: focal; IgM and C3
LM: focal segmental sclerosis

30
Q

see subendothelial deposits?

A

MPGN Type I - Hematuria and proteinuria

IF: IgG, C3, C1q +C4
LM: mesangial proliferation

31
Q

dense deposits?

A

MPGN Type II: Dense deposit disease - hematuria and renal failure

IF: C3, IgG, no C1q or C4
LM: mesangial prooliferation , GBM splitting

32
Q

mesangial and paramesangial deposits?

A

IgA nephropathy; causes recurrent hematuria

IF: IgA, IgG, IgM, C3 in mesangium
LM: focal mesangial proliferation widening

33
Q

APGN pathogenesis?

A

• Immune complex injury triggered by exogenous bacterial, viral or fungal antigen
• Poststreptococcal Glomerulonephritis:
o Group A, Beta-hemolytic Streptococcus
o appears 1 to 4 weeks after strep infection of pharynx or skin
o usually in children ages 6-10
o granular immune deposits in glomeruli
• Nonstreptococcal Acute Glomerulonephritis:
o Staph endocarditis, pneumonococcal pneumonia, Hep B, Hep C, varicella, HIV, malaria, toxoplasmosis
o Staph known to have IgA deposition – normally seen in IC people/drug users

34
Q

APGN histology?

A

• Diffuse proliferative glomerulonephritis:
• enlarged, hypercellular glomeruli:
o infiltration by leukocytes, neutrophils and monocytes
o proliferation of endothelial and mesangial cells
o Crescent formation
• IF: shows granular deposits of IgG, IgM, C3 along the GBM and mesangium
• EM: shows electron dense deposits on epithelial cell surface “humps” = Ag-Ab complexes at epithelial cell surface

35
Q

APGN clinical course?

A
  • young child develops malaise, fever, nausea, oliguria, hematuria 1-2 weeks after recovery from sore throat
  • red cell casts in urine, mild proteinuria
  • periorbital edema
  • mild/moderate hypertension
  • elevation of antistrep Ab (ASO) titers and decline in C3 concentration
  • treatment is good with conservative fluid management and most children will recover
  • Adults recover in 60% of cases, 40% of adults devlope RPGN or chronic renal disease
36
Q

RPGN

A

– Crescentic Glomerulonephritis
• rapid and progressive loss of renal fn. associated w/ severe oliguria and nephritic syndrome
• severe glomerular injury: collapsed compacted glomerular tufts
• death from renal failure occurs w/in weeks to months
• histologically see presence of crescents in glomeruli – due to proliferation of parietal and visceral epithelial cells lining Bownman capsule and infiltration of monocytes and macrophages
• rapid obliteration of urinary space
• In most cases, glomerular injury is immunologically mediated:

37
Q

RPGN Type I

A

Type I: Anti-GBM antibody induced disease:
• IF: linear deposits of IgG and often C3 in GBM

ex. Goodpasture syndrome: pulmonary hemorrhage associated w/ renal failure
o production of anti-GBM Abs to the Type IV collagen
o ages 20-40, females more common
o presents w/ pulmonary hemorrhage, recurrent hemoptysis and later dev. of RPGN

tx: plasmapheresis to remove Abs, IMsuppressive therapy, even w/ tx prognosis is poor

38
Q

RPGN Type III

A

Pauci-Immune type: 50% prevalence
• defined by lack of anti-GBM aabs or immune complexes via IF
• pt. have circulating antineutrophil cytoplasmic Abs (ANCAs) that produce cytoplasmic or perinuclear staining patterns

39
Q

RPGN Type II

A

: Immune Complex Deposition:
o ex: Idiopathic, Post-infectious GN, Lupus nephritis, Henoch-Schonlein purpura (IgA nephropathy), acute proliferative GN
o RPGN frequently shows cellular proliferation w/in the glomerular tuft in addition to crescent formation
o pt. can not normally be helped by plasmapheresis

40
Q

histology of RPGN?

A
  • kidneys enlarged and pale
  • crescents formed by proliferation of parietal (and visceral) epithelial cells and migration of monocytes and macrophages into urinary space
  • Fibrin strands are frequently prominent b/w the cellular layers of the crescents
  • EM may show ruptures in the GBM
41
Q

clinical course of RPGN?

A
  • hematuria w/ RBC casts in urine
  • moderate proteinuria occasionally reaching the nephrotic range
  • variable HTN and edema
  • in Goodpasture syndrome may see hemoptysis and life-threatening pulmonary hemorrhage
  • renal involvement is progressive and may cause severe oliguria in a few weeks
42
Q

most common nephrotic syndromes in adults?

most common in children?

A
  1. FSGS
  2. MG

children: MCD

43
Q

membranous glomerulopathy Pathogenesis/histology?

A

second most common cause of nephrotic syndrome in adults

• diffuse thickening of glomerular capillary wall due to accumulation of electron dense, Ig-containing deposits along the subepithelial side of BM
o “spikes” project from BM toward urinary space
o effaced foot processes (worn away)
o Thick BM: 5-20 fold increase in thickeness
o Subepithelial Deposits: dense aggregates of IgG → give “lumpy bumpy” spike appearance

  • Autoimmune disease linked w/ HLA-DQA1 and Abs to renal autoantigen PLA2 receptor and IgG’s
  • 85% idiopathic, no associated condition – responds poorly to steroid tx

Can be Secondary, associated with: (responds better to tx)
o Drugs: penicillamine, NSAID’s
o Malignant tumors: carcinomas of lung and colon and melanoma
o SLE
o Infections: chronic hep B, hep C, syphilis, schistosomiasis, malaria
o AI disorders (Hashimoto’s thyroiditis)

44
Q

clinical features of MG?

A
  • onset of nephrotic syndrome: nonselective proteinuria seen in 60%
  • hematuria and and mild hypertension in 15-35%
  • 40% develop renal insufficiency
  • 10% progress to ESRF
  • corticosteroids and IS tx generally no efficacious, in contrast with tx of patients with minimal change disease
45
Q

MCD path/histo?

A

most common cause of nephrotic disease in children !!!

  • peaks incidence: ages 2 to 6
  • disease sometimes follows resp. infection / prophylactic immunization

dramatic response to corticosteroid therapy – completely reversible!

Morphology:
• glomeruli are normal by light microscopy
• principle lesion is in visceral epithelial cells which show uniform and diffuse effacement of foot processes = “fusion” of foot processes

46
Q

MCD clinically?

A
  • massive proteinuria: usually selective, only albumin
  • renal fn. remains good, no HTN or hematuria
  • MCD in adults linked with Hodgkin lymphoma and lymphomas/leukemias
  • The 5 - 10% of putative minimal change disease (MCD) in children that does not respond to corticosteroid therapy generally have FSGS upon biopsy
47
Q

what treat w/ corticosteroids?

A

MCD

48
Q

FSGS path/histo?

A

focal = only some glomeruli are affected, segmental= only a portion of glomerular tuft exhibits sclerosis

most common cause of NS in adults in US!!!

  • nephrotic syndrome w/ heavy proteinuria
  • often associated with: HIV, heroin addiction, SS disease, morbid obesity

• Idiopathic FSGS is the most common cause of nephrotic syndrome in adults in US: esp. Hispanic and African-America patients

• Uncommmon inherited forms of genes that encode proteins localized in the podocyte slit diaphragms and adjacent cytoskeletal structures:
o NPHS1: nephrin, key component of slit diaphragm
o NPHS2: podocin, (accounts for 30% of steroid-resistant nephrotic syndromes in children)
o alpha-actinin 4 protein
o TRPC6 and APOL1 proteins

Pathogenesis:
• degeneration and focal disruption of visceral epithelial cells
• lesions tend to involve the juxtamedullary glomeruli
• see collapse of capillary loops
• sclerotic/nonsclerotic areas show diffuse effacement of foot processes
• in time this leads to global sclerosis of glomeruli
• collapsing glomerulopathy – subtype of FSGS

49
Q

FSGS clinically?

A

heavy, nonselective proteinuria
- can also have hematuria, reduced GFR and HTN
• generally a diagnosis that implies a poor prognosis as progressive renal disease tends to occur
• 20% of patients follow an unusually rapid course with massive proteinuria and renal failure within 2 years
• little tendency for spontaneous remission, though children have better prognosis

50
Q

how does MCD differ from FSGS?

A
  • FSGS has higher incidence of hematuria, reduced GFR and HTN
  • in FSGS proteineuria is nonselective
  • FSGS has poor response to corticosteroid therapy
  • FSGS has progression to CKD with at least 50% developing ESRD w/in 10 years
51
Q

HIV-associated nephropathy

A

• most commonly a severe form of collapsing variant of FSGS
o collapsing variant occurs in 5-10% of HIV-infected individuals and occurs more frequently in African-Americans than in Caucasians
o collapsing variant tends is NOT JUST CONFINED TO GLOMERULUS!!!
• see striking focal cystic dilation of tubule segments, filled with proteinaceous material, inflammation and fibrosis
• Pathogenesis is related to infection of glomerular and tubular cells by HIV due to podocyte expression of HIV gene products
• Human Immunodeficiency Virus (HIV) infection can directly or indirectly cause renal disease including acute renal failure and/or acute interstitial nephritis

52
Q

Membranoproliferative Glomerulonephritis (MPGN) path/histo?

A
  • mixed nephritic/nephrotic

“mesangiocapillary glomerulonephritis”

• Marked by alterations in glomerular BM, proliferation of glomerular cells and leukocyte infiltration
o glomerular proliferation is predominantly mesangial cells but may occasionally involve capillary loops

Histology:
• Mesangial cell proliferation
• Increased mesangial matrix (looks black)
• BM thickening and splitting
• Accentuation of lobular architecture
• Influx of acute inflammatory cell – neutrophils

53
Q

clinical features of MPGN?

A
  • present in adolescence/adulthood w/ nephrotic syndrome and nephritic component marked by hematuria or mild proteinemia
  • nephritic features: microscopic hematuria, HTN, oliguria, edema, renal insufficiency
  • nephrotic features: varying degrees of proteinuria
  • few spontaneous remissions
  • 50% develop CRD over 10 year span
  • high recurrence in transplant
  • no tx known
54
Q

Type I MPGN?

A
  • Subendothelial deposits

* evidence of immune complexes in the glomerulus and activation of both classical and alternative complement pathways

55
Q

Type II MPGN?

A

“Dense deposit disease”
• intramembranous deposits (in GBM)
• children and young adults
• hematuria w/ nephritic factor and/or NS or subnephrotic proteinuria
• considered a type of C3 glomerulopathy:

profound hypoclomementemia
o C3NEF or “nephritic factor” IgG autoantibody binds C3 convertase leading to continuous activation of alternative pathway

recurrence of MPGN II following renal transplant supports role of circulating factor

56
Q

secondary MPGN?

A

• occurs more in adults
• assoc.. w/ chronic antigenemia – resulting from immune complex disorders
o Hep B/C, SLE, alpha1 antitrypsin deficiency, HIV, Schistomosiasis, Malignancy, lymphorecticular lymphomas, melanoma
• poor prognosis as primary, with relentless progression to chronic renal failure (50% in 10 years)

57
Q

IgA nephropathy path/hist?

A

“Berger Disease”
• focal proliferative nephritis , most often involving mesangium and not capillary loops
• most common cause of GN worldwide
• cause of recurrent gross or microscopic hematuria
Histology
• Renal biopsy shows glomeruli/mesangial proliferation
• IF: mesangial deposits of IgA and C3
• see mesangial cell proliferation and matrix increase

58
Q

IgA nephropathy clinical features?

A
  • recurrent gross hematuria (predominantly nephritic presentation)
  • onset may follow resp. infection
  • mostly affects older children/young adults
  • more common in Caucasians/Asians
  • male predominance
  • gross hematuria after infection of respiratory, GI or urinary tract
  • hematuria typically lasts for several days and subsides, but reteurns every few months
  • slow progression to chronic renal failure in 15-40% of people within 20 years
  • onset in old age results in increased progression
59
Q

two eponymic disease assoc w/ IgA nephropathy?

A

• Berger Disease: Renal IgA nephropathy - no systemic disease
• Henoch-Schonlein purpura (HSP) - IgA nephropathy associated with systemic disease with skin (purpuric) manifestations and involvement of abdominal viscera other than kidney
o HSP is IgA mediated systemic vasculitis syndrome
o systemic childhood diseases
o onset often follows URI
o IgA nephropathy
o Ab pain, GI bleeding, arthralgia and palpable purpura on legs and buttocks
o deposition of IgA and sometimes IgG/C3 in mesangial region

60
Q

2 diseases from family hx of hematuria?

A
  1. alport syndrome (hereditary nephritis)
  2. Thin BM disease

80% with family hx of hematuria during childhood have these

61
Q

Alport Syndrome

A

Hereditary Nephritis
• Typically presents at ages 5 – 20
• Generally exhibits hematuria with progression to CRF, nerve deafness and a potential spectrum of certain eye disorders (lens dislocation, posterior cataracts, corneal dystrophy) and auditory defects
• X-linked form and gender distribution
• In X-linked forms large deletions of alpha5 chain (COL4A5) of type IV collagen imply the likelihood of ESRD at an earlier age
Histology: Irregular thickening of GBM, “moth-eaten”/ frayed

62
Q

thin BM disease

A

benign familial hematuria”
• usually a benign disease marked by diffuse thinning of GBM
• asymptomatic hematuria, mild/moderate proteineuria may exist
• prognosis is excellent – most pt. are heterozygotes for defective gene and thus are carriers
• unlike Alport, hearing loss, ocular problems, and family hx of renal failure are absent

63
Q

which glomerulonephridities most cause chronic GN?

A
  1. crescentic (RPGN)
  2. FSGS
  3. MPGN
    4/5: membranous nephropathy, IgA nephritis
64
Q

clinical course of chronic glomerulonephritis?

A 
Morphology: 
•	cortex is thinned and increase in peripelvic fat
•	obliteration of glomeruli
•	arterial/arteriolar sclerosis
•	marked atrophy of associated tubules

Dialysis changes:
• arterial intimal thickening
• deposits of calcium oxalate crystals
• acquired cystic disease

Uremic complications:
• uremic pericarditis
• secondary hyperparathyroidism
• left ventricle hypertrophy

Clinical Course:
• slowly progresses to renal insufficiency and death from uremia
• pt. presents w/ complaints of loss of appetite, anemia, vomiting, weakness, edema
• proteinuria, HTN and azotemia are discovered upon medical examination
• most patients are hypertensive and sometimes shows up cerebral and cardiovascular

65
Q

systemic diseases causing nephrotic syndrome/proteinuria?

A
  1. Diabetic Neuropathy
  2. SLE – 15% of patients
  3. Hep C- Cryoglobulinemia: Membranoproliferative Type 1
  4. HIV Nephropathy: Focal Segmental Glomerulosclerosis
66
Q

systemic diseases causing nephritic sx?

A
  1. SLE (60-70%)
  2. Bacterial Endocarditis: Acute proliferative Glomerulonephritis
  3. Goodpasture Syndrome: RPGN
  4. Henoch-Schonlein Purpura (HSP): IgA Nephropathy
67
Q

SLE

A
  • can cause damage to kidney and includes hematuria, nephritic syndrome, nephrotic syndrome, HTN and renal failure
  • in SLE see subendothelial dense deposits
  • Renal glomerular capillary BM with dense deposits are called “wire loops” – due to the deposits stiffly opening the capillary loops in the glomerulus
  • Marked increase in cellularity, glomerulus size is greatly enlarged and appears to be “stuffed” into Bowman’s capsule = decrease in urinary space
  • IF: anti-IgG Abs seen in mesangial and capillary wall (subendothelial IgG localization)
68
Q

review: what is SLE?

A

• characterized by autoantibodies that recognize ANA’s: antinuclear antibodies: directed against nuclear ags and can be grouped into four categories:
o 1: antibodies to DNA
o 2. antibodies to histones
o 3. antibodies to nonhistone proteins bound to RNA
o 4. antibodies to nucleolar antigens
• SLE starts out acutely, and becomes chronic and is characterized by febrile illness, injury to skin, joints, kidney and serosal membranes
• SLE effects women more often than men and is more predominant in black and Hispanic populations

malar rash, photosensitivity, oral ulcers, arthritis, serositis, renal disorder, seizures, hemalytic anemia,

69
Q

Diabetic nephropathy?

A

leading cause of kidney failure in US!
• non-nephrotic proteinuria, nephrotic syndrome, or chronic renal failure

• Changes to glomeruli:
o capillary BM thickening
o diffuse mesangial sclerosis
o nodular glomerulosclerosis

  • advanced renal hyaline arterosclerosis:
    o see markedly thickened afferent arterioles

Pathogenesis:
o DM glomeruosclerosis is most likely a metabolic defect due to insulin deficiency causing hyperglycemia and glucose intolerance
• see increased amounts of collagen type IV and increased ROS → damage glomerular filter: results in increased mesangial matrix

70
Q

bacterial endocarditis-associated glomerulonephritis?

A
  • immune complex nephritis initiated by complexes of bacteria Ag/Ab
  • hematuria and proteinuria
71
Q

amyloidosis

A
  • deposits of amyloid w/in the glomeruli due to renal amyloid light chain- AL
  • presents w/in the mesangium and capillary walls – eventually obliterates glomerulus completely
  • congo red – positive test
  • first present w/ nephrotic syndrome and may later die of uremia

RENAL II, Test 2 (5 decks)

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