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Delta Med - Renal > Renal 1 - Acute renal failure and Glomerulonephritis > Flashcards

Renal 1 - Acute renal failure and Glomerulonephritis Flashcards

1
Q

What are the definitions of CKD stages?

A 
Stage 1 - Kidney damage, GFR >90 (albuminuria, haem, scar)
Stage 2 - Kidney damage, GFR 60-90
Stage 3 - Moderate, GFR 30-59
Stage 4 - Severe GFR 15-29
Stage 5 - ESKD, GFR
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2
Q

What are problems with CG and MDRD in estimating GFR?

A

Accuracy significantly reduces as GFR increases.

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3
Q

What is the most prevalent stage of CKD in Australia?

A

Stage 3/3a

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4
Q

What is the importance of microalbuminuria in diabetes?

A

Heralds diabetic nephropathy.

Treating this slows the progression of DM.

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5
Q

What factors drive progression of CKD?

A

Proteinuria +++
Hypertension
Hyperglycaemia
Smoking

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6
Q

What is associated with increased CV mortality and overall mortality in CKD?

A

Reducing GFR

Increasing ACR

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7
Q

What are features of AKI?

A

Acidosis, hyperkalaemia common
Urine volume variable
Features of CRF - anaemia, PO4, PTH, Small Kidneys

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8
Q

What are causes of AKI?

A

Prerenal - hypovolaemia, CCF, sepsis, ACEi, NSAIDs, hepatorenal.
Nephrotoxins, contrast, atheroembolism
Obstruction - prostatic, others

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9
Q

What are risk factors for AKI?

A

elderly

Pre-existing CKD

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10
Q

What is the prognosis of AKI?

A

> 50% mortality if sepsis induced AKI requiring ICU
Recovery common if survival.
If dialysis dependent >60 days, ESKD

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11
Q

What is the RIFLE classification of AKI?

A

Risk – 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output

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12
Q

What is the AKIN staging system for AKI?

A

Stage 1 = serum creatinine increase >=26.5 OR increase to 1.5-2x from baseline, UO 2.0-3.0x from baseline, 3.0x from baseline OR serum creatinine >=354 with an acute increase of at least 44, or need for RRT.

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13
Q

What are some new biomarkers in AKI?

A

Urine NGAL
Plasma NGAL
Serum cystatin C

(others include IL-18 and KIM-1)

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14
Q

What area is the most sensitive to hypoperfusion in the kidney?

A

The thick ascending loop of henle - most metabolically active.

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15
Q

What are causes of acute tubular necrosis?

A 
Ischaemic:
- prolonged pre-renal
- hypotension, shock
- CCF
- CP bypass
Sepsis
Nephrotoxic
Drugs
 - Radiocontrast
 - Aminoglycosides
 - Cisplatin
 - Others
Pigment nephropathy
 - Haemoglobin
 - Myoglobin
 - Bilirubin
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16
Q

What are urine indices in ATN?

A

50% are polyuric
Urinary Na wasting
Sediment

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17
Q

What is the mortality rate in ARF vs ESRF?

A

50% in critically ill patients requiring HD
10% in ESRD patients requring HD

Significantly poorer outcomes in ATN requiring RRT

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18
Q

What is released in tumor lysis syndrome?

A

K+
PO4-
Ca2+

Largely in lymphoproliferative and leukaemic malignancies

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19
Q

What are risk factors for TLS?

A

LDH
Bone marrow disease
High chemosensitivity

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20
Q

What are methods of preventing TLS?

A 
Hydration
Allopurinol
Urinary alkalinisation
OR Rasburicase
 - recombinant urate oxidase
 - AEs - haemolysis, allergy
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21
Q

What are the 3 phases of hepatorenal syndrome?

A

1) pre-ascitic - compensated Na+ retention

2) AScities - sodium retention, mostly DCT with urinary Na

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22
Q

How is a Dx of Hepatorenal syndrome made?

A

Urinary Na

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23
Q

What are the types of hepatorenal syndrome?

A

Type I - worse than type 2, idiopathic
Type II - better prognosis than type 1 - has correctable cause

If requirement for HD for 3/12 - indication for kidney and liver transplant.

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24
Q

What is the timeframe for radio-contrast nephropathy?

A

Acute rise in serum creat 24-48hrs post contrast. Peaks in day 5-7, resolves by day 14.
3-5% post PTCA, associated with increased mortality.

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25
Q

What are clinical features/risk factors of radio-contrast nephropathy?

A

DDx = ATN, atheroembolism (weeks post insult)
Non-oliguric.

RFs =

  • dye volume and type - hypo>iso osmolar
  • heart failure, dehydration, diuretics (not ACEi)
  • CKD, diabetes, myeloma
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26
Q

How does one prevent radio-contrast nephropathy?

A

Hydration with N/S
Hydration with NaHCO3 if acidotic
N-Acetyl cysteine

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27
Q

What is useful in management of Contrast nephropathy?

A

Supportative

Haemofiltration may help

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28
Q

What is the relationship between albuminuria and proteinuria?

A

Albuminuria increases with increasing proteinuria.

Albuminuria may be more sensitive for glomerular damage at lower ranges of proteinuria.

29
Q

What are 5 clinical classifications of glomerulonephritis?

A

1) asymptomatic urinary abnormalities
2) nephritic syndrome (haematuria and proteinuria, renal impairment, salt and water retention and hypertension)
3) rapidly progressive glomerulonephritis - renal failure over days weeks, with nephritic presentation (usually), often with extensive glomerular crescent formation on Bx
4) neprotic syndrome - nephrotic range proteinuria (>3.5g/24hrs), hypoalbuminuria, hyperlipidaemia and oedema, often with predisposition to thrombosis and bacterial infection (loss of opsones)
5) Chronic glomerulonephritis - persistent proteinuria w/wo haematuria and slowly progressive loss of renal function.

30
Q

What are the 3 aspects of histological classification of Glomerulonephritis?

A

1) glomerular involvement (focal or diffuse, segmental or generalised)
2) Cell involvement - increases in cell number (proliferative), neutrophil accumulation (exudative), cell destruction (necrotising), ultrastructural damage (foot process effacement and flattening)
3) changes in non-cellular components of the glomerulus -matrix accumulation (hyalinosis) or immune deposits according to site of deposition (mesangial, sub-endothelial, sub-epithelial)

31
Q

What are examples of mesangial cell disease? (5)

A 
IgA nephropathy
IgM nephropathy
Mesangioproliferative GN
Class II lupus nephritis
Diabetic nephropathy
32
Q

What are examples of epithelial cell injury? (5)

A 
membranous nephropathy
minimal change disease
focal and segmental glomerulosclerosis
class V lupus nephritis
diabetic nephropathy
33
Q

What are examples of endothelial cell injury? (6)

A 
infection-assoc glomerulonephritis
mesangiocapillary glomerulonephritis
class III and IV lupus nephritis
anti-GBM disease
vasculitis and cryoglobulinaemia
HUS
34
Q

What is the presentation and histology of minimal change disease?

A

Presentation

  • pure nephrotic syndrome
  • 60-80% childhood NS
  • 10-20% adult NS - 10% oliguric AKI

Histology

  • normal light microscopy
  • +/- slight mesangial proliferation
  • +/- mesangial IgM
  • E.M - flattened podocytes
35
Q

What are features of treatment of minimal change disease?

A

Adults have slower response to steroids
fewer relapses
haematuria, decreased GFR, hypertension

In frequent relapses or non-response to steroids - cyclophosphamide (63% remission at 10y) or cyclosporin (nephrotoxic)

36
Q

What is the typical presentation of Focal and Segmental Glomerulosclerosis?

A

Proteinuria, nephrotic syndrome in 50%

Often hypertensive, decreased GFR, +/- haematuria

37
Q

What histology is seen in focal and segmental glomerulosclerosis?

A

focal and segmental glomerulosclerosis and hyalinosis
juxtamedullary nephrons involved first
interstitial damage and fibrosis

38
Q

What is the natural history of focal and segmental glomerulosclersosis?

A

persistent proteinuria ESRF >50%

remission portends good outcome

39
Q

What are prognostic factors in focal and segmental glomerulosclersosis?

A

decreased GFR, interstitial fibrosis on Bx
hypertension and nephrotic proteinuria (poor)
high recurrence rate in transplant (15-55%)

40
Q

What is the management of focal and segmental glomerulosclersosis?

A

ESRF >50% in untreated/non responders
Prednisone 1-2mg/kg/day for 3 months then taper for 3 months.
Cyclophosphamide 1-2mg/kg for 8 weeks in steroid non-responders (30-50% response)

cyclosporine 5mg/kg/d as BD dose

  • severely symptomatic, steroid non-responsive patients
  • high rate of relapse on withdrawal and nephrotoxicity
41
Q

What circulating receptor is seen in FSGS and is a cause of FSGS?

A 
high circulating levels of suPAR
elevated in FSGS and not other GN
higher in those with recurrence post Tx
levels fall with treatment of recurrence
causes disease in mouse models via podocyte B-3 integrin
42
Q

What is the presentation, histology and natural history of Primary membranous nephropathy?

A

Presentation - proteinuria, usually nephrotic
- common, 30% of adult nephrotic syndrome, exclude 2ndary causes

Histology:

  • thickened basement membrane
  • silver stain - intra-membranous Ig deposits, spikes
  • late - interstitial fibrosis and fewer deposits

Natural Hx:

  • variable - 25% go on to ESRF at 10 years
  • nephrosis, hypertension, low GFR and male gender portend poor prognosis and indicated treamtent
43
Q

What are 2ndary causes of GN?

A

SLE
Hepatitis
Drugs
Cancer

44
Q

What is management of primary membranous nephropathy?

A

Steroids alone offer no benefit
Cyclophosphamide plus prednisolone - improves survival and remission at 10 years. NNT 5 re: remission
Cyclosporin - slowed progression and reduced proteinuria
tacrolimus also useful with prednisone
Anticoagulation (warfarin) if serum albumin

45
Q

What antigen has been isolated in patients with idiopathic membranous nephropathy?

A

PLA2R

Also normalises when remission has been successfully induced.

46
Q

What is the presentation, histology and natural history of Mesangioproliferative GN?

A

Presentation - proteinuria and haematuria
- decreased GFR and hypertension, nephrotic syndrome uncommon

Histology - redupilication of membrane - wire loops, cellular proliferation and interstitial damage

Natural history and progression factors:

  • 40% have end stage renal disease in 10 years
  • nephrotic syndrome, decreased GFR and interstitial disease on Bx predict a poor prognosis (specific treatment is indicated)
47
Q

What is the management of mesangioproliferative GN?

A

Immunosuppression - no benefits
Aspirin +/- dipyridamole 100mg TDS
- Decreases proteinuria but likely has no effect upon GFR

48
Q

What is the presentation of IgA nephropathy?

A

asymptomatic haematuria, often synpharyngitic
hypertension, proteinuria and decreased GFR
males > females

MOST COMMON FORM OF GN

49
Q

What is the histology of IgA nephropathy?

A

mesangial hypercellularity, matrix expansion.
IgA +ve
interstitial damage and fibrosis, occasionally crescents

50
Q

What is the natural history of IgA nephropathy?

A

10 years - 20% ESRF, another 30%, reduced GFR

51
Q

What are prognostic factors in IgA nephropathy?

A 
persistent proteinuria
hypertension
decreased GFR
older age
interstitial fibrosis or crescents on Bx

Above = poor prognosis

52
Q

What is the management of IgA nephropathy?

A

RAS- inhibition - IgA with proteinuria or hypertension

Prednisolone - IgA with superimposed minimal change disease - i.e. proteinuria >3g/day, GFR >70, minor Bx changes (as per MCD)

IgA with proteinuria >1g/day, creat

53
Q

What is the pathophysiology of IgA nephropathy?

A

abnormal glycosylated IgA molecule - auto Ab developed against hinge region
formation of IgA-Ab complexes which deposit in the mesangium

54
Q

What is the presentation of rapidly progressive glomerulonephritis/crescenteric glomerulonephritis?

A

Presentation - renal failure 55 years, males = females

ANCA assoc vasculitis is the most common cause

55
Q

What are histological findings in RPGN?

A

crescents >25% of glomeruli
interstitial inflammation
vasculitis - necrosis, eosinophils, pauci-immune
Anti-GBM disease - linear IgG
SLE - mixed features - locts of complement and Ab granular)

56
Q

What is the natural history of RPGN?

A

50% ESRF may die - pulmonary haemorrhage, sepsis

57
Q

What are prognostic factors in RPGN?

A

renal function

extent of crescents on Bx

58
Q

What is the management of RPGN?

A

urgent Dx is warranted - renal Bx, SLE serology, ANCA, anti-GBM

Prednisone pulse x3, then high dose oral
Cyclophosphamide - oral for vasculitis and anti-GBM, pulse for SLE

Plasmapharesis

  • Anti-GBM if any residual function
  • ANCA +ve vasculitis - yes if there is severe renal failure
  • SLE - no proven benefit
59
Q

What are the classes of lupus nephritis?

A 
Class I - normal, minimal disease
Class II - mesangial disease with deposits/proliferation
Class III - focal proliferative GN
Class IV - diffuse proliferative GN
Class V - membranous GN
Class VI - complete sclerosis
60
Q

What is recommended initial therapy in Class III/IV lupus nephritis?

A

corticosteroids + cyclophosphamide OR MMF
In patients with worsening LN during 3 months of therapy - change to alternative recommended regime, or repeat Bx to guide further management

Use AZA or MMF + prednisone to maintain remission

Consider tapering after 1 year of maintenance.

Repeat Bx and increase treatment if there is deterioration of GFR or increased proteinuria.

61
Q

What should be used in resistance of Class III/IV lupus nephritis?

A

rituximab, IVIg, CNI

62
Q

What should be used in pregnancy in Class III/IV lupus nephritis?

A

Azathioprine and prednisone plus aspirin 100mg od

63
Q

What is the treatment of class V lupus nepritis?

A

If normal renal function and non-nephrotic range proteinuria, treat with antiproteinuric and antihypertensive medications, corticosteroids only for extrarenal manifestations of SLE.

If persistent nephrotic range proteinuria, should be treated with corticosteroids plus cyclophosphamide, CNI or MMF or AZA

64
Q

How is the diagnosis of atypical HUS made?

A 
Haematological Thrombotic Microangioathic anaemia
- thrombocytopenia =25% dec from BL
- evidence of haemolysis
 - raised serum LDH
 - OR red cell fragmentation
 - OR low haptoglobin
 - OR coombs -ve haemolytic anaemia
OR tissue Bx confirming TMA

AND Evidence of organ damage:

  • 80% kidney
  • decline in GFR or dialysis
  • or proteinuria/albuminura
  • or renal bx confirming TMA
  • Neuro changes (stroke, delirium)
  • gastrointestinal pain or pancreatitis
  • cardiac, pulmonary, PVD disease or occlusion
65
Q

What tests can excl TTP and typical HUS in suspected atypical HUS?

A

ATAMTS 13

66
Q

What are precipitants of aHUS?

A 
surgery
transplant
pregnancy
drugs
cancer
infection
APLS

causes chronic, uncontrolled activation of the complement cascade:
loss of function of CFH, CFI, MCP
gain of function Factor B, C3

67
Q

What is treatment of aHUS?

A

eculizumab - mAb directed against terminal portion of complement cascade (C5, inhibiting cleavage to C5a, C5b)

68
Q

What are conservative strategies for GN?

A

BP control

  • deterioration is slower if DBP 1g/day
  • ACEi and ARBs are best in proteinuric disease
69
Q

What role to statins have in conservative management of GN?

A

effective in treating hyperlipidaemia in proteinuric renal disease, but uncertain in effect on proteinuria and progression.
Do reduce cardiac risk

Delta Med - Renal (3 decks)

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