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Renal Flashcards

1
Q

What stimulates Na reabsorption?

A

Na reabsorption increases extracellular volume

decreased BP and decreased NaCl @ macula densa -> renin release -> aldosterone release -> more Na/K pumps

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2
Q

what increases water reabsorption?

A

increased osmolality or decreased BP

-> ADH release

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3
Q

endocrine function of the kidney?

A

secretion of renin by juxtaglomerular apparatus

EPO synthesis

1α-hydroxylation of vitamin D (controlled by PTH)

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4
Q

carbonic anhydrase inhibitors?

MOA

A

inhibit carbonic anhydrase in PCT

  • > ↓ HCO3 reabsorption → small ↑ Na loss
    e. g. acetozalamide
    use: glaucoma

SE: drowsiness, renal stones, metabolic acidosis

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5
Q

Loop diuretics MOA?

A

e.g. furosemide, bumetanide

MOA: inhibit Na/K/2Cl symporter in thick ascending limb

Effect: massive NaCl excretion, Ca and K excretion

Use: Tx of oedema – CCF, nephrotic syndrome, hypercalcaemia

SE: hypokalaemic met alkalosis, ototoxic, Hypovolaemia

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6
Q

e.g. of loop diuretics?

A

furosemide

bumetanide

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7
Q

e.g of carbonic anhydrase inhibtors?

A

acetazolamide

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8
Q

thiazide diuretics MOA?

A

e.g. bendroflumethiazide

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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9
Q

e.g. of thiazide diuretics?

A

bendroflumethiazine

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10
Q

K-sparing diuretics?

A

e.g. spironolactone - aldosterone antagonist

amiloride- blocks DCT/CD luminal Na channel

Effect: ↑ Na excretion, ↓K and H excretion

Use: used w loop or thiazide diuretics to control K loss, spiro has long-term benefits in aldosteronism (LF, HF)

SE: ↑K, anti-androgenic (e.g. gynaecomastia)

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11
Q

e.g. of k sparing diuretics?

A

spironolactone

amiloride

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12
Q

osmotic diuretics moa?

A

e.g. mannitol

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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13
Q

false +ve haematuria?

A

myoglobin, porphyria

menstrual blood

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14
Q

causes of proteinuria?

A

commonest:

DM

minimal change disease

membranous nephropathy

amyloidosis

SLE

other: HTN, UTI, ATN

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15
Q

definition of nephrotic syndrome?

A

proteinuria > 300mg/dL

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16
Q

what is a protein in the urine that wont be picked up on urine dipstick?

A

Bence-Jones proteins

(immunoglobulin light chain)

-> electrophoresis of urine

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17
Q

White cell casts in urine?

A

pyelonephritis

interstitial nephritis

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18
Q

what factors influence creatinine measurement?

A

creatinine synthesised during muscle turnover

increased muscle -> increased creatinine

age, sex, race

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19
Q

what influences urea measurement?

A

urea is produced from ammonia by liver

increases w protein meal (e.g. supplements, upper GI bleed)

decreases w hepatic impairment

decreased urine flow -> increased urea reabsorption (e.g. in dehydration)

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20
Q

raised Ur and Cr vs isolated raised Urea?

A

isolated raised urea = hypoperfusion/ dehydration -> decreased renal flow

increased urea and creatinine = decreased filtration ie. renal failure

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21
Q

causes of renal AKI?

A

glomerulonephritis

e.g. minimal change, membranous, post strep, IgA, rapidly progressive

acute tubular nephritis

interstitial disease

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22
Q

causes of post renal AKI?

A

obstruction

e.g. in renal pelvis, ureters, bladder or urethra

Stone

Inflammation: stricture

Neoplasm

Prostatic hypertrophy

Infection: TB, schisto

Neuro: post op, neuropathy

posterior urethral valves

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23
Q

causes of pre renal AKI?

A

shock

renal artery stenosis:

RAS

toxins: NSAIDS, ACEi

Thrombosis

Hepatorenal syndrome

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24
Q

presentation of renal failure?

A

uraemia

protein loss and Na+ retention

acidosis

hyperK

Anaemia

Vit D deficiency

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25
Q

how may uraemia present in a pt?

signs and symptoms

A

symptoms:

pruritus

anorexia, n/v, weight loss

lethargy

confusion

paraesthesia: neuropathy

pericarditis

signs:

pale, sallow skin

fits

coma

uraemic flap

confusion

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26
Q

how may protein loss and Na+ retention present in patients?

signs and symptoms

A

symptoms:

polyuria, polydipsia

oliguria, anuria

breathlessness

signs:

oedema

raised JVP

HTN

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27
Q

how may acidosis present in a pt?

signs and symptoms

A

signs:

Kussmaul respiration

symptoms:

breathlessness

confusion

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28
Q

how may hyperK present in a pt?

signs and symptoms

A

signs:

peaked T waves

flattened P waves

broad QRS

prolonged PR interval

sine wave pattern -> VF

symptoms:

palpitations

chest pain

weakness

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29
Q

how may anaemia present in a pt?

signs and symptoms

A

signs:

conjunctival pallor

pallor

tachycardia

flow murmurs (ESM @ apex)

symptoms:

breathlessness

lethargy

faintness

tinnitus

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30
Q

how may Vit D deficiency present in pts?

signs and symptoms

A

signs:

osteomalacia

  • looser’s zones (pseudofractures)
  • cupped metaphyses

symptoms:

bone pain

fractures

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31
Q

definition of UTI?

A

symptomatic w +ve culture or dipstick

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32
Q

what is urethral syndrome?

A

symptomatic of UTI but no bacteriuria

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33
Q

uncomplicated vs complicated UTI?

A

uncomplicated: normal GU tract and fn
complicated: abnormal GU tract, outflow obsturction, decreased renal fn, impaired host defence, virulent organism

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34
Q

presentation of pyelonephritis?

A

fever, rigors

loin pain and tenderness

vomiting

oliguria if AKI

UTI symptoms

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35
Q

presentation of cystitis?

A

freq and urgency

haematuria

dysuria

polyuria

suprapubic tenderness

foul smelling urine

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36
Q

presentation of prostatitis?

A

flu-like symptoms

low backache

dysuria

tender swollen prostate on PR

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37
Q

what may cause a sterile pyuria?

A

pus in urine, but no bacteria cultured

TB

treated UTI

appendicitis

calculi

Tubulointerstitial nephritis

PCKD

chemical cystitis e.g. cyclophosphamide

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38
Q

risk factors of UTI?

A

female

sex

pregnancy

menopause

DM
abnormal tract: stone, obstruction, catheter, malformation

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39
Q

most common organism responsible for UTI?

A

e coli

in women - 2nd most common staphylococcus saprophyticus

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40
Q

ix of UTI?

A

urine dipstick - +ve leucocytes and nitrites

send MSU for MCS

Bloods: FBC, WCC, Blood cultures (if systemic signs), U+E

US: recurrence, children, pyelonephritis

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41
Q

mx of UTI?

A

analgesia

drink plenty, urinate often

ABx: usually trimethoprim, nitrofurantoin 50mg QDS for 3 days

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42
Q

mx of pyelonephritis?

A

cefotaxime 1g IV BD for 10 d

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43
Q

prevention of UTIs?

A

drink more, urinate often

abx prophylaxis

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44
Q

what is glomerulonephritis?

A

group of disorders resulting from glomerular damage

can -> proteinuria + haematuria

can -> AKI or End stage renal failure

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45
Q

causes of glomerulonephritis?

A

idiopathic

immune: Goodpastures, SLE, Vasculitis
infection: Strep, HBV, HCV, HIV

Amyloid

Drugs: penicillamine, gold

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46
Q

ix of glomerulonephritis?

A

Bloods: FBC, U+E, ESR

Complements (C3 and C4) -> may be low in SLE

Abs: ANA, ANCA, dsDNA, GBM

serum protein electrophoresis and IgA

infection: ASOT titre
urine: dip, spot PCR, MCS, Bence-Jones protein

Imaging: CXR: infiltrates (goodpastures, wegeners)

renal US +/- biopsy

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47
Q

general mx of glomerulonephritis?

A

refer to nephrologist

tx HTN aggressively (less than 130/80)

ACEi/ ARB

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48
Q

causes of asymptomatic haematuria?

A

IgA nephropathy

Thin Basement membrane

Alport’s

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49
Q

what is IgA nephropathy?

A

aka Berger’s disease

commonest GN in developed world

young male w episodic macroscopic haematuria 24-48h after URTI

Raised IgA

can -> nephritic syndrome

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50
Q

ix of IgA nephropathy?

A

biopsy: IgA deposition in mesangium

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51
Q

mx of IgA nephropathy?

A

steroids or cyclophosphamide if renal fn impaired

HTN mx: ACEi/ ARBs (IgA nephropathy often causes high BP)

no cure: some ppl experience complete remission, some progress -> RF

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52
Q

what is thin basement membrane disease?

A

autosomal dominant

commonest cause of asymptomatic haematuria

persistent, asymptomatic microscopic haematuria

V small risk of end stage renal failure

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53
Q

what is Alport’s syndrome?

A

85% X-linked

affects type IV collagen -> basement membranes in kidney, inner ear and eye are affected

Haematuria, proteinuria -> progressive renal failure

Sensorineural deafness (bilat)

lens dislocation and cataracts

retinal ‘flecks’

females: haematuria only

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54
Q

what is nephritic syndrome?

A

haematuria + red cell casts

proteinuria -> oedema (esp periorbital)

HTN

oliguria and progressive renal impairment

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55
Q

causes of nephritic syndrome?

A
  1. Post-streptococcal
  2. Crescentic/ Rapidly progressive GN
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56
Q

features of post strep GN?

A

young child develops malaise and nephritic syndrome w smoky urine 1-2 wks after sore throat or skin infection

raised ASOT titre

low C3

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57
Q

ix of Post strep GN?

A

ASOT titre: high

Biopsy of kidney: IgG and C3 deposition at BM

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58
Q

mx of post strep GN?

A

supportive

95% children recover fully

minority develop rapidly progressive GN

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59
Q

what is rapidly progressive GN?

A

most aggressive GN which can -> end stage renal failure in days

3 types

  1. Anti-GBM (goodpastures)
  2. Immune complex deposition e.g. SLE, post strep, Bergers (45%)
  3. Pauci immune (50%)
    - e.g. Wegeners, Churg-strauss, microscopic polyangiitis
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60
Q

what is Goodpastures syndrome?

A

Anti-GBM Ab to Type IV collagen

-> haematuria and haemoptysis

CXR shows infiltrates

-> TYPE 1 Rapidly progressive GN

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61
Q

mx of goodpastures disease?

A

plasmapheresis and immunosuppression

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62
Q

What could cause Type 2 rapidly progressive GN?

A

complication of any immune complex deposition

e.g. Berger’s, post strep, infective endocarditis, SLE

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63
Q

what is Pauci immune Type 3 Rapidly progressive GN?

A

may be due to cANCA +ve: Wegener’s

or pANCA +ve: microscopic polyangiitis, Churg-Strauss

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64
Q

what is nephrotic syndrome defined by?

A

proteinuria: PCR > 300mg/dL
hypoalbuminaemia: <35g/L

Oedema: periorbital, genital, ascites, peripheral

(JVP not raised - intravascularly depleted)

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65
Q

complications of nephrotic syndrome?

A

Infection: low Ig, low complement activity

VTE: up to 40%

Hyperlipidaemia: high cholesterol and triglycerides

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66
Q

ix of nephrotic syndrome?

A

Bloods: FBC, U+E, ESR

Complements (C3/4), lipid levels

Urine dip, MCS, Spot PCR

Imaging: Renal US +/- biopsy

  • all adults should get biopsied
  • steroids 1st in children: mostly minimal change
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67
Q

most common cause of nephrotic syndrome in children?

A

minimal change disease

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68
Q

causes of nephrotic syndrome?

A

primary:

minimal change disease

membranous nephropathy

Focal segmental glomerulosclerosis

Membranoproliferative/ mesangiocapillary GN

secondary:

DM: glomerulosclerosis

Amyloidosis

SLE: membranous

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69
Q

what is minimal change GN?

A

commonest cause of nephrotic syndrome in children

assoc w URTI

oedema - periorbital, genital

could present w AKI and High BP

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70
Q

biopsy of kidney showing normal BM on light microscopy, fusion of podocytes

A

Minimal change disease

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71
Q

mx of minimal change glomerulonephritis?

A

1st line: corticosteroids

2nd: cyclosporine

symptomatic mx: salt and fluid restriction to control swelling

in adults with high BP: ACEi

reduce risk of thrombosis, infection, hyperlipidaemia

1% -> ESRF

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72
Q

what is membranous nephropathy?

A

20-30% of adult nephrotic syndrome (common)

assoc w

Ca: lung, colon, breast

autoimmune: SLE, thyroid disease
infections: HBV
drugs: penicillamine, gold

biopsy shows: subepithelial immune complex deposits

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73
Q

mx of membranous nephropathy?

A

immunosuppression if renal function declines

prognosis: 40% spontaneous remission

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74
Q

what is focal segmental glomerulosclerosis?

A

commoner in Afro carribeans

Biopsy shows: focal scarring of the glomerulus, IgM + C3 deposition in the sclerotic segment

idiopathic or secondary: chronic pyelonephritis, vesicourethral reflux, berger’s, Sickle cell, HIV

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75
Q

mx of focal segmental glomerulosclerosis?

A

steroids or cyclosporin/ cyclophosphamide

30-50% -> ESRF (may recur in transplants)

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76
Q

What is membranoproliferative GN?

A

deposits in kidney glomerular mesangium and BM thickening, activating complement and damaging the glomeruli

may -> nephrotic or nephritic syndrome

assoc w HBV, HCV, endocarditis

50% -> ESRF

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77
Q

mx of nephrotic syndrome?

A

monitor U+E, BP, fluid balance, weight

treat underlying cause

symptomatic tx:

  • oedema: fluid and salt restrict + furosemide

proteinuria - ACEi/ ARB decrease proteinuria

high lipids: statin

VTE: tinzaparin

tx HTN

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78
Q

definition of AKI?

A

significant decline in renal function over hrs or days manifesting as an abrupt and sustained increase in serum urea and creatinine

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79
Q

most common cause of AKI?

A

pre renal

due to shock, hypovolaemia or renovascular compromise (e.g. NSAIDS, ACEi)

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80
Q

what drugs may cause AKI?

A

contrast dye

gentamicin

Hb from rhabdomyolysis

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81
Q

causes of chronic renal failure?

A

diabetes

HTN

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82
Q

clinical assessment of AKI?

A

acute or chronic?

  1. Assess fluid status
    - JVP, postural hypotension, tachycardia, poor skin turgor, dry mucous membranes, decreased UO
  2. GU tract obstruction?
    - suprapubic discomfort (urinary retention?)

palpable bladder

enlarged prostate

catheter blocked?

complete anuria?

  1. Rare cause?
    - proteinuria + haematuria
    vasculitis: rash, arthralgia, nosebleed
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83
Q

ix of AKI?

A

Bloods: FBC, U+E, LFT, Glucose, Clotting, ESR, Ca

ABG: hypoxia (oedema), acidosis, K+

GN screen: if cause unclear

Urine: Dip, MCS, PCR, osmolality

ECG: hyperK

CXR: pulmonary oedema

Renal US (hydronephrosis)

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84
Q

classification of AKI?

A

RIFLE classification

3 grades and 2 outcomes

Risk: UO < 0.5ml/kg/h for 6h

Injury: UO < 0.5 ml/kg/h for 12h

Failure: UO < 0.3ml/kg/h for 24h or anuria for 12h

Loss: persistent acute renal failure = loss of renal fn > 4 wks

End stage renal disease: complete loss of renal fn > 3 mo

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85
Q

Mx of AKI?

A

identify cause and treat e.g post/ prerenal cause

urgent renal US

tx exacerbating factors e.g. sepsis

give PPIs

stop nephrotoxins: NSAIDs, ACEi, gent, vanc

stop metformin if Cr>150mM

tx complications e.g. hyperK, pulmonary oedema

Monitor: catheterise and monitor UO, consider CVP

fluid balance and daily weights

86
Q

what is impt to monitor in pt w AKI?

A

catheterise - Urine Output

Consider CVP

Fluid balance and daily weights

87
Q

mx of HyperK?

A

10ml 10% Calcium Gluconate - to stabilise myocardium w cardiac monitoring

100ml 20% glucose with 10 u Insulin (Actrapid)

salbumatol 5mg nebulizer

calcium resonium 15g PO

may need haemofiltration

88
Q

Mx of Pulmonary Oedema?

A

sit up and give O2

Morphine 2.5mg IV (+ metoclopramide 10mg IV)

Frusemide 40-80mg IV

GTN spray +/- isosorbide mononitrate iv infusion (unless SBP <100)

if no response consider:

CPAP

Haemodialysis

89
Q

Indications for Acute Dialysis?

A

AEIOU

Acidosis: severe metabolic acidosis (pH <7.2)

Electrolytes: Persistent HyperK (>7)

Intoxicants: Poisons e.g. aspirin

Oedema: Refractory pulm oedema

Uraemia: Symptomatic e.g. encephalopathy, pericarditis

90
Q

Tx of Bleeding due to AKI?

A

increased urea impairs haemostasis

Give FFP + platelets as needed

transfuse to maintain Hb <10

91
Q

commonest causes of post renal AKI?

A

stone

catheter

malignancy

92
Q

commonest cause of AKI renal?

A

ATN

TIN

GN

93
Q

Mx of Acute Renal failure

A to E approach?

A

Resus assess fluid status

A: decreased GCS may need airway mx

B: pulmonary oedema- sit up, high flow O2

C: assess fluid status (JVP, postural BP, HR, mucous membranes, skin turgot, CRT)

Urine output

Tx lifethreatening complications

e.g. HyperK, pulmonary oedema

Tx shock or dehydration:

fluid bolus 500 ml over 15 min

monitoring: cardiac, urine, CVP, fluid balance

Post renal causes: catheter in situ, prostate, bladder

Hx and Ix

tx sepsis: blood cultures and empirical abx

call urologists if obstructed despite catheter

care w nephrotoxic drugs e.g. gentamicin

94
Q

evidence of acute vs chronic renal failure?

A

previous blood results

duration of symptoms

co morbidities

95
Q

What is tubulointerstitial nephritis?

A

immune mediated hypersensitivity w either drugs or other antigens

e. g. NSAIDs, Abx, diuretics
infections: staph, strep

96
Q

Causes of tubulointerstitial nephritis?

A

Drug hypersensitivity in 70%:

NSAIDS

abx: cephs, penicillins, rifampicin, sulphonamide

Diuretics: furosemide, thiazide

allopurinol

cimetidine

infections: staph, strep

Immune: SLE, Sjogrens

97
Q

presentation of tubulointerstitial nephritis?

A

fever, arthralgia, rashes

AKI -> olig/ anuria

uveitis

98
Q

ix of tubulointersitial nephritis?

A

raised IgE: eosinophilia

urine dip: haematuria, proteinuria, sterile pyuria

99
Q

mx of tubulointerstitial nephritis?

A

stop offending drug

prednisolone

100
Q

what is chronic tubulointerstitial nephritis?

A

fibrosis and tubular loss

commonly caused by: reflux and chronic pylenonephritis

DM

SCD

101
Q

what is nephrocalcinosis?

A

diffuse renal parenchymal calcification

progressive renal impairment

causes:

Malignancy

high PTH

Myeloma

Sarcoid
Vit D intoxication

102
Q

what is acute urate crystal nephropathy?

A

AKI due to urate precipitation

usually after chemo-induced cell lysis

Mx: hydration, urinary alkalinsation

103
Q

What is analgesic nephropathy?

A

prolonged heavy ingestion of compound analgesics

often a hx of chronic pain

sterile pyuria +/- mild proteinuria

slowly progressive chronic renal failure

sloughed papilla can -> obstruction and renal colic

Ix: CT w/o contrast (papillary calcifications)

tx: stop analgesics

104
Q

E.g.s of endogenous nephrotoxins

A

either directly toxic -> ATN

of cause hypersensitivity -> TIN

Haemoglobin, myoglobin

Urate

Ig e.g. light chains in myeloma

105
Q

E.g.s of exogenous nephrotoxins?

A

either directly toxic -> ATN

or cause hypersensitivity -> TIN

NSAIDs

Abx: AVASTA

Aminoglycosides e.g. Gentamicin, Kanamycin

Vancomycin

Aciclovir

Sulphonamides

Tetracycline

Amphotericin

ACEi

Immunosuppressants: Ciclosporin, Tacrolimus

Contrast media

Anaesthetics: enflurane

106
Q

what antimicrobials are nephrotoxin?

A

AVASTA

Aminoglycosides e.g gent, kanamycin

Vancomycin

Aciclovir

Sulphonamides

Tetracycline

Amphotericin

107
Q

pathogenesis of rhabdomyolysis?

A

skeletal muscle breakdown -> release of

  • K+, PO4, urate
  • myoglobin, creatinine kinase
  • > AKI
108
Q

causes of rhabdomyolysis?

A

ischaemia: embolism, surgery
trauma: immobilisation, crush, burns, seizures, compartment syndrome

Toxins: Statins, fibrates, ecstacy, neuroleptics

109
Q

features of rhabdomyolysis?

A

muscle pain, swelling

red/ brown urine

AKI occurs 10-12 h later

110
Q

ix of rhabdomyolysis?

A

urine dip: +ve Hb, -ve RBCs

bloods: raised CK, K, PO4, urate

111
Q

mx of rhabdomyolysis?

A

tx hyperK

IV fluids

CVP monitoring if oliguric

IV NaHCO3 may be used to alkalinize urine and stabilise a less toxic form of myoglobin

112
Q

Classification of chronic renal failure?

A

Stage 1: GFR >90

2: 60-89
3a: 45-59
3b: 30-44
4: 16-29
5: <15

113
Q

what stage of CKD do you start getting symptomatic?

A

stage 4

stage 5 = End stage renal failure, need for Renal replacement therapy

114
Q

Causes of chronic renal failure?

A

Common:

Diabetes mellitus

HTN

other:

Glomerulonephritis

PCKD

Drugs: e.g. analgesic nephropathy

Pyelonephritis: usually 2º to VUR

SLE

Myeloma + Amyloidosis

115
Q

Hx in chronic renal failure?

A

Past UTI

HTN, DM

FH

DH

Symptoms

116
Q

Bloods in chronic renal failure?

A

low Hb (low EPO)

U+E, ESR, glucose

low Ca/ high phosphate

high Alk Phos

high PTH

Immune screen

Film: burr cells

117
Q

Urine Ix in chronic renal failure?

A

Urine dip, MCS, PCR, bence jones proteins

118
Q

imaging of chronic renal failure?

A

CXR: pulmonary oedema, cardiomegaly

AXR: calcification from stones

Renal US: usually small, may be large - polycystic, amyloid

Bone Xrays: renal osteodystrophy

CT KUB: e.g. cortical scarring from pyelonephritis

renal biopsy: if cause unclear and size normal

119
Q

complications of Chronic renal failure?

A

CRF HEALS

Cardiovascular disease

Renal osteodystrophy

Fluid (oedema)

HTN

Electrolyte disturbances: K, H, phosphate

Anaemia

Leg restlessness

Sensory neuropathy

120
Q

features of renal osteodystrophy?

A

2/3º hyperPTH -> osteitis fibrosa cystica

subperiosteal bone resorption

acral osteolysis: short stubby fingers

pepperpot skull

121
Q

mechanism of renal osteodystrophy?

A

decreased 1a-hydroxylase -> decreased Vit D activation -> low Ca

-> high PTH

Phosphate retention also -> high PTH

  • > activation of osteoclasts
  • > increased bone resorption
122
Q

general mx of chronic kidney failure?

A

tx reversible causes

stop nephrotoxic drugs

lifestyle: exercise, healthy weight, stop smoking

Na, fluid and phosphate restriction

CV risk: statins (irrespective of lipids), low dose aspirin, tx DM

HTN: target <140/90 (<130/80 if DM) -> ACEi/ARB

Oedema: furosemide

Bone disease: Alfacalcidol, phosphate binders, ca supplements

Anaemia: EPO

Restless Legs: Clonazepam

123
Q

mx of anaemia due to CKD?

A

exclude IDA and ACD

EPO to raise Hb to 11

124
Q

mx of bone disease due to CKD?

A

Phosphate binders: Calcichew

Vit D analogues: Alfacalcidol (1-OH Vit D3)

Ca supplements

**rare: cincalcet: ca mimetic

125
Q

mx of HTN in CKD?

A

in DM: always give ACEi/ARB

if not, give if >140/90

126
Q

Mx of CV risk due to CKD?

A

statins -irrespective of lipids

low dose aspirin

127
Q

contraindications for renal transplant?

A

active infection

untreated malignancy

severe heart failure

128
Q

assessment prior to Renal transplant?

A

ABO and HLA matching

CVD?

Virology status: CMV, HCV, HBV, HIV, VZV, EBV

TB

129
Q

types of grafts for renal transplant?

A

cadaveric: brainstem death w CV support

Live donor: HLA matched, optimal surgical timing, improved graft survival

130
Q

Immunosuppression pre-renal transplant?

A

Induction drugs e.g. alemtuzumab Anti-CD52

131
Q

immunosuppression post op renal transplant?

A

prednisolone short term

tacrolimus/ ciclosporin long term

132
Q

complications of renal transplant?

A

post op: bleeding, graft thrombosis, infection, urinary leaks

rejection

ciclosporin/ tacrolimus nephrotoxicity

immunosuppression: increased risk of infection & malignancy

Cardiovasc disease: HTN, atherosclerosis

133
Q

what type of infections are immunosuppressed ppl at risk of?

A

opportunistic

fungi

134
Q

differential of rising creatinine in transplant pt?

A

rejection

obstruction

ATN

drug toxicity

135
Q

pathology of diabetic nephrology?

A

conglomerate of lesions occuring concurrently

hyperglycaemia -> renal hyperperfusion -> hypertrophy and increased renal size

hypertrophy and metabolic defects include reactive oxygen species production

-> glomerulosclerosis and nephron loss

nephron loss -> RAS activation -> HTN

136
Q

features of diabetic nephropathy?

A

microalbuminuria (30-300mg/d)

*strong independent RF for CV disease

progresses to proteinuria (>300mg/d)

diabetic retinopathy usually coexists and HTN is common

137
Q

screening in DM for nephropathy?

A

T2DMs should be screened for microalbuminuria every 6 months

138
Q

Mx of diabetic nephropathy?

A

Good glycaemic control delays onset and progression

BP target 130/80

start ACEi/ARB even if normotensive

stop smoking

139
Q

features of amyloidosis?

A

renal involvement caused by AL / AA Amyloid

proteinuria

nephrotic syndrome

progressive renal failure

140
Q

diagnosis of amyloidosis causing renal impairment?

A

large kidneys on US

biopsy

141
Q

How could malignancy affect kidneys?

A

direct:

renal infiltration: leukaemia, lymphoma

obstruction: pelvic tumour

mets

nephrotoxicity:

toxic chemo, analgesics, tumour lysis syndrome

142
Q

how may sarcoidosis affect kidneys?

A

raised Ca and tubulointerstitial nephritis

143
Q

pathology of multiple myeloma?

A

excess production of monoclonal abs +/- light chains

(detected in most as urinary BJP)

light chains block tubules and have direct toxic effects -> ATN

-> AL Amyloidosis

myeloma also assoc w raised Ca

144
Q

mx of multiple myeloma causing renal failure?

A

ensure fluid intake of 3L/ d to prevent further impairment

dialysis may be required in acute renal failure

145
Q

how may Rheumatoid arthritis lead to kidney problems??

A

NSAIDs -> ATN

Penicillamine and gold -> membranous GN

AA Amyloidosis occurs in 15%

146
Q

how may SLE affect kidneys?

A

involves glomerulus in 40-60% -> ARF/CRF

proteinuria and raised BP common

may -> Type 2 rapidly progressive GN

147
Q

tx of SLE kidney disease?

A

proteinuria: ACEi

aggressive GN: immunosuppression

148
Q

diffuse systemic sclerosis and kidneys?

A

renal crisis: malignant HTN + ARF

  • > commonest cause of death
    tx: ACEi if high BP/ renal crisis
149
Q

HTN and kidney disease?

A

HTN can be both cause and effect of renal damage

renal diseases are commonest cause of secondary HTN

  • > activation of RAS
  • > retention of Na and water due to decreased excretion
150
Q

cause of renovascular disease? activation of RAS System

A

atherosclerosis in 80%

fibromuscular dysplasia

thromboembolism

external mass compression

151
Q

features of renovascular disease?

A

refractory HTN

worsening renal function after ACEi/ARB

flash pulmonary oedema (no LV impairment on echo)

152
Q

gold standard ix of renovascular disease?

A

renal angiography

153
Q

ix of renovascular disease?

A

US + doppler: small kidney + low flow

renal angio: gold std

154
Q

mx of renovascular disease?

A

tx medical CV risk factors

angioplasty and stenting

155
Q

what is haemolytic uraemic syndrome?

A

E coli O157:H7 verotoxin -> endothelial dysfunction

young children eating undercooked meat

bloody diarrhoea and abdo pain precedes:

  • MAHA
  • thrombocytopenia
  • renal failure
156
Q

ix findings of HUS?

A

schistocytes, low platelets

low Hb

normal clotting

157
Q

what is Thrombotic Thrombocytopenic Purpura?

A

genetic or acquired deficiency of ADAMTS13 -> giant vWF multimers

(ie. antibodies inhibiting ADAMTS13)

blood clots form in small blood vessels throughout body -> kidney, heart and brain dysfunction

+ low Pl, low Hb

adult females

pentad: fever

CNS signs: confusion

MAHA

thrombocytopenia

renal failure

158
Q

what is the Pentad found in thrombotic thrombocytopenic purpura?

A

fever

cns signs: confusion, seizures

MAHA

thrombocytopenia

renal failure

159
Q

mx of haemolytic uraemic syndrome?

A

usually resolves spontaneously

may need dialysis or plasma exchange

160
Q

mx of thrombotic thrombocytopenic purpura?

A

plasmapheresis

immunosuppression e.g. corticosteroids, rituximab

splenectomy

pl transfusions generally not recommended

161
Q

what is Polycystic Kidney Disease?

A

most commonly autosomal dominant

defect in PKD1 gene on Chr 16 (80%)

or PKD2 gene on chr4

cystic changes are bilat

162
Q

clinical presentation of PCKD?

A

bilateral upper quadrant masses (cystic enlargement of the kidneys)

dull loin pain

frank haematuria (from rupture of a cyst into the renal pelvis)

infected cyst

hypertension and eventually chronic renal failure (in 10% of cases)

Anuerysms: Berry -> SAH

UTIs/ Stones

20 % cystic livers + possibly, pancreas and spleen

163
Q

pathology of autosomal dom PCKD?

A

PKD1 gene on chr 16 affected

-> polycystin 1 affected

large cysts arise from all parts of nephron

-> progressive decline in renal fn

70% ESRF by 70 yrs

164
Q

causes of minimal change disease?

A

majority: idiopathic

10-20% cause is found:

  • drugs: NSAIDs, rifampicin
  • Hodgkin’s lymphoma, thymoma
  • infectious mono
165
Q

Pathophysiology of minimal change disease?

A

T cell and cytokine mediated damage to the glomerular BM -> polyanion loss

reduction of electrostatic charge of BM -> increased glomerulat permeability to serum albumin

166
Q

what does electron microscopy show for kidney biopsy of minimal change disease?

A

fusion of podocytes

167
Q

what drugs should be stopped in AKI due to increased risk of toxicity (but does not usually worsen AKI itself)

A

Metformin (increased risk of lactic acidosis)

Lithium

Digoxin

168
Q

what does calcium resonium do in the acute stage of hyperK?

A

removes K from the body

169
Q

why does VTE occur in nephrotic syndrome?

A

loss of antithrombin III, proteins C and S

and an associated rise in fibrinogen levels predispose to thrombosis

170
Q

mx of acute graft failure?

A

may be reversed by steroids and immunosuppression

171
Q

what drugs should be stopped in AKI as may worsen renal function?

A

NSAIDs (afferent constriction)

Aminoglycosides

ACEi (efferent dilatation)

Angiotensin II receptor blockers

Diuretics (intravasc depletion)

172
Q

Risk factors for AKI?

A

Chronic Kidney disease

other organ failure e.g. heart/liver

chronic disease- diabetes

hx of AKI
use of drugs w nephrotoxic potential

use of iodinated ocntrast agents within past wk

age 65 or over

173
Q

Features of PCKD in kidneys?

A

large bilateral masses

flank pain

infected cyst

Haemorrhage into cyst -> haematuria

stones

High BP

174
Q

features of PCKD extra renally?

A

Berry aneurysms: SAH

cysts in liver (70%)/ pancreas

cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection

175
Q

mx of PCKD?

A

general:

Increase water intake, decrease Na/ caffeine

Monitor BP and U+E

Genetic counselling

MRA screen for Berry Aneurysms

Medical: Tx HTN aggressively (<130/80)

ACEi best.

Tx infections

Surgical: pain may be helped by laparoscopic cyst removal/ nephrectomy

ESRF in 70% by 70 yrs

-> dialysis or transplant

176
Q

what is autosomal recessive PCKD?

A

presents in infancy

development of kidneys and liver is abnormal

  • > underdeveloped lungs
  • > High BP, CKD
  • > problems w liver
177
Q

Differentials for renal enlargement?

A

PHONOS

polycystic kidneys: PCKD (AD/AR), tuberous sclerosis

Hypertrophy 2º to contralat renal agenesis

Obstruction (hydronephrosis)

Neoplasia: RCC, myeloma

Occlusion: renal vein thrombosis

Systemic: early DM, Amyloid

178
Q

what is Tuberous Sclerosis?

A

Autosomal dominant condition w hamartomas in skin, brain, eye, kidney

Skin: Nasolabial adenoma sebaceum, ash leaf macules, peri ungual fibromas

Neuro: low IQ, epilepsy

Renal: Cysts, angiomyolipomas

179
Q

How is Tuberous sclerosis inherited?

180
Q

what is a medullary sponge kidney?

A

multiple cystic dilatations in the collecting ducts in the medulla

typically presents in 20-30s

often asymptomatic, but predisposes to

  • Hypercalciuria + stones
  • recurrent UTIs and pyelonephritis
  • haematuria

renal fn is usually normal

181
Q

what is renal tubular acidosis?

A

impaired acid excretion -> hyperCl met acidosis

both -> RAS activation -> K+ wasting and hypokalaemia

182
Q

features of Fanconi Syndrome?

A

Disturbance of PCT function -> generalised impaired reabsorption of aas, K+, HCO3, Phosphate, glucose

features of:

  • polyuria (osmotic diuresis)
  • hypophosphataemic rickets (Vit D resistant)
  • Acidosis, low K
183
Q

types of renal tubular acidosis?

A

-> hyperCl met acidosis

Type 1: Distal collecting tubule

Type 2: Proximal collecting tubule

184
Q

Features of Type 1 renal tubular acidosis?

A

inability to excrete H+ even when acidotic

causes: hereditary - Marfans, Ehlers Danlos

AI: sjogrens, SLE, thyroiditis

Drugs

features of rickets/ osteomalacia (bone buffering)

renal stones and UTIs

nephrocalcinosis -> ESRF

185
Q

diagnosis of renal tubular acidosis (type 1 vs 2)?

A

I: failure to acidify urine (pH> 5.5) despite acid load

2: urine will acidify w acid load (pH <5.5)

186
Q

features of type 2 renal tubular acidosis?

A

defect in proximal collecting tubule

  • defect in HCO3 reabsorption

tubules can reabsorb some HCO3 so can acidify urine in systemic acidosis when HCO3 is low

187
Q

what are the hereditary hypoK tubulopathies?

A

Bartter’s Syndrome: HYPOK and met alkalosis

Gitelman Syndrome: HypoK and met alkalosis + hypocalciuria

both normal BP

188
Q

3 main causes of nephrotic syndrome?

A

minimal change: more common in kids

membranous

focal segmental: more common in adults

189
Q

causes of focal segmental glomerulosclerosis?

A

causes nephrotic syndrome

Causes:

idiopathic

secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy

HIV

heroin

Alport’s syndrome

sickle-cell

190
Q

when to urgently refer someone to urology?

A

Aged >= 45 years AND:

unexplained visible haematuria without urinary tract infection, or

visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

191
Q

what are the six classes of SLE glomerulonephritis?

A

WHO classification

class I: normal kidney

class II: mesangial glomerulonephritis

class III: focal (and segmental) proliferative glomerulonephritis

class IV: diffuse proliferative glomerulonephritis

class V: diffuse membranous glomerulonephritis

class VI: sclerosing glomerulonephritis

Class IV most common and severe

193
Q

prevention of nephrotoxicity due to contrast media?

A

IV 0.9% NaCl pre and post procedure

194
Q

mx of high PTH in CKD?

A

Alfacalcidol

195
Q

when starting pts with CKD on ACEi, what fall in glomerular filtration pressure (GFR) and rise in creatinine is acceptable?

A

decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable

although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs). A rise greater than this may indicate underlying renovascular disease.

196
Q

most common organism causing peritonitis in peritoneal dialysis?

A

Staphylococcus epidermidis

(staph aureus is another common cause)

197
Q

features of rhabdomyolysis?

A

acute renal failure with disproportionately raised creatinine

elevated CK

myoglobinuria

hypocalcaemia (myoglobin binds calcium)

elevated phosphate (released from myocytes)

198
Q

mx of rhabdomyolysis?

A

IV fluids to maintain good urine output

urinary alkalinization is sometimes used

199
Q

features of Wilms Nephroblastoma?

A

typically presents in children under 5 years of age, with a median age of 3 years old.

abdominal mass (most common presenting feature)

flank pain

painless haematuria

other features: anorexia, fever

unilateral in 95% of cases

metastases are found in 20% of patients (most commonly lung)

200
Q

what is a common immunosuppressant induction regime before transplant?

A

Campath Alemtuzumab anti-CD52

201
Q

regimen for immunosuppression post-transplant?

A

initial: ciclosporin/tacrolimus with a monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus

add steroids if more than one steroid responsive acute rejection episode

202
Q

pts undergoing longterm immunosuppression should undergo regular monitoring for?

A

Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia. Patients must be monitored for accelerated cardiovascular disease.

Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney

Malignancy - patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas

203
Q

what does haemodialysis involve?

A

most common form of renal replacement therapy

regular filtration of the blood through a dialysis machine in hospital

most often 3 x 3-5h / wk,

pt needs surgery to create AV fistula for site of haemodialysis

204
Q

what is involved in peritoneal dialysis?

A

RRT where filtration occurs in patient’s abdomen

Dialysis solution is injected into the abdominal cavity through a permanent catheter

The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum.

After several hours of dwell time, the dialysis solution is then drained, removing the waste products from the body, and exchanged for new dialysis solution.

205
Q

what are the different types of peritoneal dialysis?

A
  • Continuous ambulatory peritoneal dialyssi (CAPD): each exchange ~30-40 mins and each dwell time 4-8h. normal activities w dialysis soln inside abdomen
  • Automated peritoneal dialysis: a dialysis machine fills and drains the abdo while pt is sleeping, 3-5 exchanges over 8-10h per night
206
Q

What is involved in Renal transplantation?

A

receipt of a kidney from either a live or deceased donor

donor kidney transplanted into the groin, with the renal vessels connected to the external iliac vessels

Following transplantation, the patient must take life-long immunosuppressants to prevent rejection of the new kidney

average lifespan of a donor kidney is 10-12 years from deceased donors and 12-15 years from living donors.

207
Q

Complications of haemodialysis?

A

Site infection

endocarditis

stenosis at site

hypotension

cardiac arrhythmia

air embolus

anaphylactic reaction to sterilising agents

Disequilibration syndrome

208
Q

Complications of peritoneal dialysis?

A

peritonitis

sclerosing peritonitis

catheter infection

catheter blockage

constipation

fluid retention

hyperglycaemia

hernias

back pain

malnutrition

209
Q

Complications of renal transplantation?

A

DVT/PE

immunosuppression: opportunistic infection, malignancies (skin ca, lymphoma), bone marrow suppression

recurrence of original disease

Urinary tract obstruction

CV disease

graft rejection

210
Q

1st line Renal replacement therapy for independent pts?

A

Peritoneal dialysis

211
Q

contraindications to peritoneal dialysis?

A

IBD

diverticulitis

ischaemic bowel

abdo abscess

212
Q

Causes of cranial DI?

A

idiopathic

post head injury

pituitary surgery

craniopharyngiomas

DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

Medicine (16 decks)

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