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Renal > Nephrotic Syndrome > Flashcards

Nephrotic Syndrome Flashcards

1
Q

Define nephrotic

A

protein in urine > 3.5 g/24 hrs

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2
Q

What is selective nephrotic proteinuria?

A

albumin is being excreted

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3
Q

What is non selective nephrotic proteinuria?

A

proteins other than albumin, i.e. immunoglobulins, complement etc

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4
Q

What causes edema in nephrotic disease?

A

loss of vascular oncotic pressure due to proteinuria

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5
Q

Define nephritic

A

RBC in urine (hematuria) either gross or microscopic

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6
Q

What are consequences of nephritic hematuria?

A

azotemia
edema
HTN

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7
Q

At what point in the filtration system does filtrate become ultrafiltrate/early urine

A

between the visceral epithelial cells (podocytes) and the parietal epitheliacl cells of the Bowman’s capsule

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8
Q

What are podocytes

A

visceral epithelial cells lining the GBM on the bowman’s capsule side, but not the actual capsule itself

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9
Q

What is the parietal epithelium?

A

the epithelial cells lining the actual capsule, just beyond the podocytes

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10
Q

Where are mesangial cells located?

A

in the center of the glomerulus, where they provide support to other cells

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11
Q

Why are the papillary prone to papillary necrosis?

A

an electrolytically hostile region containing the loop of Henle, with high solute concentrations and low blood flow, prone to toxic and ischemic insult – ‘papillary necrosis’

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12
Q

Define glomerular sclerosis

A

fibrotic obliteration of capillary loop and increased matrix

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13
Q

Define a crescent

A

proliferation of parietal epithelial cells which compresses the glomerular tuft

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14
Q

Define the mesangial area

A

stalk region of capillary loop which contains mesangial cells and matrix; supports the tuft

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15
Q

Define subendothelial relative to the glomerulus

A

between vascular endothelial cells and GBM

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16
Q

Define subepithelial in the glomerulus

A

between the podocytes and the GBM

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17
Q

What is Tamm-Horsfall protein?

A

uromodulin - protein secreted by tubular epithelium; accumulates as dense pink homogenous material inside tubules in disease

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18
Q

Define tram track appearance

A

double contouring of the GBM, generally seen on EM or silver stains

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19
Q

Define wire loop appearance

A

thickened rigid-appearing capillary loops due to subendothelial deposits

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20
Q

What are the 2 types of immune complex deposition in situ?

A

Anti-GBM and anti-other

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21
Q

What are the two types of immune complex deposition in situ?

A

anti glomerular and planted

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22
Q

What % of loss can be tolerated without significant adverse events via glomerular compensation?

A

60 to 70%

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23
Q

Why does hyperlipidemia occur in nephrotic syndromes?

A

Hyperlipidemia is thought to occur as a by-product of increased synthetic activity of the liver to replace lost albumin.

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24
Q

When is minimal change disease generally seen in children?

A

following a URI

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25
Q

What is collapsing FSGS? what is a risk factor associated with it?

A

A complicatin of other GN’s that is drug induced, generally as HIV + heroin use

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26
Q

Does FSGS respond to steroids?

A

no

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27
Q

What is the pathophysiology of FSGS?

A

Pathophysiology is thought to involve a circulating mediator: the disease may recur in transplanted organ.

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28
Q

What are the histology findings in minimal change disease?

A

LM: normal
FM: negative
EM: podocyte effacement

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29
Q

What role do plasma proteins and lipids play in FSGS?

A

In primary cases is thought to occur through injury to the visceral epithelium (podocytes). As damage accrues, plasma proteins and lipids accumulate and appear as sclerosis; mesangial cells respond by proliferation and matrix formation (scar).

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30
Q

What is the most benign form of FSGS?

A

“tip lesion”

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31
Q

What are the LM findings for FSGS?

A

sclerosis affecting some parts of some glomeruli

32
Q

What are the FM findings for FSGS?

A

non-specific (may include IgG, IgM, C’), but will in part depend on underlying disease: increased IgA in IgA- induced nephropathy, “full house” (IgG, IgM, IgA, and C’ components) if happens as consequence of SLE

33
Q

What are the EM findings in FSGS?

A

loss of foot processes and podocyte detachment – the loss of foot processes has given rise to a hypothesis that FSGS is a severe variant of MCD

34
Q

What exogenous antigens can cause membranous NP?

A

hep B and C

35
Q

What endogenous antigens can cause membranous NP?

A

SLE or hashimoto’s

36
Q

Describe membranous nephropathy

A

Slowly progressive condition in adults with refractory proteinuria resulting from IC deposition,

37
Q

Other than antigens,what exposures can cause membranous NP?

A

heavy salts (gold and mercury) or drugs (penicillamine, captopril, NSAIDs)

38
Q

What causes the damage to the glomerulus in membranous NP?

A

MAC seems to induce mesangial cells to secrete proteases and oxidants, which damage the GBM. So the ICs may not necessarily be the agent of direct damage to the GBM, but instead act as an inciting agent.

39
Q

What is the LM finding for membranous NP?

A

diffuse thickening of the capillary wall – wire-loop appearance of the capillary tuft

40
Q

What is the FM finding for membranous NP?

A

granular deposits of C3 and IgG; may also have IgM and C1q if secondary to Lupus (‘full house’), or none

41
Q

What is the EM finding for membranous NP?

A

subepithelial deposits along the GBM containing IG imparting a ‘spike-and-dome’ pattern, where the dense (dark) deposits are progressively surrounded by lighter basement membrane materials and eventually resorbed.

42
Q

What are the two processes contained within membranoproliferative GN?

A

IC mediated

C mediated

43
Q

What is type I MPGN?

A

circulating ICs = complication of SLE, HBV, and HCV, prolonged infections or idiopathic

44
Q

What pathogens are associated with MPGN IC?

A

SLE
HBV
HCV

45
Q

What are C3 glomerulopathies?

A

Pathogenesis involves dysregulation of the alternative C’ pathway (either due to an autoantibody or a genetic predisposition and depletion of complement components. May present as nephritic syndrome or may have a mild proteinuria.

46
Q

What kind of membranoproliferative glomerulonephritis tends to recur in transplant organs?

A

C3 glomerulopathies

47
Q

What are the LM findings for MPGN?

A

increased cellularity of glom, with pronounced lobulation; GBM may show ‘tram-track’ appearance on silver stain

48
Q

How can the two types of MPGN be differentiated?

A

FM - c3 = c3 glomerulopathy

IgG = type I MPGN IC

49
Q

What are the EM findings for MPGN?

A

variable: both can have subepithelial, subendothelial, or intra-GBM deposits

50
Q

What are the LM findings for diabetic nephropathy?

A

diffuse thickening of GBM (a reflection of thickening of basement membrane throughout the body); this results in capillary leakage of proteins into the urine – proteinuria. Mesangial cells increase matrix production and glomerulosclerosis ensues. Eventually, nodules form – nodular sclerosis (Kimmelstiel-Wilson lesion): nodules of dense pink hyaline-appearing material in the mesangium.

51
Q

What are the main findings that confirm diabetic nephropathy?

A

nodular sclerosis; mesangial matrix production, and diffuse GBM thickening

52
Q

Why are diabetics predisposed to UTIs?

A

This results in favorable environment for bacteria, predisposing diabetics to urinary tract infections including pyelonephritis (with an occasional complication by necrotizing papillitis).

53
Q

What can chronic glomerulonephritis lead to?

A

end stage state

54
Q

What are the LM findings for chronic glomerulonephritis?

A

Diffuse sclerosis of majority of glomeruli, interstitial fibrosis, and tubular atrophy; at this point it is generally not possible to tell what the originating process was.

55
Q

What are the 2 divisions of tubulointerstitial disease?

A

infectious and non infectious

56
Q

What are the 2 types of infectious tubulointerstitial diseases?

A

acute pyelo

chronic pyelo + reflux nephropathy

57
Q

What are the non infectious causes of tubulinterstitial disease?

A

drug induced
ischemia
metabolic derangements
physical damage (i.e. radiation, etc)

58
Q

In severe cases, what can reflux nephropathy, medications and diabetes cause?

A

papillary necrosis

59
Q

What is the pathophysiology for analgesic induced nephropathy?

A

Acetaminophen/phenacetin cause oxidative damage and aspirin is a prostaglandin synthesis inhibitor resulting in vasoconstriction and reduction of blood flow to an already ischemic papilla.

60
Q

What are causes of acute tubular necrosis?

A

ischemia, drug/toxicity, consequences of severe glomerular diseases, acute papillary necrosis.

61
Q

What are the 3 phases of acute tubular necrosis?

A

initation x 36 h
maintenance x day 2 to 6 w
recovery at week 3 to 7

62
Q

What happens during initiation of ATN?

A

urine output begins to fall at this time. Tubular epithelium appears apoptotic/necrotic, nuclear features degenerate, basement membrane may fragment.

63
Q

What happens during the maintenance phase of ATN?

A

urine output is dramatically reduced; patients are uremic, fluid overloaded, and commonly need dialysis.

64
Q

What happens during the recovery phase of ATN?

A

marked by increased in urine production and metabolic derangements due to poor electrolyte control – need close observation by nephrologist. Tubules re-epithelialize in this phase if the basement membrane is intact; if not – scarring.

65
Q

“dults, slowly progressive nephrotic state with immune complexes depositing within GBM, key feature – ‘wire loop’ appearance of glom on LM and ‘spike-and-dome’ subepithelial deposits appearance on EM.” What disease is this?

A

membranous glomerulonephritis

66
Q

“Kids, relatively benign – responds to steroids – post-infectious nephrotic state, key feature – effacement of podocyte foot processes on EM with a normal glom on LM.” What disease is this?

A

minimal change disease

67
Q

“Kids or adults, key features – thickened GBM with ‘tram- track’ appearance and increased cellularity of the glom.” What disease is this?

A

membranoproliferative glomerulonephritis (MPGN)

68
Q

“damage to the glom by circulating ICs due to various long-standing immune activation conditions (autoimmune or infectious); key feature: IgG and C3 on FM”. What disease is this?

A

MPGN type I

69
Q

“damage to the glom due to C3 activation; key feature: C3 on FM”. What disease is this?

A

MPGN type II

70
Q

“Adults, poor response to steroids, a complication of many
infectious, autoimmune, or primary renal disorders; key feature – partial sclerosis of some gloms on LM and
effacement of podocyte foot processes on EM.” What disease is this?

A

Focal segmental glomerulosclerosis

71
Q

What are some of the currently thought mechanisms of glomerular damage in immune complex glomerlonephritis’s?

A

Antibody-antigen complex formation (either in plasma with subsequent deposition in the glom or in-situ either to filtered hapten or to intrinsic glomerular protein), cell-mediated damage, renal ablation, or direct epithelial (or endothelial) injury by toxins, medications/drugs, ischemia, or radiation. These ICs deposit themselves in various compartments within the glomerulus and either interfere with filtration directly, cause toxic damage to cellular components, induce proliferation of the mesangial cells, or incite inflammatory response which then damages the glomerulus – or any and all of the above.

72
Q

In absence of clinical history, what is the main morphologic difference between MCD and FSGS?

A

Light microscopy will assist in differentiation: in MCD, the glomerulus appears normal, whereas in FSGS parts of some glomeruli are fibrotic (both have effacement of foot processes by EM, and FM may be non-specific).

73
Q

When approached with a patient with nephrotic syndrome, what are main thoughts when considering the causes?

A

The main objective is to identify whether the patient’s nephrotic syndrome is due to any treatable causes, such as infection or autoimmune disorder or toxic exposure, because many types of renal damage may be halted or even reversed upon successful treatment of underlying disorder. Possibly, the reason why primary renal disorders progress to renal failure is because the underlying disease was not identified or is not yet known.

74
Q

What are signs and symptoms of nephrotic syndrome?

A

Nephrotic-range proteinuria (>3.5 g per day of protein), lipiduria and hyperlipidemia, and edema.

75
Q

What are some of the key components of the nephron and specifically – of the glomerulus?

A

Nephron consists of a filtration unit (glom), the concentrating units (convoluted tubules and loops of Henle), and collecting unit – collecting duct. Glomerulus consists of a capillary tuft lined by vascular endothelial cells with fenestrae, attached to glomerular basement membrane, on the other side of which are podocytes (visceral epithelial cells) with interdigitating foot processes holding up a lattice of proteins including nephrin, all encased in a layer of parietal epithelial cells (Bowman’s capsule).

76
Q

What is the danger of long-term use of high-dose combination of analgesics, including acetaminophen and aspirin?

A

These patients are at risk of analgesic-induced nephropathy.

Renal (28 decks)

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