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RENAL Flashcards

1
Q

definition of AKI clinical and laboratory

A

clinical = urine output below 0.5ml/kg/hr for over 6 hours

lab= serum creatinine rise of over 50% from baseline within 48 hours

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2
Q

Pre renal causes AKI

A

Pump failure:

  • MI
  • CHF

Leaky:
- Nephrosis, gasatrosis, cirrhosis

Hole:
- Diarrhoea, dehydration, diuresis, haemorrhage

Clog:
- Fibromuscular dysplasia, Renal artery stenosis

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3
Q

Intra renal causes AKI

A

Glomerulonephritis

acute interstitial nephritis

acute tubular necrosis

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4
Q

Post renal causes AKI

A

Cancer
stones
BPH
neurogenic bladder

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5
Q

Fluid status examination

A 
eyes
mucous membranes
skin turgor 
respiratory rate and sounds
heart rate and sounds
oxygen sats
urine output
cap refill
pulse
BP
JVP
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6
Q

AKI investigations

A

Urine dipstick MCS - infection
FBC - infection
CRP - infection
Blood cultures - infection
ECG - hyperkalaemia
U&E - hyperkalaemia
ABG - hyperkalaemia and acidosis
abdominal uss - obstruction
CK - rhabdomyolysis
LFTs - hepatorenalsyndrome

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7
Q

3 signs of hyperkalaemia ECG

A

tall tented t waves
widened QRS complexes
flattened P waves

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8
Q

Treatment for hyperkalaemia IV

A

10mls 10% calcium gluconate

10 units actrapid(insulin) in 50ml 50% glucose

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9
Q

Treatment for hyperkalaemia if no IV available

A

salbutamol neubliser

calcium resonium + laxatives po

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10
Q

Management of acute renal failure

A

fluids
ABx
calcium gluconate + actrapid
catheterise/nephrostomy

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11
Q

indications for dialysis

A 
A - acidosis (pH < 7.1 HCO3 <12)
E- electrolytes (K+ > 7 Na+)
I - Intoxication
O- Overload
U - uraemia (urea >45)
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12
Q

Diagnosing cause of AKI

A 
Pre:
BUN:Cr - >20
Urine Na - <10
Fraction excreted Na - <1%
Fraction excreted urea - <35%

Post:
USS
CT

Intra:
diagnosis of exclusion 
use history and physical 
RBC casts likely glomerulonephritis
WBC casts + WBC + eosinophils likely AIN
Muddy brown casts likely ATN
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13
Q

Basics of the glomerulus

A

Epithelial pouch invaginated by capillary tuft
Semi-permeable filter
Endothelium
Basement membrane Epithelium
Mesangial cells are specialised smooth muscle cells that support the glomerulus and regulate blood flow and GFR

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14
Q

Filtration of blood in kidneys

A

Receive 25% CO
20% blood volume is filtered (250ml/min)
Basement membrane is negatively charged so anionic proteins are retained eg albumin
Filtration key to excrete waste and it remains constant over 80-200mmHg
Flow of filtrate will depend on Na and water reabsorption

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15
Q

Sodium reabsorption

A

Main factor for determining extracellular volume

Low BP and low NaCl at macula densa (DCT) ==> renin release ==> aldosterone release ==> upregulate Na/K pumps

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16
Q

Water reabsorption

A

Determines ECF osmolality

High osmolality or low BP ==> ADH release

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17
Q

Nephron PCT

A

reabsorption of filtrate

  • Na/K pump basolateral keeps Na low
  • Na can move in at apical membrane down conc gradient
  • Can use secondary active transport to move AA, glucose, Cl-
  • 70% total Na reabsorption
  • Reabsorption of amino acids, glucose, cations
  • Bicarbonate reabsorbed using carbonic anhydrase
  • Water follows by osmosis
  • Small proteins absorbed, lysed and back into circulation
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18
Q

Thick ascending limb

A

Creation of osmolality gradient

  • 20% sodium reabsorption
  • Na/K/2Cl triple symporter
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19
Q

DCT function

A

5% Na reabsorption
Apical NaCl co-transporter
Ca reabsorption under control of PTH

In very close opposition to the glomerulus
1st part is macula densa cells provides feedback for GFR and fluid flow, based on Na levels

2nd part overlap in function with ascending limb
Continues to dilute the fluid

IS susceptible to ADH action
ACID BASE regulation

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20
Q

Medullary collecting duct

A

Na reabsorption coupled to K or H excretion
Basolateral aldosterone sensitive Na/K pump

Intercalated cells - acidification of urine and acid base balance

Principal cells - role in Na balance and ECF volume regulation

ADH can act here
Also permeable to urea

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21
Q

Cortical CD

A

Water reabsorption controlled by aquaporin 2 channels

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22
Q

Endocrine function of the kidneys

A
  • Secretion of renin by juxtaglomerular apparatus
  • EPO synthesis
  • 1 alpha hydroxylation of vitamin D controlled by PTH
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23
Q

Carbonic anhydrase inhibitor diuretics (acetazolamide)

A

MOA: inhibit carbonic anhydrase in PCT
Effect: ↓ HCO3 reabsorption → small ↑ Na loss
Use: glaucoma
SE: drowsiness, renal stones, metabolic acidosis

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24
Q

Loop diuretics (frusemide)

A

MOA: inhibit Na/K/2Cl symporter in thick ascending limb
Effect: massive NaCl excretion, Ca and K excretion
Use: Rx of oedema – CCF, nephrotic syndrome,
hypercalcaemia
SE: hypokalaemic met alkalosis, ototoxic, Hypovolaemia

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25
Q

Thiazide diuretics (bendroflumethiazide)

A

MOA: inhibit NaCl co-transporter in DCT
Effect: moderate NaCl excretion, ↑ Ca reabsorption
Use: HTN, ↓ renal stones, mild oedema
SE: ↓K, hyperglycaemia, ↑ urate (CI in gout)

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26
Q

K+ sparing diuretics ( spironolactone)

A

MOA
Spiro: aldosterone antagonist
Amiloride: blocks DCT/CD luminal Na channel
Effect: ↑ Na excretion, ↓K and H excretion
Use: used ̄c loop or thiazide diuretics to control K loss,
spiro has long-term benefits in aldosteronsim (LF, HF)
SE: ↑K, anti-androgenic (e.g. gynaecomastia)

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27
Q

Osmotic diuretics (mannitol)

A

MOA: freely filtered and poorly reabsorbed
Effect: ↓ brain volume and ↓ ICP
Use: glaucoma, ↑ICP , rhabdomyolysis
SE: ↓Na, pulmonary oedema, n/v

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28
Q

Renal causes of haematuria

A 
Congenital: PCK
  Trauma
  Infection: pyelonephritis
  Neoplasm
  Immune: GN, TIN
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29
Q

Extra-renal causes of haematuria

A

Trauma: stones, catheter
Infection: cystitis, prostatitis, urethritis
Neoplasm: bladder, prostate
Bleeding diathesis (tendency)
Drugs: NSAIDs, frusemide, cipro, cephalosporins

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30
Q

Proteinuria classification

A

30mg/dL = 1+
300mg/dL = 3+
PCR < 20mg/mM is normal, >300 = nephrotic

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31
Q

Causes of proteinuria

A 
Diabetes
amyloidosis 
SLE
HTN
ATN
fever
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32
Q

Microalbuminuria

A

albumin 30-300mg/24 hr

Causes DM, raised BP, minimal change glomerulonephritis

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33
Q

Causes of casts

A

RBC- glomerular haematuria
WBC - interstitial nephritis , pyelonephritis
tubular - ATN

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34
Q

Creatinine

A

synthesised during muscle turnover
freely filtered and small proportion secreted by PCT
take in to account, muscle mass, age, sex, race
Plasma Cr wont rise above normal until 50% decrease in GFR

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35
Q

Urea

A

Produced from ammonia by liver
Increased with protein meal
Decreased with hepatic impairment
10-70% is reabsorbed - depends on urine flow
decreased flow == increased urea reabsorption so high urea in dehydration

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36
Q

Interpreting urea and creatinine

A

Isolated increase urea = low flow (hypoperfusion / dehydration )
Increased urea and creatinine = low filtration = renal failure

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37
Q

Creatinine clearance

A

measuring creatinine clearance helps to give estimate of GFR

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38
Q

Modification of diet in renal disease equation (MDRD)

A

takes into account serum Cr, sex, age, race

elucidates need for urine collection

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39
Q

Presentation of renal failure URAEMIA (GFR<15ml/min)

A

Symptoms

  • pruritus
  • confusion
  • lethargy
  • paraesthesia
  • bleeding
  • hiccoughs

Signs

  • pale
  • striae
  • pericardial rub
  • fits
  • coma
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40
Q

Presentation of renal failure PROTEIN LOSS and NA+ RETENTION

A

Symptoms

  • polyuria
  • polydipsia
  • breathlessness

signs

  • oedema
  • raised JVP
  • HTN
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41
Q

Presentation of renal failure ACIDOSIS

A

symptoms

  • breathlessness
  • confusion

signs
- kussmaul breathing

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42
Q

Presentation of renal failure hyperkalaemia

A

symptoms

  • palpitation
  • chest pain
  • weakness

signs

  • peaked T waves
  • flattened P waves
  • increased PR interval
  • broad QRS complex
  • can enter VF == death
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43
Q

Presentation of renal failure ANAEMIA

A

symptoms

  • breathlessness
  • lethargy
  • faintness
  • tinnitus

signs

  • pallor
  • tachycardia
  • flow murmurs (mitral )
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44
Q

Presentation of renal failure vitamin D deficiency

A

symptoms

  • bone pain
  • fractures

signs

  • osteomalacia
  • cupped metaphyses
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45
Q

Presentation of renal failure overview

A 
Uraemia
Proteinuria + High Na+
Acidosis
Hyperkalaemia
Anaemia
Vitamin D deficiency
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46
Q

Urine output

A

1ml/min
1.5L/day

0.5-1ml/kg/hr

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47
Q

2 types of nephron

A

Cortical - 85%
- short loop of henle

Juxtamedullary - 15%

  • long loop of henle
  • vasa recta develops alongside it
  • able to reabsorb more water due to larger surface area
  • these are the predominant nephrons in desert animals
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48
Q

Fanconi syndrome

A

All the normal PCT reabsorptive mechanisms are defunct
all solutes now found in urine, eg Na, glucose etc

Many causes

  • inherited
  • medications eg valproate
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49
Q

Medullary osmotic gradient

A

interstitium of the medulla becomes more hypertonic as you move down up to 1200mOsm/kg

this is created by countercurrent multiplier

this gradient helps as CD passes alongside and water is free to move out and dilute

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50
Q

Countercurrent multiplier

A

Thick ascending limb is impermeable to water but pumps out a load of solutes (Na/K/2Cl) especially lower down where it has more solutes to pump = (1200mOsmol)

Thin descending limb is permeable so water moves out in to interstitium to dilute, more water is lost at the superior aspect.

Tonicity of tubule fluid rises then falls, it is always 200 less in ascending vs descending.

Gradient is maintained by the vasa recta which is permeable to both

  • absorbs solutes as it descends
  • releases solutes as it ascends
51
Q

GFR regulation

A

Intrinsic control

  • autoregulation by vasoconstriction of afferent arteriole
  • tubulo-glomerular feedback

Extrinsic control
- renal sympathetic vasoconstrictor nerve activity

autoregulation when we have high blood pressure get afferent vasoconstriction to prevent overload of DCT and CD due to too much fluid flowing through

if mean arterial pressure drops towards 70mmHg afferent vasodilation to encourage blood flow through kidneys

52
Q

Calculating MAP

A

SBP + 2(DBP)/3

53
Q

Glomerulus filtration sieve

A

fenestration of epithelia

negatively charged basement membrane

podocyte epithelium has filtration slits 4nm wide made up of protein rungs and if these rungs damaged == nephrotic syndrome

54
Q

Measuring GFR with inulin

A

GFR = Uin x Flow rate / Pin

55
Q

disadvantages of using inulin for gfr

A

prolonged infusion
repeated plasma samples
difficult for routine clinical use

56
Q

advantages of using creatinine for gfr

A 
intrinsic inert substance 
released at steady state from skeletal muscle 
no infusion needed 
freely filtered 
Not reabsorbed in the tubule
57
Q

Disadvantages of creatinine for gfr

A

Some is secreted in to tubule
gives overestimate of gfr
also need to remember different muscle masses and MDMR score

Also trimethoprim acts as a competitive inhibitor of creatinine secretion

58
Q

Glucose transport maximum in nephron

A

20mM
but can see glucose in urine from 10mM + due to different transport maximum values between the 2 million nephrons you have

PCT Na-Glucose co transporter

then GLUT2 on basolateral membrane

59
Q

Familial renal glycosuria

A

SGLT2 protein mutation

also a drug target for T2DM treatment SGLT2 inhibitors help lower blood glucose levels

eg dapagliflozin

60
Q

Dapagliflozin

A

SGLT2 inhibitor in PCT

Diabetes drug to increase glycosuria and lower blood glucose

61
Q

Blood buffers

A

Bicarbonate buffers

Phosphate buffers

Protein buffers (inc Hb)

62
Q

Using Henderson Hasselbach equation what is the normal clinical ratio of HCO3:CO2

A

20:1

63
Q

Acid base control in PCT

A

In lumen brush border carbonic anhydrase creates CO2 + H2O
CO2 is reabsorbed and used to generate HCO3 and H+ in cell
H2CO3 moves into blood with Na symporter
H+ moves into filtrate with Na antiporter or via ATP H+ pump

64
Q

Acid base control intercalated A cell

A

CO2 reabsorbed and used to generate HCO3 in the cell
HCO3 reabsorbed using Cl- antiporter
H+ out via ATP channel (this is upregulated by aldosterone)
or out via ATP and K+ antiporter

thus aldosterone helps lower blood acidity and increase pH.

Phosphate is also excreted into filtrate which buffers the excess H+ in the filtrate to keep pH above 4.5 whilst still secreting H+ ions

pH of urine cannot fall below 4.5 or gives lots of damage

65
Q

Ammonia buffers

A

Glutamine breakdown on intercalated cells gives 2 x HCO3 and 2 x NH3
HCO3 is made de novo from glutamine and is reabsorbed using Na symporter

NH3 + H+ = NH4+ ammonium salts excreted into filtrate using Na antiporter

66
Q

Intercalated B cells

A

Carbonic anhydrase in cell generates HCO3- and H+
HCO3- pumped out into filtrate with Cl antiporter

H+ back into blood using ATP pump

This cell type is upregulated during alkalosis in order to try and decrease the pH by reabsorbing H+

67
Q

Role of aldosterone in kidney acid base

A

Aldosterone upregulates the function of the ATP H+ apical transport channel in intercalated A cells

Aldosterone also upregulates Na H+ antiporter in the PCT

Thus it acts to raise pH and remove acid

68
Q

Medulla respiratory regulation

A

charged ions cannot cross BBB but CO2 does and is converted to H+ by CSF carbonic anhydrase

In acidotic times CSF pH decreases
Medulla recognises this and increases ventilation

The increase in ventilation can also be triggered by peripheral chemoreceptors in aortic arch and carotid bodies, and these detect H+ directly rather than CO2.

Increase ventilation helps blow off CO2 and return ECF pH to normal range.

69
Q

Renal tubular acidosis

A

Caused by lack or fault in the acid- base regulating enzymes

type 1= Collecting ducts
type 2= PCT
type 4= deficiency of aldosterone

70
Q

Respiratory acidosis causes

A 
respiratory depression
copd
nm disorder
airway obstruction 
restrictive lung disease
71
Q

Respiratory alkalosis causes

A 
anxiety
hypoxaemia
pneumothorax (causes hyperventilation)
V:Q mismatch (hyperventilation)
hypotension 
high altitude
72
Q

Normal anion gap

A 
cation = Na 140
anion = Cl- + HCO3 = 108 + 24 = 132

normal anion gap = 8-12

73
Q

Non anion gap acidosis causes

A

this is when HCO3 drops but Cl- will increase so overall there is no change in the anion gap

causes

  • renal tubular acidosis 1 and 2
  • diarrhoea
  • acetazolamide (CAi) therapy

all cause decrease of HCO3

74
Q

causes of anion gap metabolic acidosis

A 
MUDPILES 
or KARMEL 
Ketoacidosis
Aspirin
Renal failure
Methanol 
Ethylene glycol 
Lactic acidosis (sepsis)
75
Q

Glomerulonephritis definition

A

Group of disorders resulting from glomerular membrane damage
Can give proteinuria and haematuria
Can give AKI and ESRF

76
Q

Glomerulonephritis causes

A 
Immune - SLE, goodpastures, vasculitis 
Infection - Hepatitis , Streptococcus, HIV
Idiopathic
Drugs- penicillin, gold
Sarcoidosis
77
Q

Presentation glomerulonephritis

A

Asymptomatic haematuria
Nephrotic syndrome
Nephritic syndrome

78
Q

Glomerulonephritis Ix

A 
Bloods:
  Basic: FBC, U+E, ESR
  Complement (C3 and C4)
  Abs: ANA, dsDNA, ANCA, GBM
  Serum protein electrophoresis and Ig
  Infection: ASOT, HBC and HCV serology
Urine
  Dipstick: proteinuria ± haematuria
  Spot PCR
  MCS
  Bence-Jones protein

Imaging
CXR: infiltrates (Goodpasture’s, Wegener’s)
Renal US ± biopsy

79
Q

3 causes of asymptomatic haematuria

A

IgA nephropathy
Thin BM disease
Alport’s disease

80
Q

Features of IgA nephropathy

A

Young males with recurrent macroscopic haematuria

Often follows URTI (strep)

Rapid recovery between episodes

Can occassionally lead to nephritic syndrome

81
Q

Diagnosing IgA nephropathy

A

Biopsy shows IgA in mesangium

82
Q

Treatment IgA nephrop;athy

A

Steroids or cyclophosphamide if decreased renal function

83
Q

Thin basement membrane disease features

A

Autosomal dominant condition
Commonest cause of asymptomatic haematuria

Persistent asymptomatic microscopic haematuria

Very small risk of ESRF

84
Q

Alport’s syndrome features

A

85% X linked inheritance

Progressive proteinuria and haematuria ==> progressive renal failure

Sensorineural deafness
Lens dislocation and cataracts
Retinal flecks

85
Q

Nephritic syndrome features

A

Haematuria (macro / micro) + red cell casts
Proteinuria → oedema (esp. periorbital)
Hypertension
Oliguria and progressive renal impairment

86
Q

Causes of nephritic syndrome (acute GN)

A

proliferative - post strep

Crescenteric - RPGN

87
Q

Proliferative nephritic syndrome

A

usually young child following URTI strep
malaise and smoky urine

Raised ASOT
Decreased C3

88
Q

Biopsy proliferative nephritic syndrome

A

shows IgG and low C3

89
Q

Prognosis proliferative nephritic syndrome

A

95% children will fully recover

minority go on to develop RPGN

90
Q

3 types of RPGN (crescenteric nephritic syndrome)

A

Anti-GMN – goodpasture’s syndrome
Immune complex deposition
Pauci immune

91
Q

Goodpastures syndrome features

A

5% of RPGN cases
Ab against collagen 4
Gives haematuria and haemoptysis
CXR shows infiltrates

Treat with plasmaphoresis and immunosuppression

92
Q

Immune complex deposition RPGN

A

45% RPGN cases
Any predisposing condition to give immune deposition
eg SLE.. endocarditis

93
Q

Pauci immune RPGN

A

cANCA: Wegener’s
pANCA: microscopic polyangiitis, Churg-Strauss Even if ANCA+ve, may still be idiopathic
i.e. no features of systemic vasculitis

94
Q

Nephrotic syndrome features

A

Proteinuria – PCR >300mg/mM or >3g/24h

Hypoalbuminaemia: <35g/L

Oedema: periorbital, genital, ascites, peripheral
Often intravascularly depleted ̄c ↓ JVP (cf. CCF)

95
Q

Nephrotic syndrome complications

A

Infection: ↓ Ig, ↓ complement activity
VTE: up to 40%
Hyperlipidaemia: ↑ cholesterol and triglycerides

96
Q

Clinical assessment for AKI

A

acute or chronic?

volume depleted?

GU tract obstruction ?

Rare cause?

97
Q

Mx acute renal failure

A

ABC

Treat life threatening states
- hyperkalaemia, pulmonary oedema, bleeding

Treat shock and dehydration

Monitor
- cardiac, catheter, fluid balance

Look for evidence post renal causes

Hx and Ix

Treat sepsis

Call urologists

98
Q

Acute interstitial or tubulointerstitial nephritis

A

immune mediated hypersensitivity to either drugs or other haptens

99
Q

Causes ATN

A

70% drugs

  • NSAIDS
  • ABx
  • Diuretics

Infections 15%
- staph

Immune
- sle, sjogrens

100
Q

ATN overview

A

People will come in with arthralgia, rash and oliguria and maybe uveitis

Ix

  • look for raised IgE and eosinophilia
  • also will have haematuria and proteinuria

Need to stop the offending drug
offer prednisolone

101
Q

Analgesic nephropathy

A

Arises following chronic use of complex analgesia

gives mild proteinuria and slowly progressive CRF

Sloughed papilla can lead to obstruction of urinary tract

Ix- non contrast CT shows calcified papilla

Mx - stop analgesia

102
Q

Rhabdomyolysis pathogenesis

A

Skeletal muscle breakdown gives release of K+, phosphate, urate, myoglobin and CK

103
Q

Rhabdomyolysis clinical features

A

Red-brown urine
Muscle pain and swelling
AKI occurs 10-12 hours later

104
Q

Rhabdomyolysis Ix

A

Dipstick: +ve Hb, -ve RBCs

Blood: ↑CK, ↑K, ↑PO4, ↑urate

105
Q

Rhabdomyolysis Rx

A

Rx hyperkalaemia
IV rehydration: 300ml/h
CVP monitoring if oliguric
IV NaHCO3 may be used to alkalinize urine and stabilise a less toxic form of myoglobin.

106
Q

Chronic renal failure features

A

Kidney damage for more than 3 months indicated by reduced function
Symptoms usually only seen at stage 4 <30ml
Stage 5 or need for RRT == ESRF

107
Q

CKD classification

A 
1- >90
2- 60-89
3a - 45-59
3b- 30-44
4- 16-29
5- <15
108
Q

Ix CKD

A

Bloods:
↓Hb, U+E, ESR, glucose, ↓Ca/↑PO4, ↑ALP, ↑PTH
Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep
Film: burr cells

Urine: dip, MCS, PCR, BJP

Imaging
CXR: cardiomegaly, pleural/pericardial effusion, oedema
AXR: calcification from stones
Renal US
Usually small (<9cm)
May be large: polycystic, amyloid
Bone X-rays: renal osteodystrophy (pseudofractures)
CT KUB: e.g. cortical scarring from pyelonephritis
Renal biopsy: if cause unclear and size normal

109
Q

Complications CKD

A 
CRF HEALS
Cardiovascular disease
Renal osteodystrophy 
Fluid oedema
Hypertension 
Electrolyte disturbances 
Anaemia
Leg restlessness
Sensory neuropathy
110
Q

Renal osteodystrophy mechanism

A

1 alpha hydroxylase deficiency less calcium so more PTH

Phosphate retention

  • decreased calcium
  • increased PTH directly

More PTH = bone resorption

this whole process gives acidosis

111
Q

Management CKD

A

General
- stop toxic drugs

Lifestyle

  • exercise
  • stop smoking
  • Na, fluid and PO4 restriction

CV risk

  • statins
  • low dose aspirin

HTN
- target 140/90

Oedema
- furosemide

Bone disease

  • phosphate binders- calcichew
  • alfacalcidol - (vit d analog)
  • Cinacalcet - calcium analog

Anaemia
- EPO

Restless legs
- Clonazepam

112
Q

Renal transplant assessment

A

Virology status: CMV, HCV, HBV, HIV, VZV, EBV
CVD
TB
ABO and HLA haplotype

113
Q

Renal transplant CI

A

active current infection
cancer
severe heart disease or other significant co-morbidity

114
Q

Renal transplant types of graft

A

LIVE

  • related has best outcomes
  • unrelated

CADAVERIC

  • Deceased brain dead
  • Deceased cardiac dead
115
Q

Renal transplant pre-op immunosuppression

A

Alemtuzumab (anti CD52)

116
Q

Renal transplant post-op immunosuppression

A

Short term
- prednisolone

Long term

  • tacrolimus
  • ciclosporin
117
Q

Renal transplant prognosis

A

cadaveric graft

15 years

118
Q

Renal transplant post-op complications

A

bleeding
graft thrombosis
infection
urinary leaks

119
Q

Renal transplant hyperacute rejection

A

Occurs within minutes
due to ABO incompatibility

gives thrombosis and SIRS
- systemic inflammatory response syndrome

120
Q

Acute rejection renal transplant

A

Occurs within 6 months
presents with increasing Creatinine
- with fever and graft pain

Cell mediated response

DOES respond to immunosuppression

121
Q

Chronic rejection renal transplant

A

> 6 months

Interstitial fibrosis + tubular atrophy

Gradual increase in Cr

DOESN’T respond to immunosuppression

122
Q

Ciclosporin and Tacrolimus nephrotoxicity

A

Acute
- reversible afferent arteriole constriction == decreased GFR

Chronic
- tubular atrophy and fibrosis

123
Q

Immune complications of renal transplant

A

increased susceptibility to infection
- opportunists, fungi, warts

Increased risk of malignancy

  • BCC
  • SCC
  • EBV

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