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Imperial Medicine Year 3 > Nephrology AS cards > Flashcards

Nephrology AS cards Flashcards

1
Q

Renal Physiology - Na Reabsorption

A
  • Main factor determining extracellular volume
  • Decreased BP and decreased NaCl @ macula densa –> increased renin release –> aldosterone release –> more Na, less K (insertion of pumps).
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2
Q

Renal Physiology - Water Reabsorption

A
  • Determines ECF osmolality

- Increased osmolality or decreased BP –> ADH release

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3
Q

What is absorbed at the PCT?

A

Reabsorption of filtrate

  • 70% of total Na+ reabsorption
  • reabsorption of amino acids, glucose, cations.
  • Bicarbonate reabsorbed using carbonic anhydrase
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4
Q

What is absorbed at the thick ascending limb?

A

Creates osmolality gradient

  • 20% of Na reabsorption
  • Na/K/2Cl triple symporter
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5
Q

What is absorbed at the distal convoluted tubule?

A

pH control and Ca reabsorption

  • 5% of Na reabsorption
  • Apical NaCl co-transporter
  • Ca2+ reabsorption under control of PTH
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6
Q

What is absorbed at the medullary collecting duct?

A

pH and K regulation

  • Na reabsorption coupled to K or H excretion
  • Basolateral aldosterone-sensitive Na/K pump.
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7
Q

What is absorbed at the cortical collecting duct?

A

Regulation of water reabsorption

- Water reabsorbed by aquaporin-2 channels.

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8
Q

Endocrine function of the kidney?

A
  • Secretion of renin by juxtaglomerular apparatus
  • EPO synthesis
  • 1a-hydroxylation of vitamin D (controlled by PTH).
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9
Q

What are the classes of diuretics?

A
  • Carbonic Anhydrase Inhibitors
  • Loop Diuretics
  • Thiazide diuretics
  • K-Sparing diuretics
  • Osmotic Diuretics
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10
Q

MOA and example of Carbonic Anhydrase Inhibitors (acetazolamide)

A

MOA: inhibit carbonic anhydrase in PCT
Effect: decreased HCo3 reabsorption –> small increase in Na loss.
Used in glaucoma
SE: drowsiness, renal stones, metabolic acidosis

Acetazolamide

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11
Q

MOA and example of Loop diuretic?

A

Examples: furosemide, bumetanide

  • MOA: inhibits Na/K/2CL symporter in thick ascending limb
  • Effect: massive NaCl excretion, Ca and K excretion.
  • Use: Management of oedema - CCF, nephrotic syndrome and hypercalcaemia
  • SE: hypokalaemic metabolic alkalosis, ototoxic, hypovolaemia, hypocalcaemia, renal impairment from dehydration + toxic effect, gout
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12
Q

MOA and examples of thiazide diuretics?

A

Bendroflumethazide, indapamide

  • MOA: Inhibits NaCl co-transporter in Distal Convoluted Tubule
  • Effects: moderate NaCl excretion, increased Ca reabsorption
  • Use: HTN, decreased renal stones, mild oedema
  • SE: decreased K, hyperglycaemia, increased urate (CI in gout). Can cause hypercalcaemia, hypokalaemia, hyponatraemia.
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13
Q

What are the K-sparing diuretics?

A

Spironolactone and amiloride

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14
Q

What is the MOA of K-sparing diuretics?

A

Spiro: Aldosterone antagonist
Amiloride: blocks DCT/CD luminal Na channels
Eplerenon - K-sparing diuretic.

Effect: Increased Na excretion, decreased K and H excretion

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15
Q

What are K-sparing diuretics used for?

A

Used with loop or thiazide diuretics to control K loss.
Spiro has long-term benefits in aldosteronism (LH, HF)

Use spironolactone in ascites.

Ascites = Fluid leaves the intravascular space = Decreased blood pressure = activates RAAS and increased aldosterone resulting in further fluid retention which worsens ascites. SO give aldosterone antagonist stops the RAAS overactivation

SE: increased K, anti-androgenic (gynaecomastia)

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16
Q

What are osmotic diuretics? Give examples?

A

Mannitol

MOA: freely filtered and poorly reabsorbed
Effect: decreased brain volume and decreased ICP
USe: glaucoma, increased ICP, rhabdomyolysis
SE: decreased Na, Pulmonary oedema, n/v.

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17
Q

Causes of haematuria - renal?

A

Transient or spurious non-visible haematuria

  • UTI
  • Menstruation
  • Vigorous exercise
  • Sexual intercourse.

Renal:

  • Congenital: PCK
  • Trauma
  • Infection: pyelonephritis
  • Neoplasm
  • Immune: GN, TIN

Extra-renal

  • Trauma: stones, catheter
  • Infection: Cystitis, prostatitis, urethritis
  • Neoplasm: bladder, prostate
  • Bleeding diathesis
  • Drugs: NSAIDs, frusemide, cipro, cephalosporins

Painless, frank haematuria. Warrants an urgent referral on the cancer pathway due to his age.

Gold standard = bladder cancer diagnosis = Cystoscopy.

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18
Q

What can give you a false positive for haematuria?

A

Myoglobin, porphyria

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19
Q

Proteinuria 1+ meaning?

A

30mg/dL

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20
Q

Proteinuria 2+ meaning?

A

300mg/dl

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21
Q

What is proteinuria defined as?

A

Urine protein: creatinine ratio <30 mg/mmol.

PCR <20mg/mM is normal. >300 = nephrotic.

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22
Q

Commonest causes of proteinuria?

A
  • DM
  • Minimal change
  • Membranous
  • Amyloidosis
  • SLE
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23
Q

Other causes of proteinuria?

A 
HTN 
ATN 
TIN
UTI
Fever, orthostatic
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24
Q

False positive for proteinuria?

A

Bence-Jones protein

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25
Q

Definition of microalbuminuria?

A

30-300mg/24hr

Earliest detectable sign of deterioration in DM

Other causes:

  • HTN
  • minimal change GN
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26
Q

What are the 3 types of casts?

A

RBC, WBC or Tubular.

RBC: glomerular haematuria
WBC: Interstitial nephritis or pyelonephritis
Tubular: ATN

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27
Q

Differential from urine if glomerular in nature?

A
  • Haematuria, proteinuria, red cells/casts.
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28
Q

Differential from urine if tubular in nature?

A

White cell casts, small protein, leucocyturia

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29
Q

Differential from urine if pre-renal in nature?

A

Nothing

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30
Q

What is creatinine?

A
  • Synthesised during muscle turnover
  • Freely filtered and small proportion secreted by PCT
  • Increased muscle –> Increased creatinine: age, sex, race
  • Plasma Cr doesn’t increase above normal until 50% increased in GFR
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31
Q

What is urea?

A
  • Produced from ammonia by liver in ornithine cycle
  • Increased with protein meal (upper GI bleed or supplements)
  • Decreased with hepatic impairment
  • 10-70% is reabsorbed: depends on urine flow
  • Decreased flow –> increased urea reabsorption (in dehydration)
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32
Q

How do you interpret isolated increased urea?

A

Decreased flow = Hypoperfusion/dehydration

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33
Q

How do you interpret increased urea and increased creatinine?

A

Decreased filtration (renal failure)

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34
Q

What is creatinine clearance?

A
  • Vol of blood that can be cleared of a substance in 1min
  • CrC roughly approximates GFR as it is freely filtered and only a small proportion secreted (~10%)
  • Required urine concentration from 24hr collection
  • Can use radiolabelled EDTA: very rarely done.
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35
Q

What is eGFR

A
  • Modification of Diet in Renal Disease (MDRD) equation
  • CAGE = serum creatinine, age, gender, ethnicity!
  • Obvious need for urine collection.
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36
Q

What are the problems with eGFR?

A
  • Validated for patients with established renal failure: ?applicable to general population
  • Most elderly people are in >stage 3 CFR by eGFR: may npt progress or impinge on their health.
  • eGFR is too pessimistic in mild renal impairment.
  • Factors which may affect the result
    = pregnancy, muscle mass, eating red meat 12 hrs prior to sample being taken.
    Higher creatinine in body builder = artificially lower eGFR.
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37
Q

What are the causes of Renal Disease? - Pre-renal

A

Pre-renal

  • Shock
  • Renal vascular: RAS,
  • Toxins: NSAIDs, ACEi
  • Thrombosis
  • Hepatorenal syn
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38
Q

What are the causes of Renal Disease? - Renal

A

Glomerulonephritis
Acute Tubular Necrosis
Interstitial disease

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39
Q

What are the causes of Renal Disease? -Post-renal

A 
Disease of renal papillae, pelvis, ureters, bladder or urethra. 
SNIPPIN 
- Stone
- Neoplasm
- INflammation: stricture
- Prostatic hypertrophy
- Posterior urethral valves
- Infection: TB, schisto
- Neuro: post-op, neuropathy
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40
Q

What are the presentations of renal failure?

A
  • Uraemia
  • Protein loss and Na+ retention
  • Acidosis
  • Hyperkalaemia
  • Anaemia
  • Vitamin D deficiency
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41
Q

Symptoms of uraemia?

A 
Pruritis
N/V
Anorexia
Lethargy
Confusion
restless legs
Metallic taste
Paraesthesia: neuropathy
Bleeding
Chest pain: serositis
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42
Q

Signs of uraemia?

A 
Pale skin, 
Striae
Pericardial/Pleural rub
Fits
Coma
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43
Q

Symptoms of protein loss and Na+ retention.

A

Symptoms

  • Polyuria, polydipsia
  • Oliguria, anuria
  • Breathlessness
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44
Q

Signs of protein loss and Na+ retention.

A
  • Oedema
  • INcreased JVP
  • HTN (or decreased BP)
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45
Q

Symptoms of acidosis?

A

Breathlessness

Confusion

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46
Q

Signs of acidosis?

A

Kussmaul respiration?

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47
Q

Symptoms of hyperkalaemia?

A

Palpitations
Chest pain
Weakness

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48
Q

Signs of hyperkalaemia - ECG?

A 
Peaked T waves
Flattened P waves
Increased PR interval
Widened QRS
Sine-wave pattern --> VF
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49
Q

Symptoms of anaemia?

A 
Breathlessness
Lethargy
Faintness
Tinnitus
Aortic flow murmur
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50
Q

Signs of anaemia?

A

Pallor
Tachycardia
Flow murmurs (ESM @ apex)

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51
Q

Vitamin D deficiency symptoms?

A

Bone pain

Fractures

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52
Q

Signs of vitamin D Deficiency?

A

Osteomalacia

  • Looser’s zones (pseudo #)
  • Cupped metaphyses
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53
Q

What is bacteriuria?

A

Bacteria in urine, symptomatic or asymptomatic

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54
Q

What is a UTI?

A

Symptomatic with +ve culture or dipstick

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55
Q

What is Urethral syndrome

A

Symptomatic but no bacteriuria

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56
Q

What is the classification of UTIs?

A
  • Uncomplicated: Normal GU tract + functioning.
  • Complicated: abnormal GU tract, outflow obstruction, decreased renal function, impaired host defence
  • Recurrent: further infection with new organism
  • Relapse: further infection with same organism
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57
Q

Types of Presentation of UTI?

A

Pyelonephritis
Cystitis
Prostatitis

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58
Q

Presentation of pyelonephritis?

A
  • Fevers, rigors
  • Loin pain and tenderness
  • Vomiting
  • Oliguria if ARF
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59
Q

Presentation of cystitis?

A
  • Frequency and urgency
  • Polyuria
  • Haematuria
  • Dysuria
  • Suprapubic tenderness
  • Foul smelling urine
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60
Q

Presentation of Prostatitis?

A
  • Flu-like symptoms*
  • Low backache
  • Dysuria
  • Tender swollen prostate on PR
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61
Q

Sterile Pyuria - what can cause it?

A

Presence of leukocytes without infection

  • TB
  • Treated UTI
  • Appendicitis
  • Calculi
  • Tubulointerstitial nephritis
  • Papillary necrosis
  • Polycystic Kidney
  • Chemical cystitis (cyclophosphamide)
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62
Q

Risk factors for UTI?

A 
Female
Sex
Pregnancy
Menopause
DM
Abnormal tract: stone, obstruction, catheter
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63
Q

Organisms for UTI?

A
  • E.coli
  • Staphylococc Saprophyticus
  • Proteus (Struvite renal stones)
  • Klebsiella
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64
Q

Investigations for UTI?

A
  • Dipstick
  • MSU for MCS
  • Bloods: FBC, U+E, Blood cultures (if systemic signs)
  • US: Children, men, recurrence, pyelonephritis
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65
Q

Positive cultures of a UTI?

A
  • 10^4 cfu/ml for most
  • Women with symptomatic UTI >10^2 cfu/l
  • Men >10^3 cfu/ml (if 80% of growth due to a single organism)
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66
Q

Management of UTI? Cystitis

A

General: drink plenty of water

Cystitis

  • Management for 3-6 days
  • Trimethoprim 200mg BD
  • Nitrofurantoin 50mg QDS (not in RF) - Causes lung fibrosis.
  • Cefalexin 500mg BD (good in RF)
  • Co-amoxiclav 625mg TDS
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67
Q

Management of UTI? Pyelonephritis?

A

Cefotaxime/Ceftriaxone 1g IV BD for 10days
No response: Augmentin 1.2g TDS + gentamicin.

Gentamicin can cause an intrinsic AKI.

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68
Q

UTI prevention?

A

Drink more
Abx prophylaxis
? Cranberry juice

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69
Q

Features of Glomerulonephritis?

A
  • group of disorders resulting from glomerular damage
  • Can –> Proteinuria ± haematuria
  • Can –> AKI or ESRF
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70
Q

Presentations of glomerulonephritis?

A

Asymptomatic haematuria
Nephrotic syndrome
Nephritic syndrome

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71
Q

Those glomerulonephritidies that cause nephrotic syndrome?

A

Most common cause = Diabetes.

  • Deposition disease - Amyloidosis
  • Minimal change disease (child with nephrotic syndrome)
  • Focal and segmental glomerulosclerosis (may be idiopathic or secondary to HIV)
  • Membranous nephropathy (presentation: proteinuria/nephrotic syndrome/chronic kidney disease)
  • Membranoproliferative GN (generally mixed picture)
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72
Q

Those that mainly cause Nephritic syndrome?

A
  • Postinfectious GN
  • IgA nephropathy/ young adult with haematuria following URTI
  • Rapidly progressive GN (rapid onset, often presenting as acute kidney injury).
    Causes include Goodpasture’s ANCA positive vasculitis.
  • Vasculitis (Wegener’s + nose bleeds).
  • Anti-glomerular basement membrane (GBM)
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73
Q

Investigations for Glomerulonephritis?

A

Urinanalysis
- Haematuria, proteinuria, dysmorphic RBC, leukocytes, RBC casts. Bence-Jones proteins.

Bloods
- Basic: FBC (anaemia) , U+E (elevted creatinine, liver enzymes for Hep B/C), ESR (ESR elevated)

  • Complement (C3 and C4) for immune complex GN
  • Abs: ANA, dsDNA, ANCA (pauci immune or anti-glomerular basement membrane) , GBM (GBM)
  • Serum protein electrophoresis and Ig
  • Infection: ASOT (post-strep) HBC, and HCV

Imaging

  • CXR: infiltrates (Goodpasture’s, Wegener’s)
  • Renal US ± Biopsy
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74
Q

General management for glomerulonephritis?

A

Refer to nephrologist
Rx HTN aggressively (<130/80)
Include ACEi/ARA.

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75
Q

Asymptomatic Haematuria causes?

A
  1. IgA nephropathy
  2. Thin BM
  3. Alports
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76
Q

What is the commonest GN in the developing world?

A

IgA nephropathy/Berger’s Disease

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77
Q

What are the features of IgA nephropathy?

A
  • Young male with episodic macroscopic haematuria occuring a FEW DAYS after URTI
  • Rapid recovery between attacks.
  • increased IgA
  • Can occassionally lead to nephritic syndrome.
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78
Q

What do you find on biopsy for IgA nephropathy?

A

IgA Deposition in mesangium

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79
Q

Treatment for IgA nephropathy?

A

If low risk of progression - supportive.
If HTN or proteinuria develops - all patients should receive ACEi and ARBS.

  • Steroids or cyclophosphamide if decreasing renal function (6 months)
  • Prognosis = 20% ESRF after 20yrs.
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80
Q

What is Thin BM disease?

A
  • AD disease, commonest cause of asymptomatic haematuria
    -Features
    Persistent, asymptomatic microscopic haematuria.
    V. small risk of ESRF.
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81
Q

What is Alport’s syndrome?

A

X-linked inheritance

  • Haematuria, proteinuria = progressive renal failure NOT APKD
  • Sensorineural deafness
  • Lens dislocation + Cataracts (lenticonus)
  • Retinal flecks
  • Females: haematuria only.

Alport’s patient with a failing renal transplant - caused by presence of anti-GBM anitbodies leading to Goodpasture’s syndrome like picture.

Can’t see - Lenticonus
Can’t pee - CKD, hematuria
Can’t hear a high C - sensorineural deafness

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82
Q

What is nephritic syndrome/Acute Glomerulonephritis?

A
  • Haematuria (macro/micro) + red cell casts
  • Proteinuria –> Oedema (especially periorbital)
  • HTN
  • Oliguria and progressive renal impairment
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83
Q

Causes of nephritic syndrome?

A
  • Proliferative/post strep

- Crescentic/Rapidly Progressive Glomerulonephritis.

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84
Q

What are the features of proliferative/post-strep GN?

A
  • Young child develops malaise and nephritic syndrome with smoky urine
  • 1-2 WEEKS AFTER sore throat or skin infection.
  • Delayed antibody-mediated syndrome. Pyelonephritis and a UTI would present differently including symptoms such as fever, dysuria and pain.
  • Present with headache, malaise, haematuria, proteinuria, HTN, Low C3, raised ASO
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85
Q

Investigations for proliferative/post-strep glomerulonephritis?

A

Increase ASOT
Decreased C3

Biopsy shows: IgG and C3 deposition.

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86
Q

Management of post-strep/proliferative GN?

A
  • Supportive management
  • Consider antibiotics
  • ACEi to treat proteinuira >1g/day
    Minority develop RPGN
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87
Q

What is crescentic/RPGN?

A

Most aggressive GN which can lead to ESRF in a few days.

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88
Q

What are the types of RPGN?

A

Type 1: Anti-GBM - (Goodpasture’s) - 5% Presents with haemoptysis and haematuria Rare condition associated with pulmonary ahemorrhage and RPGlomerulonephritis.

Factors increasing likelihood of pulmonary haemorrhage.
- Smoking, LRTI, Pulmonary oedema, inhalation of hydrocarbons.

Manage = plasma exchange, steroids, cyclophosphamide.

Type 2: Immune Complex deposition (complication of any immune complex deposition = Berger’s, post-strep, endocarditis, SLE)

Type 3: Pauci Immune - 50%

  • cANCA: Wegener’s (Granulomatosis with Polyangiitis)
  • pANCA: microscopic polyangiitis, Churg-Strauss
  • Even if ANCA+ve, may still be idiopathic: no features of systemic vasculitis
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89
Q

Investigations and management of RPGN?

A
  • Manage with Corticosteroids and other immunosuppressants.

- Manage CVS factors - lifestyle measures, statins, BP control.

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90
Q

What is the definition of nephrotic syndrome?

A
  • Proteinuria (>3.5g/24hr)
  • Hypoalbuminaemia (<30g/L)
  • Peripheral oedema (periorbital, genital, ascites, peripheral).
  • Hyperlipidaemia
  • Lipiduria
    Often intravascularly depleted with decreased JVP (CCF).
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91
Q

What are the investigations for nephrotic syndrome?

A

Same as glomerulonephritis

  • Basic bloods: FBC, U+E, ESR
  • Complement (C3 and C4)
  • Abs: ANA, dsDNA, ANCA, GBM
  • Serum protein electrophoresis and Ig
  • Infection: ASOT, HBC, HCV.

All adults get biopsy.
Steroids 1st with children: mostly minimal change.

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92
Q

Complications of nephrotic syndrome?

A
  • Hyperlipidaemia: increased cholesterol and triglycerides
  • Infection: decreased Ig, decreased complement activity
  • VTE: up to 40%. - Therefore prophylactic LMWH required. Due to loss of anti-thrombin III, protein C&S, rise in fibrinogen
  • Loss of thyroxine-binding globulin = low total, but not free, thyroxin level

HIT.

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93
Q

Nephrotic syndrome secondary to systemic disease?

A

DM: glomerulosclerosis

SLE: Membranous - Present with proteinuria on urinalysis. Pre-eclampsia cannot occur before 20 weeks therefore cannot be possible. Can cause deranged TFTs due to urinary loss of thyroid-binding globulins, leading to a low total T4 level.

Amyloidosis

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94
Q

Causes of nephrotic syndrome?

A
  1. Minimal change glomerulonephritis (common cause in children) - can be due to NSAIDs, Hodgkin’s lymphoma, EBV.

Offer prednisolone and only if poor prognosis then give biopsy.

  1. Membranous Nephropathy (most common cause of adults - due to malignancy, but also diabetic nephropathy)
  2. Focal Segmental GS
  3. Membranoproliferative/ Mesangiocapillary GN/ Berger’s/ IgA nephropathy.
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95
Q

Summary of minimal change glomerulonephritis?

A
  • Commonest cause of nephrotic syndrome in children

Causes:

  • URTI - infectious mononucleosis
  • drugs - NSAIDs, rifampicin
  • Hodgkin’s lymphoma, thymoma
  • Biopsy: normal light micro, fusion of podocytes on EM
  • Management: Steroids (cyclophosphamide if steroid unresponsive)
  • Prog: 1% –> ESRF.

1/3 of patients have infrequent relapses and 1/3 of patients have frequent relapsed (2/3) with recurrent episodes.

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96
Q

Summary of membranous nephropathy?

A 
20-30% of adult nephrotic syndrome 
- Associations: Mainly malignancy 
Ca: lung, colon, breast
Autoimmune: SLE, thyroiditis, rheumatoid
Infections: HBV, malaria, syphilis
Drugs: Penicillamine, gold, NSAIDs

On biopsy: Subepithelial immune complex deposits, basement membrane thickening on light microscopy. Subepithelial spikes on silver stain. Positive immunohistochemistry for PLA2

Management:
- All patients should receive an ACEi or an ARB.
- immunosuppression if renal functions declines. E.g steroid + cyclophospamide.
Prognosis: 40% spontaneous remission.

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97
Q

Summary of focal segmental glomerulonephritis?

A

If adult with nephrotic syndrome think focal segmental.

  • Commoner in Afro-Caribbeans
  • Common nephrotic syndrome in adults
  • Idiopathic or Secondary: VUR, Berger’s, SCD, HIV.
  • Biopsy: focal scarring, IgM deposition
  • Management: Steroids or cyclophosphamide/cyclosporin
  • Prognosis: 30-50% –> ESRF (may recur in transplants).
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98
Q

Summary of membranoproliferative GN?

A
  • Rare
  • May lead to nephrotic or nephritic syndrome
  • Associated with HBV, HCV, Endocarditis
  • Prognosis: 50% –> ESRF
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99
Q

What is the general management of nephrotic syndrome?

A
  • Monitor U+E, BP, fluid balance, weight
  • Treat underlying cause:
    Majority are steroid-responsive.
  • Symptomatic/complication management:
    Oedema: Salt and fluid restrict + furosemide
    -
    Proteinuria: ACEi/ARA decreased proteinuria
    Increased lipids: Statin
  • VTE: Tinzaparin (risk of clotting)

Management HTN.

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100
Q

What is the definition of AKI?

A

Significant decline in renal function over hrs or days manifesting as an abrupt and sustained increased in serum urea and creatinine and/or a fall in urine output.

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101
Q

What are the causes of AKI?

A

Pre-renal
Renal
Post-renal

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102
Q

Causes of pre-renal AKI

A
  • Shock (hypovolaemia, haemorrhage, sepsis, 3rd space filling)
  • renovascular compromise (NSAIDs, ACEi, bilateral renal artery stenosis + ACEi.

In pre-renal urea:creatinine ratio indicated a pre-renal cause.
Normally in pre-renal kidneys will try to hold onto sodium and there will be low fractional sodium excretion.

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103
Q

Causes of Renal AKI?

A

ATN:
Ischaemia: shock, HTN, HUS, TTP
Direct nephrotoxin: drug hypertensitivity

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104
Q

Causes of post-renal AKI?

A

SNIPPIN

  • Stone
  • Neoplasm
  • Inflammation: Stricture
  • Prostatic hypertrophy
  • Posterior urethral valves
  • Infection: TB, Schisto
  • Neuro: Post-op, neuropathy
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105
Q

How does AKI present?

A
  • Uraemia
  • Acidosis
  • Hyerkalaemia
  • Fluid overload
    Oedema, including pulmonary
    Increased BP (or decreased)
    S3 gallop
    Increased JVP
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106
Q

Clinical assessment of AKI? How do you decide if acute or chronic?

A

Can’t tell for sure?: Manage as acute.

Features of chronic AKI?

  • Hx of comorbidity: DM, HTN
  • Long duration of symptoms
  • Previously abnormal bloods (GP records)
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107
Q

Volume depletion assessment in AKI?

A
  • Postural hypotension
  • Decreased JVP
  • increased pulse
  • Poor skin turgor, dry mucous membranes
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108
Q

How to assess for GU tract obstruction in AKI?

A 
Suprapubic discomfort
Palpable bladder
Enlarged prostate
Catheter
Complete anuria (rare in ARF)
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109
Q

What are the rare causes of AKI?

A

Associated with proteinuria±haematuria

Vasculitis: rash, arthralgia, nosebleed.

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110
Q

What are the investigations for AKI?

A

Bloods: FBC (anaemia, leucocytosis), U+E, (creatinine, potassium, urea), urea to creatinine ratio, LFTs, Glucose, Clotting, Ca, ESR

ABG: hypoxaemia (oedema), acidosis, increased K+

GN screen: if cause unclear

Urine dip: Dip, MCS, chemistry (U+E, PCR, Osmolality, BJP)

ECG: Hyperkalaemia

CXR: pulmonary oedema

Renal US: renal size, hydronephrosis** - must be done within 24h of assessment if no identifiable cause/ at risk of urinary tract obstruction

NB: in pre-renal failure, urine is concentrated and Na is reabsorbed –> increased osmolality, Na <20mM.

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111
Q

What is the classification of AKI?

A

RIFLE Classification

  • 3 grades of AKI and 2 outcomes
  • Classification determined by worst criteria
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112
Q

RIFLE Classification - Those at risk of AKI?

A

Risk:

  • Increased Cr x 1.5
  • Decreased GFR >25%
  • UO: <0.5ml/kg/h x 6hr

In the 1s

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113
Q

RIFLE Classification - Those with acute kidney injury?

A

Injury:

  • Increased Cr x 2
  • Decreased GFR >50%
  • UO: <0.5ml/kg/h x 12hrs

In the 2s

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114
Q

RIFLE Classificaiton - Those with acute kidney failure?

A

Failure:

  • Increased Cr x 3
  • Decreased GFR >75%
  • UO: <0.3ml/kg/h x 24hr, or anuria x 12hr.

In the 3s

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115
Q

RIFLE classification - acute kidney loss?

A
  • Persistent ARF = complete LOF > 1month
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116
Q

RIFLE classification - End stage kidney disease

A
  • LOF >3 months.
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117
Q

General management of AKI?

A
  • Identify and manage pre-renal or post-renal causes
  • Urgent US
  • Manage exacerbating factors: sepsis
  • Give PPI
  • Stop nephrotoxins: NSAIDs, ACEi, Gent, Vank
  • Stop meformin if Cr >150mM.

Pre-renal

  • Volume expansion - Offer fluid 500ml 09% saline over 15mins.
  • Vasopressors (severe hypotension)
  • Diuretic if overloaded
  • Renal replacement therapy (haemodialysis)

Manage hyperkalaemia.

118
Q

What to monitor in AKI?

A

Cathereise and monitor UO
Consider CVP
Fluid balance
Weight

119
Q

What are the ECG signs in hyperkalaemia?

A

ECG feature (in order)

  • Peaked T waves
  • Flattened P waves
  • Increased PR interval
  • Widened QRS
  • Sine-wave pattern - VF
120
Q

What is the management of hyperkalaemia?

A

If K+ >6.5 or if there are ECG changes
- Then admin

  • 10ml 10% calcium gluconate
    Protective effect begins in minute.
  • 100ml 20% glucose + 10u insulin (Actrapid) .
  • Salbutamol 5mg nebs (helps to lower potassium through intracellular migration of potassium).

Removal of potassium from body

  • Calcium resonium - enemas are more effective than oral as potassium is secreted by rectum.
  • Loop diuretics
  • Dialysis

Calcium resonium 15g PO or 30 PR
Haemofiltration (usually needed if anuric)

121
Q

How to manage pulmonary oedema?

A
  • Sit up and give high-flow O2
  • Morphine 2.5mg IV (±metoclopramide 10mg IV)
  • Furosemide 120-250mg IV over 1hr
  • GTN spray ± ISMN IVI (unless SBP <100)
  • If no response consider:
    CPAP
    Haemofiltration/haemodialysis ± venesection
122
Q

How to manage bleeding in AKI?

A

Increased urea impaires haemostasis
FFP + plats as needed
Transfuse to maintain hb>10

123
Q

What are the indications for acute dialysis?

A
  • Persistent Hyperkalaemia >7mM
  • Refractory pulmonary oedema (as a result of volume overload).
  • Symptomatic uraemia: encephalopathy, pericarditis
  • Severe metabolic acidosis
  • Poisoning (e.g aspirin, methylglycol)

AEIOU

124
Q

What are the common causes of acute renal failure?

A

Pre-renal: Shock or renovascular (HTN, GM, HRS)
Renal: ATN, GN
Post-renal: Obstruction, stone, neoplasm, catheter

125
Q

Presentation of acute renal failure?

A
  • Presents in the context of critical illness
  • Uraemia
  • Hyperkalaemia
  • Acidosis
  • Oedema and increased BP
126
Q

Management of Acute Renal Failure? - Resus

A

Resuscitate and assess fluid status
- A: GCS increased may need airway management
- B: pulmonary oedema - sit up, high flow oxygen
- C: fluid status?
CVS: Postural BP, JVP, HR
Tissues: CRT, cold/warm hands, skin turgor, mucus membranes

127
Q

Management of life-threatening complications of acute renal failure?

A
  • Hyperkalemia
  • Pulmonary oedema
  • Consider need for rapid dialysis

Manage shock or dehydration

  • Fluid challenge 250-500ml over 30 mins
  • Repeat as necessary: aim for CVP of 5-10cm
  • Continue @ 20ml +UO/h
128
Q

What to monitor in acute renal failure?

A
  • Cardiac monitor
  • Urinary catheter
  • Consider CVP
  • Start fluid balance chart
129
Q

Further management of AKI?

A

Look for evidence of post-renal cause

  • Palpable ± tender bladder
  • Enlarge prostate/anuria, catheter
  • Hx
    Evidence of acute vs chronic
    = renal ultrasound = most patients with CRF have bilateral small kidneys.
    May also have hypocalcemia.
  • Ix
    Bloods, ABG, Urine dip, ECG, CXR, Renal US

Manage sepsis
Further management
- Call urologists if obstructed despite cather.

130
Q

What are the interstitial nephritides?

A

Acute Intersitial/Tubulointerstital nephritis and eventually necrosis.

  • Immune mediated hypersensitivity with either drug or other Ag acting as haptans. Usually have rash, fever and eosinophilia. Can be due to penicillins.
  • ATN = Reversible or irreversible type of renal failure caused by ischaemic or toxic injury to the renal tubular epithelial cells. Injury results in cell death or detachment from basement membrane.
131
Q

What causes ATN?

A

Ischaemia - Hypoperfusion, or kidney structural damage.

Exogenous toxins
- Nephrotoxins = intrarenal vasoconstriction, tubular toxicity (Aminoglycosides, amphotericin B, chemo drugs, NSAIDS.

Endogenous toxins
- Rhabdomyolsis (myoglobin) - this can be due to compartment syndrome producing myoglobinuria. Muddy brown casts. Leads to tubular cell necrosis.

  • Increased uric acid (gout)
  • Increased light chain proteins (myeloma).
132
Q

What causes Tubulointerstitial nephritis/ AIN?

A

Drug hypersensitivity in 70%

  • NSAIDS
  • Abx: ceph, penicillin, rifampicin, sulphonamides
  • Diuretics: frusemide, thiazide
  • Allopurinol
  • Cimetidine

Infections in 15%
- Staphs, Streps, hantavirus

Immune disorders
- SLE, Sjogren’s, Sarcoid

133
Q

How does ATN present?

A

Occurs 2* to prolonged renal ischaemia
2* to either continuing pre-renal injury or by direct toxicity
2* to sepsis or nephrotoxins

  • Oliguria
  • Hypotension
  • Tachycardia
  • Oedema
  • Orthopnoea/dyspnoea
  • granular/ tubular casts
134
Q

How does Tubulointerstitial nephritis present?

A
  • Fever, arthralgia
  • Rash
  • AKI –> Oliguria/Anuria
  • Uveitis
  • eosinophilia
135
Q

Investigations for tubulointerstitial nephritis?

A
  • Increased IgE, Eosinohilia

- Dip: haematuria, proteinuria, WCC, IgE, esoniphils

136
Q

Ix for ATN?

A
  • Urea + creatinine: raised urea/creatinine, hyperkalaemia, metabolic acidosis.
  • Elevated sodium in urine
  • Coagulation - Prolonged PTT
137
Q

Management of tubulointerstitial nephritis?

A

Stop offending drug

Prednisolone

138
Q

Management of ATN?

A

Supportive care
Stop drugs
Manage volume

139
Q

What causes chronic tubulointerstitial nephritis

A 
Fibrosis and tubular loss
Commonly caused by: 
- Reflux and chronic pyelonephritis 
- DM 
- SCD or trait
140
Q

What is analgesic nephropathy?

A
  • Prolonged heavy ingestion of compound analgesics
  • Often a Hx of chronic pain: headache, muscle pain.

Features:

  • Sterile pyuria ± mild proteinuria
  • Slowly progressive CRF
  • Sloughed papilla can –> Obstruction + renal colic.

Ix: CT w/o contrast (papillary calcifications)

Rx: Stop analgesics

141
Q

What is Acute Urate Nephropathy?

A
  • AKI due to urate precipitation
  • Usually after chemo-induced cell lysis
    Rx: Hydration, urinary alkalinisation
142
Q

What are the causes of nephrocalcinosis?

A
  • Diffuse renal parenchymal calcification
  • Progressive renal impairment
  • Causes:
    Malignancy
    Increased PTH
    Myeloma
    Sarcoidosis
    Vit D intoxification
    RTA
143
Q

What types of nephrotoxins do you have?

A

Those that are directly toxic –> Leading to ATN

Those that cause hypersensitivity –> Tubulointerstitial nephritis

144
Q

What are some exogenous nephrotoxins?

A
  • NSAIDs
  • Antimicrobials: AVASTA
  • ACEi
  • Immunosuppresssants
    Ciclosporin
    Tacrolimus
  • Contrast media
  • Anaesthetics: enflurane

DAMN drugs to be stopped in AKI

  • Diuretics
  • ACEi
  • Metformin (if Cr >150)
  • NSAIDs
145
Q

Which antibiotics are nephrotoxic?

A
  • Aminoglycosides (Gent, Tobramycin)
  • Vancomycin
  • Acyclovir
  • Sulphonamides (trimethoprim)
  • Tetracycline (doxycycline)
  • Amphotericin
146
Q

What are the endogenous nephrotoxins?

A

Myoglobin
Urate
Ig - eg light chains in myeloma

147
Q

Rhabdomyolysis pathogenesis?

A

Skeletal muscle breakdown –> Release of:
K+, PO4, urate
Myoglobin, CK

Increased K+ and AKI. Can also lead to DIC, renal failure.

148
Q

Causes of rhabdomyolysis?

A

> Ischaemia: embolism, surgery

> Toxins: statins, fibrates, ecstasy, neuroleptics

> Trauma: immobilisation, crush, burns, seizures, compartment syndrome, falls

149
Q

Clinical signs of rhabdomyolysis?

A
  • Muscle pain, swelling
  • Red/brown urine
  • AKI occurs 10-12hr later
150
Q

Investigations for rhabdomyolysis?

A

Dipstick: +ve Hb, -ve RBCs.
Bloods: Increased CK (increased 5x normal is diagnostic) , increased K, increased Po4, Increased Urate.

Urine - Myoglobin increased in blood or urine.

151
Q

Management of rhabdo?

A
  • Manage hyperkalaemia
  • IV rehydration: 300ml/h to maintain good urine output
  • CVP monitoring if oliguria
  • IV NaHCO3 may be used to alkanalise urine and stabilise a less toxic form of myoglobin.

?Furosemide

152
Q

Chronic renal failure - definition?

A
  • Kidney damage >3 months indicated by decreased function.
  • Symptoms usually only occur by stage 4 (GFR <30)
  • ESRF is stage 5 or need for RRT.
153
Q

What are the stages of chronic renal failure?

A

Stage 1 = GFR >90 (with some sign of kidney damage on other tests) - if all kidney tests are normal there is no CKD.

Stage 2 = GFR >60-89 (with some sign of kidney damage)

Stage 3a = 45-59

Stage 3b = 30-44
Stage 4 = 16-29
Stage 5 = <15

154
Q

Stages of chronic Renal failure shorthand?

A

> 90–> <90 –> 60 –> 30 –> 15

If patient falls below eGFR of 30 or progressively by >15 in a year refer to a nephrologist.

155
Q

Causes of Chronic renal failure - common?

A

DM

HTN

156
Q

Other causes of chronic renal failure that are less common?

A
  • Renal artery stenosis
  • GN
  • Polycystic disease
  • Drugs: e.g analgesic nephropathy
  • Pyelonephritis: usually 2ndry to VUR
  • SLE
  • Myeloma and amyloidosis
157
Q

Investigations for chronic renal disease?

A

Bloods:

  • Hb decreased
  • U+E (elevated creatinine), decreased GFR
  • ESR
  • Glucose
  • Decreased Ca/PO4 (AKI) If phosphate is high it is chronic.
  • Increased ALP
  • Increased PTH

Urine
- Microalbuminuria, proteinuria, haematuria. Protein:creatinine ratio - 300 means you are nephrotic.

Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep

Film: burr cells

158
Q

Imaging in chronic renal disease?

A 
CXR: Cardiomegaly, pleural/pericardial effusion, oedema
AXR: calcification from stones
Renal US
- Usually small (<9cm) 
- May be large: polycystic, amyloid

Bone X-rays: renal osteodystropy (pseudofractures)

CT KUB: cortical scarring from pyelonephritis

For contrast-enhanced CT - prevention of contrast induced nephropathy: volume expansion with 0.9% saline at a rate of 1mL/kg/hr for 12 hours pre- and post- procedure.

Renal biopsy: if cause unclear and size normal

159
Q

What are the complications of chronic renal disease?

A

CRF HEALS

  • Cardiovascular disease - leading cause of death.
  • Renal osteodystrophy
  • Fluid (oedema)
  • HTN
  • Electrolyte disturbance
  • Anaemia
  • Leg restlessness
  • Sensory neuropathy
160
Q

What are the features of renal osteodystrophy?

A

Osteoporosis: decreased mineral density
Osteomalacia: Decreased mineralisation of osteiod
2ndry/3rdy HPT –> Osteitis fibrosa cystica
- Subperiosteal bone resorption
- Acral osteolysis: short stubby fingers
- Pepperpot skull

May get osteosclerosis –> Rugger Jersey spine
= Sclerotic vertebral end-plate with lucent centre.

161
Q

What is the mechanism of renal osteodystrophy?

A
  • Reduced 1a hydroxylase –> decrease vit D activation –> decreased Ca –> increased PTH.
  • Phosphate retention –> Decreased Ca and increased PTH
  • Increased PTH –> activation of osteoclasts ± osteoblasts
  • Also acidosis –> Bone resorption.
162
Q

What is the management of chronic renal failure? General measures and lifestyle?

A
  • Management of reversible causes
  • Stop nephrotoxic drugs

Lifestyle

  • Exercise
  • Healthy weight
  • Stop smoking
  • Na, Fluid, PO4 restriction
163
Q

How do you manage the cardiovascular risk factors of chronic renal failure?

A
  • Statins
  • Low-dose aspirin
  • Manage DM

Target for HTN (<140/90) - <130/80 if DM.
In DM kidney disease give ACEi/ARB

164
Q

How to manage oedema in chronic renal failure?

A

Furosemide

165
Q

How to manage bone disease in chronic renal failure ?

A

Pathophysiology:

  • 1-alpha hydroxylation normally occurs in kidneys -> CKD leads to low Vit D
  • kidneys normally excrete phosphate but CKD -> high phosphate

Other problems:
> High phosphate level in CKD drags calcium from bones -> osteomalacia
> low Ca - due to low vit D, high phosphate
>2* hyperPTH - due to low Ca, high phosphate and low vit D

Mx:
> reduce phosphate intake
> Phosphate binders: calcichew. As they are calcium based they can lead to hypercalcaemia symptoms. (Sevelamer is a non-calcium based phosphate binder.)
> Vit D analgoues: calcitriol or Alfacalcidol.
> Ca supplements/Cinacalcet: Ca Mimetics

> parahytoidectomy may be needed in some ccases

166
Q

How to manage anaemia in chronic renal failure?

A

Anaemia
- Exclude IDA and ACD
- EPO to raise Hb to 11g/dL
epoetin alpha

167
Q

How to manage restless legs in chronic renal failure?

A

Clonazepam

168
Q

Renal transplant assessment?

A
  • Virology status: CMV, HCV, HIV, VZV, EBV
  • CVD
  • TB
  • ABO and HLA haplotype
169
Q

What are the contraindications to a renal transplant?

A

Active infection
Malignancy
Severe HD or other co-morbidities

170
Q

What sort of grafts can you use in a renal transplant?

A
  • Cadaveric: brainstem death with CV support
  • Non-heart beating donor :no active circulation
  • Live-related
    Optimal surgical timing
    HLA-match
    Improved graft survival
  • Live unrelated
171
Q

What is used for immunosuppression pre-op?

A

Campath/alemtuzumab (anti-CD52)

172
Q

What is used for immunosuppression post-op?

A
  • Prednisolone short-term and tacro-ciclo long-term
173
Q

What are the complications of renal transplant? Early?

A

Hyperacute:
due to pre-existent antibodies against donor HLA type 1 antigens (a type II hypersensitivity reaction)
rarely seen due to HLA matching

Post-op

  • Bleeding
  • Graft thrombosis
  • Infection
  • Urinary leaks

Hyperacute rejection

  • ABO incompatibility
  • Thrombosis and SIRS
174
Q

What are the complications of renal transplant? Medium (6 months)

A

Acute Rejection

  • Increased Cr (± fever and graft pain) - appears like infection but sterile pyuria
  • confirm diagnosis on biopsy of transplanted kidney
  • Cell-mediated response
  • Responsive to immunosuppression.
175
Q

What are the complications of a renal transplant? Chronic >6 months)

A
  • Interstitial fibrosis + tubular atrophy
  • Gradual increase in Cr and proteinuria
  • Not responsive to immunosuppression

Initial management is steroid treatment - chronic rejection presents insidiously with deteriorating renal function.

176
Q

What are the complications of renal transplant? Ciclosporin/tacrolimus nephrotoxicity

A

Acute: reversible afferent arteriole constriction –> decreased GFR
Chronic: tubular atrophy and fibrosis

177
Q

Complications of renal transplant? Decreased immune function?

A

Increased risk of infection: Opportunistic, fungi, warts

Increased risk of malignancy: BCC, SCC, Lymphoma (EBV)

178
Q

What are the complications of renal transplant? Cardiovascular disease?

A

HTN and Atherosclerosis

179
Q

What are the differentials for rising Cr in Tx patient?

A
  • Rejection
  • Obstruction
  • ATN
  • Drug Toxicity
180
Q

What percentage of end stage renal failure is caused by diabetes?

A

20%

Advanced/ESRF occurs in 40% of T1 and T2 DM.

181
Q

Pathology of diabetic nephropathy?

A
  • Diabetes nephropathy describes conglomerate of lesions occuring concurrently
  • Hyperglycaemia –> renal hyperperfusion –> hypertrophy and increased renal size.

This is in constrast to chronic kidney disease where they have bilateral small kidneys.

  • Hypertrophy and metabolic defects including ROS production –> glomerulosclerosis and nephron loss.
  • Nephron loss –> RAS activation –> HTN
182
Q

What is the clinical progression of diabetes nephropathy?

A
  • Microalbuminuria (30-300 mg/d
    = (albumin: creatinine >2.5)
    Strong independent RF for CV disease.

Therefore measure urinary albumin/creatinine ratio on a spot urine sample. If abnormal, repeat with a first-pass morning urine specimen.
ACR should be used to screen nephropathy.

Microalbuminuria is the EARLIEST clinically detectable sign of classic diabetic nephropathy. Rise in albumin loss to 30-300mg per day.

  • All diabetic patients require annual screening for albumin:creatinine ratio in early morning specimens.
  • Progresses to proteinuria (albuminuria >300mg/d)
  • Diabetic retinopathy usually co- exists and HTN is common
183
Q

What should diabetics be screened for to reduce complications of diabetic nephropathy?

A

all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

184
Q

How would you manage diabetic nephropathy?

A
  • Good glycaemic control delays onset and progression
    (keep HbA1c)
  • BP control below 130/80
  • Start ACEi/ARB even if normotensive
  • Stop smoking (associated with reduced GFR)
  • Can use peritoneal dialysis or haemodialysis
  • Finally - consider pancreas-kidney transplantation.
185
Q

What are the associations with amyloidosis and the kidney?

A
  • Renal involvement usually caused by AL/AA amyloid.
  • Features:
  • Proteinuria
  • Nephrotic syndrome
  • Progressive renal failure

55yr old with progressive weakness and dyspnea, hepatomegaly, proteinuria and worsening renal function.

Commonly present with dyspnoea, hepatomegaly, proteinuria, worsening renal function.

186
Q

How do you diagnose amyloidosis associated nephropathy?

A
  • Large kidneys on US

- Biopsy

187
Q

Pathophysiology of amyloid associated nephropathy?

A

Primary target for AL. Monoclonal light chain assembles and deposits extracellularly, resulting in disruption of the glomerular basement membrane.

AL produce immunoglobulin light chains - prone to misfolding from a native alpha-helical state into an insoluble beta-pleated sheet.

188
Q

What is secondary amyloidosis

A

AA

  • Improper processing of serum amyloid A protein.
  • Rather than being broken down it cannot.
  • Commonly related to long-standing infections such as bronchiectasis, osteomyelitis, IBD.
189
Q

What is cardiac amyloidosis?

A

Resembles idiopathic restrictive cardiomyopathy. Impairment in longitudinal functioning. Also causes conduction abnormalities.

190
Q

Diagnosis of amyloid on biopsy?

A

Congo Red - demonstrates green birefringence when viewed under green birefringence.

191
Q

What infections can cause golmerulonephritis?

A 
Post Strep
HCV
HBV
HIV
SBE/IE
Visceral abscess
192
Q

Which infections can cause a vasculitis?

A

HBV
HCV
Post-strep

193
Q

Which infections can cause a tubulo-interstital nephritis?

A

Bacterial pyelonephitis
CMV
HBV
Toxo

194
Q

What direct impacts can systemic malignancy have on the renal system?

A

Renal infiltration: Leukaemia, lymphoma
Obstruction: Pelvic tumour
Mets

Nephrotoxicity

  • Due to toxic chemo
  • Analgesics
  • Tumour Lysis Syndrome
195
Q

Other renal complications of systemic disease?

A

Hyperparathyroidism –> hypercalcaemia

Sarcoidosis
–> increased Ca and TIN

196
Q

Myeloma and Renal disease?

A

Pathology

  • Excess production of monoclonal AB ± light chains (excreted and detected in 60% as urinary BJP)
  • Light chains block tubules and have direct toxic effects –> ATN
  • Myeloma also associated with increased Ca2+ (through stimulating osteoclastogenesis).

Presentation

  • ARF/CRF
  • Amyloidosis

Management

  • Ensure fluid intake of 3L/d to prevent further impairment
  • Dialysis may be required in ARF.
197
Q

Which rheumatological diseases are associated with renal complication?

A

Rheumatoid
SLE
Diffuse Systemic Sclerosis

198
Q

How is rheumatoid arthritis associated with renal complications?

A
  • NSAIDS –> ATN
  • Penicillamine + gold –> membranous GN
  • AA amyloidosis occurs in 15%
199
Q

How is SLE associated with renal complications?

A
  • Involves glomerulus in 40-60% –> ARF/CRF
  • Proteinuria + increased BP common
  • Management
    Proteinuria - ACEi
    Aggressive GN: immunosuppression
200
Q

How is Diffuse Systemic Sclerosis associated with renal complications?

A
  • Renal crisis: Malignant HTN + ARF (commonest cause of death)
  • Rx: ACEi if increased BP or renal crisis.
201
Q

What are the renal vascular diseases?

A
  • Hypertension
  • Renal artery stenosis
  • Haemolytic Uraemic Syndrome
  • Thrombotic Thrombocytopenic Purpura
202
Q

HTN and renal vascular disease?

A
  • Can be both cause and effect of renal damage
  • Renal diseases are commonest cause of 2ndry HTN
    (through activation of RAS, leading to retention of Na and water due to decreased excretion).
203
Q

What are the causes of renal artery stenosis?

A
  • Atherosclerosis in 80%
  • Fibromuscular dysplasia
  • Thromboembolism
  • External mass compression
204
Q

What are the clinical features of renal artery stenosis?

A
  • Refractory HTN
  • Worsening renal function after ACEi/ARB
  • Flash pulmonary oedema (no LV impairment on Echo)
205
Q

What are the investigations for renal artery stenosis?

A
  • Bloods: Creatinine to estimate GFR, serum potassium for activation of RAS, should be low due to increased sodium. Aldosterone-to-renin <20 excludes primary aldosteronism.
  • ie if renin is high = RAS.
  • US + Doppler: small kidney + reduced flow
  • CT/MR angio
  • Renal angiography: gold standard.
206
Q

What is Haemolytic Uraemic SYndrome (HUS) caused by?

A

E.coli 0157: h7 verotoxin –> endothelial dysfunction . Shiga Toxin

This leads to cell damage, microvascular thrombosis and resulting MAHA (Microangiopathic haemolytic anaemia).

Haemolysis, anaemia, thrombocytopenia, raised LDH, Urea and Creatinine raised.

Ix

  • FBC = anaemia, thrombocytopenia, fragmented blood film
  • U&E = AKI
  • stool culture

Management

  • Fluids, blood transfusion and dialysis.
  • No role for antibiotics.
  • Indication for plasma exchange in severe HUS usually when there is no diarrhoea present.
  • Eculizumab

Different to TTP = neuro signs.

DIC = pancytopaenia

207
Q

What is the management of renal artery stenosis?

A

Use medical treatment with CV risk factors. (Ue ACEi and attempt to keep HTN below 130/80).
Use statin, antiplatelet (aspirin

2nd line: Then angioplasty + stenting. Consider when refractory HTN on >3 medications, progressive CKD, AKI on ACEi, flash pulmonary oedema, bilateral RAS.
- Give post-stenting clopidogrel

3rd line: surgical reconstruction of renal arteries (eg when AAA involved)

208
Q

What are the clinical features of HUS?

A
  • Young children eating undercooked burgers
  • Bloody diarrhoea + abdominal pain precedes:
    MAHA, thrombocytopenia, renal failure.
209
Q

What are the investigations for HUS?

A
  • Schistocytes (RBC fragments) and are seen in haemolytic anaemia
  • decreased platelets
  • decreased Hb,
  • Renal failure
  • Normal clotting (rule out other causes of thrombocytopenia such as DIC)
  • PCR for Shiga Toxin
210
Q

Management of HUS?

A
  • Usually resolves spontaneously
  • RBC transfusion
  • Dialysis or plasma exchange may be needed (if TTP) or eculizumab
211
Q

What is TTP?

A

Thrombotic Thrombocytopenic Purpura.

  • Clinical syndrome characterised by MAHA, thrombocytopenic purpura, renal failure, fever, CNS signs: confusion, seizures).
212
Q

What is TTP pentad?

A 
MAHA
Thrombocytopenic purpura
Neurological dysfunction
Renal dysfunction
Fever
213
Q

What is the aetiology of TTP?

A

May involve unusually large vWF multimers.

This may also be due to lack of ADAMTS-13 cleaving enzyme for von Willebrand factor.

214
Q

What is the role of vWF?

A

1) Carrier protein for Factor VIII, protecting it from degradation.
2) Bridge connecting platelets to damaged endothelium.

Large vWF leads to aggregation of circulating platelets at sites of high intravascular shear stress. This leads to thombi in the microvascular system.

215
Q

What is the investigations for TTP?

A
  • Blood: Platelets decreased, anaemia,
  • Smear: schistocytes, reticulocyte count raised,
  • Coombs: negative
  • Normal clotting
216
Q

Management of TTP?

A
  • Plasmapherisis/Plasma exchange
  • Immunosuppression (prednisolone/ Caplacizumab which interacts with vWF).
    If steroids unsuccessful use vincristine/rituximab/cyclophosphamide/ciclosporin.
  • Splenectomy - will need polyvalent pneumococcal vaccine, Hib, meningococcal.
217
Q

What are the renal tubular acidosis diseases?

A

Renal tubular acidosis

  • Type 1 (Distal)
  • Type 2 (Proximal)
  • Fanconi’s syndrome
  • Hereditary Hypokalaemic tubulopathies
218
Q

What is the pathophysiology behind renal tubular acidosis?

A
  • Impaired acid excretion
    leads to a hypercholaraemic metabolic acidosis
  • Both –> RAS activation –> K wasting and hypokalaemia. (as potassium cannot be reclaimed)
219
Q

Classical Distal RTA (type 1) pathophysiology?

A
  • Inability to excrete H+, even when acidotic
  • Mutations of proton pump or moving bicarb into blood.
  • May complicate other renal disorders
    Either:
  • 1) hereditary
  • 2) AI: Sjorgen’s, SLE, thyroiditis
  • 3) Drugs
220
Q

What are the features of Type 1 Classical RTA?

A
  • Hyperchloraemic metabolic acidosis + hypokalaemia
  • Urine alkalotic regardless of systemic acidosis.
  • Rickets/osteomalacia (bone buffering)
  • Renal stones and UTIs
  • Leading to nephrocalcinosis –> ESRF. This is because calcium stones have a propensity to form in alkaline urine.
221
Q

What is the diagnosis/management of Type 1 Classical RTA?

A
  • Diagnosis = Failure to acidify urine (pH >5.5) despite acid load.
  • Ix = serum bicarb, chloride, ABG, K.

Management - Sodium alkali or potassium containing alkali solution.

222
Q

What is the pathophysiology of proximal Type 2 RTA?

A

Defect in HCO3 reabsorption in the PCT.
Tubules can reabsorb some HCo3 so can acidify urine in systemic acidosis when HCO3 is reduced.
- Usually associated wtih Fanconi Syndrome.

223
Q

Diagnosis of Fanconi’s Syndrome?

A

Diagnosis

Urine will acidify with acid load

224
Q

What is Fanconi Syndrome?

A

Disturbance of PCT function – > generalised impaired reabsorption.

  • Amino acids
  • k+
  • HCO3
  • Phosphate
  • Glucose
225
Q

What are the causes of Fanconi Syndrome?

A
  • Idiopathic
  • Inherited: inborn errors, Wilson’s
  • Acquired: tubule damage (Drugs, myeloma)
226
Q

What are the features of Fanconi’s Syndrome?

A
  • Polyuria
  • Hypophosphataemic rickets (vit D resistant)
  • Acidosis
  • Decreased K
227
Q

Management of proximal RTA + Fanconi’s syndrome?

A

Sodium alkali and/or potassium-containing alkali solution.

228
Q

What are the Hereditary Hypokalaemic Tubulopathies?

A

Bartter’s Syndrome

Gitelman Syndrome

229
Q

What is Bartter’s Syndrome?

A
  • Blockage of NaCL reabsorption in loop on Henle (as if taking furosemide)
  • Congenital salt wasting –> RAS activation –> hypokalaemia and metabolic alkalosis
  • Normal BP
230
Q

What is Gitelman Syndrome?

A
  • BLockage of NaCl reabsorption in DCT (taking thiazides)
  • COngenital salt wasting –> RAS activation –> hypokalaemia + metabolic alkalosis + hypocalcirua (due to increased Ca reabsorption)
  • Normal BP
231
Q

Renal Cystic Disease?

A

AD PKD
AR PKD
Medularry Sponge Kidney
Tuberous Sclerosis

232
Q

AD PKD overview?

A

Age - Adults 40-60 yrs
Genetics
- PKD1 on Chr 16
- PKD2 on Chr 14

Path

  • Large cysts arising from all parts of nephron
  • Progressive decline in renal function
  • 70% ESRF by 70yr.
233
Q

Presentation of AD PKD

A
  • Mass: abdo mass + flank pain
  • Infected cyst
  • Stones
  • SBP increased
  • Haematuria or haemorrhage into cyst
  • Aneurysm: Berry –> SAH
  • Polyuria + nocturia
  • Extra-renal cysts:liver
  • Systolic murmur: Mitral valve prolapse
234
Q

General Management of AD PKD?

A

General

  • Increased water intake, decreased Na, Decreased Caffeine (may decreased cyst formation)
  • Monitor U+E, BP
  • Genetic counselling
  • MRI screen for Berry aneurysms
235
Q

Medical management of AD PKD?

A
  • Rx HTN aggressively: <130/80 ACEi best
  • Rx infection
  • Urine alkalinasation for nephrolithiasis
236
Q

Surgical management of AD PKD?

A

Pain may be helped by laparoscopic cyst removal or nephrectomy

  • ESRF in 70% by 70 yrs, therefore dialysis or transplant.
237
Q

AR PKD info?

A

Prev: 1:40,000
Infancy
renal cyst and congenital hepatic fibrosis

238
Q

What is Medullary sponge kidney?

A

Multiple cystic dilatations of the CDs in the medulla
- Typically presents in 20-30s
- commoner in femals
- often asymptomatic but predisposes to:
Hypercalciruia, nephrolithiasis, recurrent UTIs and pyelonephritis
Haematuria

Renal function usually normal.

239
Q

What is tuberous sclerosis?

A

AD condition with hamartomas in skin, brain, eye, kidney.

Skin: Nasolabial adenoma sebaceum, ash-leaf macules, peri-ungal fibromas

Neuro: decreased IQ, epilepsy

Renal: cysts, angiomyolipomas

240
Q

What are the differentials for renal enlargement?

A
  • Polycystic kidney: ADPKD, ARPKD, TS
  • Hypertrophy 2nd to contralateral renal agenesis
  • Obstruction (hydronephrosis)
  • Neoplasia: RCC, myeloma, amyloidosis
  • Occlusion (renal vein thrombosis)
  • HIV associated
  • Systemic: early DM, amyloid.
241
Q

Presentation of Renal Case

A

This is a patient with end stage renal disease.

The likely current mode of renal replacement therapy is a renal transplant as evidenced by a scar in the right iliac fossa with an underlying mass consistent with a kidney. The mass was ovoid, smooth and non-tender.

I noted a matured radio-cephalic AV fistula in the left arm, which did not have any puncture marks that would suggest recent use.

The current mode of renal replacement therapy appearance to be adequate as the patient is euvolaemic.

I noted evidence of immunosuppression in the form a fine postural tremor that may be suggestive for tacrolimus use.

The patient did not appear cushingoid.

I could not identify a cause of the ESRF and would therefore like to take a history from the patient to enquire about risk factors for CKD, such as diabetes and HTN.

To complete my exam
- Request Urine Dip for glucosuria, which may suggest diabetes as the underlying case, or blood or protein whch may indicate an underlying glomerulonephritis.

Request an ECG + exam CVS system, as CKD is an independent factor for IHD**

242
Q

Signs on inspeciton on ESRF

A

Asian patient - DM prick marks - Diabetes

  • Palpate kidneys - APCKD risk of ICH, HTN + family US renal screening.
  • Purpura - Vasculitis/SLE
  • Stroke/CABG - vascular disease
243
Q

Graft function of renal patient

A 
Tenderness/heat over graft = rejection 
ACTIVE RRT methods - suggests a failed graft. 
- Tesio catheter
- Fistula - palpable bruit/sign of use
- Tenchkoff catheter

Anaemia, fluid overload, uraemia signs = graft failure

244
Q

Uraemia signs

A 
Hiccups 
Pruritis 
Loss of appetite
Malaise
Lemon tinged skin
245
Q

Immunosuppression

A
  • Steroids - remember violacious striae
  • Ciclosporin - gum hypertrophy, tremor, Peripheral neuropathy, HTN
  • Azothioprine = Anaemia, liver fibrosis
  • Tacrolimus - DM, tremor
  • Increased risk of malignacy with all of them (Esp cutaneous) Skin and colorectal.
246
Q

RIF Masses?

A

Caecal Malignancy (cachexia)
Crohns -clubbing, EN, PG.
Adenopathy
Transplanted Kidney

247
Q

Indications for RRT?

A

When you need dialysis

  • Uraemia with complications - encephalopathy/pericarditis
  • Refractory hyperkalaemia
  • Refractory pulmonary oedema
  • Refractory Metabolic acidosis
  • Drugs
248
Q

RRT options

A
  • Emergency: CVVHF (ITU) - filtrations (continuous veno-veno haemofiltration). Slower + a lot more gentle than dialysis.
  • Haemodialysis - 3x per week - Tesio line or fistula
    Risk of endocarditis (TR). More efficient. Regular filtration of the blodo through dialysis mahcine in hospital 3x a week for 3-5hrs.
  • Peritoneal dialysis: Continuous ambulatory peritoneal dialysis (CAPD) or automated. Can laso have APD (automated) - whilst patient is sleeping. 3-5 exchanges over 8-10hrs.

If the patient has Crohn’s won’t be suitable.

  • Sclerosing peritonitis, Hyperglycaemia (makes diabetes worse)

Renal transplant

249
Q

Renal cell cancer

A

Painless haematuria
HTN, polycythaemia, hyperCa

Stauffer syndrome: Cholestasis/HSM.

Von-Hippel Lindau
Tuberous Sclerosis

250
Q

Complications of haemodialysis?

A 
Site infection 
Endocarditis
Stenosis at site
Hypotension
Cardiac arrhythmia
Air embolus
Anaphylactic reaction to sterilising agents
Disequilibration syndrome
251
Q

Complication of peritoneal dialysis?

A

Peritonitis - most common cause is due to coagulase-negative staphylococcus. = Staph epidermidis. Staph A is another common cause.

  • Sclerosing peritonitis
  • Catheter infection
  • Catheter blockage
  • Constipation
  • Fluid retention
  • Hyperglycaemia
  • Hernia
252
Q

Complications of renal transplantation

A 
DVT
PE
Opportunistic infections 
Malignancies
Bone Marrow suppression 
Recurrence of original disease
Urinary tract obstruction
CVS
Graft rejection
253
Q

Symptoms of inadequate management with RRT?

A 
breathlessness
fatigue
insomnia
pruritus
poor appetite
swelling
weakness
weight gain/loss
abdominal cramps
nausea
muscle cramps
headaches
cognitive impairment
anxiety
depression
sexual dysfunction
254
Q

Fluid therapy requirements?

A
  • 25-30ml/kg/day of water
  • 1mmol /kg/day of potassium, sodium and chloride.
  • k = max rate of K infusion via a peripheral line is 10mmol/hour on a standard ward. 40mmol of K over 4 hrs.
  • IN ITU may give it quicker - max 20 mmol/hr
  • 50-100g/day of glucose to limit starvation ketosis. Irrespective of glucose requirements.

When administering NaCL - risk of hyperchloraemic metabolic acidosis.

255
Q

Henoch-Schonlein Purpura

A

Palpable purpuric rash
Abdo pina
polyarthritis
features of IgA nephropathy (Haematuria, renal failure)

256
Q

Acute clot retention?

A

Continuous bladder irrigation is the treatment of acute clot retention.

3 way foley catheter.

257
Q

Testing for haematuria?

A

urine dipstick is the test of choice for detecting haematuria

  • persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
  • renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked

urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

258
Q

Urgent referral for haematuria?

A

Urgent referral (i.e. within 2 weeks)

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
- non-visible haematuria AND either dysuria or a raised white cell count on a blood test

259
Q

Non-urgent referral for haematuria?

A

Non-urgent referral

Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

Since the investigation (or not) of non-visible haematuria is such as a common dilemma a number of guidelines have been published. They generally agree with NICE guidance, of note:
patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care

260
Q

Referral to urology or renal?

A

Haematuria >40 -=urology

Haematuria <40 = renal

261
Q

Causes of hypokalaemia?

A
  1. ) Increased potassium loss:
    - Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
    - GI losses: diarrhoea, vomiting, ileostomy
    - Renal causes: dialysis
    - Endocrine disorders: hyperaldosteronism, Cushing’s syndrome
  2. ) Trans-cellular shift
    - Insulin/glucose therapy
    - Salbutamol
    - Theophylline
    - Metabolic alkalosis
  3. ) Decreased potassium intake
  4. ) Magnesium depletion (associated with increased potassium loss)
262
Q

Management of hypokalaemia?

A
  • Mild to moderate hypokalaemia 2.5 - 3.4 mmol/l can be treated with oral potassium provided the patient is not symptomatic and there are no ECG changes.
  • Severe hypokalaemia (<2.5mmol/l) or symptomatic hypokalaemia should be managed with IV replacement. The patient should be managed in an area where cardiac monitoring can take place. If there are no contraindications to fluid therapy (e.g. volume overload, heart failure) potassium should be diluted to low concentrations as higher concentrations can be phlebitic. The infusion rate should not exceed 20mmol/hr. In this case, 3 bags of 1L 0.9% Saline with 40mmol KCL over 24hrs is the correct answer.
263
Q

Differences between ATN and prerenal uraemia?

A

Pre-renal uraemia

  • <20 urinary sodium
  • > 500 urine osmolality
  • <1% sodium excretion
  • Good response to fluid challenge
  • Raised urea/creatinine ratio

In pre-renal = kidney’s hold on to sodium to preserve volume.

Acute tubular necrosis (damage to tubular cells due to prolonged ischaemia or toxins).
- Kidneys can no longer concentrate urine or train sodium.

  • > 40 mmol/L
  • <350 mOsm/kg
  • > 1%
  • Poor response to fluid
  • Normal serum urea/creatinine ratio
  • fractional urea >35%
264
Q

Diabetes insipidus? nephrogenic

A

Kidneys inability to respond to vasopressin.
Give the patient thiazide diuretic works as polyuria is a symptom of the disorder.

Causes of nephrogenic DI
> genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
> electrolytes: hypercalcaemia, hypokalaemia
> drugs: demeclocycline, lithium
> tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

Investigation

  • High plasma osmolality, low urine osmolality
  • a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  • water deprivation test

Management

  • nephrogenic diabetes insipidus: thiazides, low salt/protein diet
  • central diabetes insipidus can be treated with desmopressin
265
Q

Causes of cranial DI?

A 
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
histiocytosis X
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)
haemochromatosis
266
Q

How long does it take for a fistula to be fully functioning after surgery?

A

6-8 weeks. The AV fistula causes arterialisation of the vein due to the high pressure of the artery. The shunted blood flow causes an increase in growth factors and further hypertrophy of the venous wall. It takes 6 to 8 weeks post-surgery to allow full maturation to take place where the fistula can withstand a dialysis flow rate of 500ml/min.

Preferred method of access for haemodialysis.

267
Q

Complications of AV fistula?

A
  • infection
  • thrombosis = may be detected by the absence of a bruit
  • stenosis = may present with acute limb pain
  • steal syndrome
268
Q

Erythropoietin use and SE?

A

Haematopoeitic growth factor that stimulates the production of erythrocytes.

Treats CKD associated anaemia and improves exercise tolerance. DOes not improve renal function.

Secreted by kidney in response to cellular hypoxia. Used to treat anaemia associated with CKD.

SE:

  • accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
  • bone aches
  • flu-like symptoms = skin rashes, urticaria
  • pure red cell aplasia* (due to antibodies against erythropoietin)
  • raised PCV increases risk of thrombosis (e.g. Fistula)
  • iron deficiency 2nd to increased erythropoiesis
269
Q

Reasons why patients fail to respond to erythropoietin?

A
  • iron deficiency
  • inadequate dose
  • concurrent infection/inflammation
  • hyperparathyroid bone disease
  • aluminium toxicity
270
Q

Metabolic acidosis?

A

Normal anion gap = hyperchloraemic metabolic acidosis

Normal anion gap = 8-14.
Causes of normal anion gap acidosis: [ABCD]
- Addison’s disease - this is because loss of aldosterone function, causing less sodium but increased potassium. The acidosis is also due to loss of aldosterone function, more Na excreted and more H+ retention.
- Bicarbonate loss (GI): diarrhoea, ureterosigmostomy, fistula.
- Chloride (ammonium) injection
- Drugs e.g acetazolamide
- Renal tubular acidosis

Raised anion gap

  • Lactate: shock, hypoxia, sepsis or tissue ischaemia.
  • ketones: diabetic ketoacidosis, alcohol
  • Urate: Renal failure
  • Acid poisoning: salicylate, methanol.

For salicylate poisoning - common presentation presenting with nausea, vomiting, tinnitus and headache. Hyperventilation and secondary resp alkalosis.
Over 24hrs, progresses to a metabolic acidosis and hypokalemia.

Management - if recent give activated charcoal. Significant overdose may require alkalinisation with IV sodium bicarb.

271
Q

Metabolic alkalosis?

A 
vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
diuretics
liquorice, carbenoxolone
hypokalaemia
primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
congenital adrenal hyperplasia
272
Q

Respiratory acidosis

A

Respiratory acidosis may be caused by a number of conditions:

  • COPD
  • decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
  • sedative drugs: benzodiazepines, opiate overdose
273
Q

Respiratory alkalosis?

A 
Common causes
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
274
Q

ADPKD?

  • Features
  • extra-renal manifestations
  • Ix
  • screening/ diagnostic criteria
  • mx
A

Features

  • HTN
  • Recurrent UTIs
  • Abdo pain
  • Renal stones
  • Haematuria
  • CKD

Extra-renal manifestation

  • Liver cysts (70%) - leads to hepatomegaly.
  • Berry aneurysms (8%)
  • CVS system: Mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilatation, aortic dissection
  • Cysts in other organs, pancreas, spleen and rarely thyroid, oesophagus, ovary

Ultrasound is the screening test for adult PKD***

Genes are PKD1 and PKD2 which code for polycystin-1 and polycystin 2.

Screening investigation is abdo ultrasound.

US Diagnostic criteria

  • 2 cyst, unilateral or bilateral if age <30
  • 2 cysts in both kidneys if aged 30-59 yrs
  • 4 cysts in both kidneys if aged >60

Management

  • Tolvaptan may be an option.
  • CKD stage 2 or 3.
  • Evidence of rapidly progressing disease.
275
Q

Nephrotoxicity due to contrast media?

A

25% increases in creatinine occurring within 3 days of the intravascular administration of contrast media.

RF:

  • Known renal impairment (esp diabetic nephropathy)
  • Age >70
  • Dehydration
  • Cardiac failure
  • Use of nephrotoxic drugs
276
Q

Fibromuscular dysplasia?

A

Consider in a young female patient who develops AKI after initiation of an ACEi.

In older patient suspect atherosclerosis of renal arteries.

Fibromuscular dysplasia - proliferation of cells in the wall of arteries causing the vessels to bulge or narrow and commonly affects women. Classic description includes string of beads appearance.

Feature

  • HTN, CKD or acute renal failure secnondary to ACEi.
  • Flash pulmonary oedema.
277
Q

Drugs to stop in an AKI?

A

ACEi reduce GFR by causing vasodilation of efferent arteriole and reducing glomerular filtration.

Diuretics have a nephrotoxic effect as they prevent fluid being reabsorbed into capillaries.

Metformin is renally cleared and would risk causing a lactic acidosis.

Low dose aspirin is safe.

278
Q

Hereditary haemochromatosis and cranial diabetes insipidus?

A

Lethargy + arthraglia is a common presentation of HH. Cause of central insipidus.

AR so skips generations. Grandmother has bloodletting.

279
Q

Renal colic with patients with bilateral urinary tract obstruction?

A

Check U+E to look for underlying AKI.

Both renal tracts may be compromised so important to look at creatinine to look for post-renal AKI.

280
Q

Renal cell carcinoma?

A

Renal cell carcinoma

  • Haematuria, loin pain, abdo mass.
  • Pyrexia or unknown origin
  • Left varicocele - due to compression of left testicular vein (or right)
  • Endocrine effects - EPO secretion (polycythaemia), PTH hormone (hypercalcaemia), renin, ACTH
  • 25% have mets at presentation.
281
Q

Renal artery stenosis vs Bilateral adrenal hyperplasia?

A

Primary and secondary aldosteronism can be differentiated by looking at the renin levels.

If renin is high then a secondary cause is more likely - renal artery stenosis.

282
Q

Hyaline casts

A
  • Patients on loop diuretics
  • after exercise
  • during fever
283
Q

Causes for persistent non-visible haematuria?

A
  • cancer (bladder - frank haematuria in >60Y is bladder cancer until proven otherwise, renal, prostate)
  • strones
  • BPH
  • prostatitis
  • urethritis - e.g. Chlamydia
  • renal causes - IgA nephropathy, thin basement membrane disease
284
Q

Causes of transient/ spurious microscopic/ non-visible haematuria?

A
  • UTI
  • menstruation
  • vigorous exercise (normally settles after ~3d)
  • sexual intercourse
285
Q

Causes of spurious (red/orange) urine - blood not on dipstick?

A
  • Foods = beetroot, rhubarb

- Drugs = rifampicin, doxorubicin

286
Q

How to differentiate acute from chronic kidney injury?

A

Check calcium
if hypocalcaemia - more likely to be chronic

Renal failure -> reduced metabolised 1,25OH-2D = reduced calcium reabsorption in kidneys

287
Q

Causes of polyuria?

A

Common:

  • diuretics, caffeine, alcohol
  • DM
  • Lithium
  • Heart failure

Infrequent:

  • Hypercalcaemia
  • hyperthyroidism

Rare:

  • chronic renal failure
  • primary polydipsia
  • hypokalaemia

Very rare:
- diabetes insipidus

288
Q

Fluid maintenance for children?

A

FIRST 10kg = 100ml/kg
SECOND 10kg = 50ml/kg
EVERY OTHER kg = 20ml/kg

289
Q

Imaging of choice for reflux nephropathy?

A

Micturating cystography

290
Q

What is reflux nephropathy?

A
  • caused by recurrent UTI in young children
  • urine flows backwards from bladder towards kidneys
  • over time causes scarring
  • renal scar -> increased renin -> HTN
  • strong genetic disposition

Ix = micturating cystogram

291
Q

What is dialysis disequilibrium syndrome?

A

A rare but serious complication of haemodialysis -> cerebral oedema (mechanism unclear)

Features = headache, drowsiness

292
Q

Stages of AKI?

A

According to serum creatinine change ± production of urine

1 = Cr rise by 1.5-1.9x baseline = urine <0.5ml/kg/hr for >6h
2 = Cr rise <3x baseline = urine <0.5ml/kg/hr for >12hr
3 = Cr rise >3x baseline or >354 = urine <0.3ml/kg/hr for >24h or anuric for 12h

Pt deemed in stage 3 AKI if commenced on RRT irrespective of urine/ creatinine.

Imperial Medicine Year 3 (35 decks)

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