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Renal Medicine Flashcards

1
Q

How do you tell the difference between AKI and dehydration on bloods?

A

AKI - creatinine will be much higher than urea
Dehydration - urea will be much higher than creatinine

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2
Q

How do you tell the difference between AKI and CKD?

A

CKD patients will have bilateral small kidneys except those with:
- ADPKD
- Early diabetic nephropathy
- Amyloidosis
- HIV nephropathy

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3
Q

What is a common cause of fragility fractures?

A

CKD induced secondary hyperparathyroidism

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4
Q

What is a common cause of drug-induced AKI?

A

Acute interstitial nephritis

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5
Q

What drugs cause acute interstitial nephritis?

A
  • Antibiotics including penicillin, rifampicin
  • NSAIDs
  • Allopurinol
  • Furosemide
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6
Q

Causes of acute interstitial nephritis?

A

drugs; systemic disease eg. SLE, scaroidosis, Sjogrens; infection eg. Hanta virus, staphlococci

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7
Q

What does histology show for acute interstitial nephritis?

A

marked interstitial oedema and interstitial infiltrate in connective tissue between renal tubules

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8
Q

Acute interstital nephritis Ix?

A

sterile pyuria and white cell casts

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9
Q

How are diabetic patients screened for diabetic nephropathy?

A

albumin:creatinine ratio (ACR) in early morning specimens

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10
Q

What are the ECG changes of hypokalaemia?

A

U waves
T wave flattening
ST segment changes

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11
Q

What is the most common cause of nephrotic syndrome with malignancy?

A

Membranous nephropathy

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12
Q

What would biopsy show for someone with membranous nephropathy?

A

subepithelial immune complex deposits

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13
Q

What drugs should be withheld with AKi?

A
  • Diuretics
  • Aminoglycosides (gentamicin) and ACE/ARB
  • Metformin
  • NSAIDs
    DAMN AKI
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14
Q

What drug is most commonly used to decrease phosphate levels?

A

Sevelamer - a non calcium based binder which binds to dietary phosphate and prevents it being absorbed

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15
Q

How can stages 1 and 2 of CKD be diagnosed?

A

GFR range PLUS if kidney tests must be abnormal

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16
Q

What are causes of focal segmental gomerulosclerosis?

A

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

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17
Q

What is the risk of using 0.9% NaCl fluid therpay in patients who need large volumes?

A

Hyperchloremic metabolic acidosis

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18
Q

What can alcohol bingeing lead to?

A

ADH suppression in the posterior pituitary leading to polyuria as well as hypernatremia

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19
Q

What is the classic triad for HUS?

A
  • AKI
  • Haemolytic anaemia
  • Thrombocytopenia
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20
Q

What organism typically causes HUS?

A

E coli

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21
Q

What medication should be used as an alternative to spironolactone for patients with gynaecomastia?

A

Eplerenone

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22
Q

How does membranous glomerulonephritis present on histology?

A

basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2

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23
Q

What is hyperacute transplant rejection?

A

Rejection within minutes to hours

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24
Q

What is the cause of hyper acute transplant rejection?

A

pre-existing antibodies against ABO or HLA antigens

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25
Q

What type of hypersensitivity reaction of hyper acute transplant rejection?

A

Type 2

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26
Q

Why does rhabdomyolysis cause renal failure?

A

Tubular cell necrosis

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27
Q

What is the prognosis for HSP?

A

Full renal recovery

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28
Q

What is the diuretic of choice in ascites?

A

Spironolactone

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29
Q

When is a renal biopsy indicated for those with minimal change disease?

A

If the response to steroids is poor

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30
Q

What HLA subtype is the most important for transplants?

A

HLA-DR

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31
Q

What are the side effects of EPO?

A
  • Accelerated hypertension
  • Bone aches
  • Flu like symptoms
  • Skin rash
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32
Q

What medication can be used for recurrence of hyperkalaemia?

A

Calcium resonium

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33
Q

How does acute tubular necrosis respond to fluid challenge?

A

Poorly

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34
Q

What is prerenal uraemia?

A

Where the kidneys hold onto sodium to preserve volume

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35
Q

Prerenal uraemia vs ATN?

A
  • Prerenal responds well to fluid challenge
  • Urine osmlaitity will be raised
  • Urine sodium will be low
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36
Q

Why should metformin be stopped in AKI?

A

Due to increased risk of toxicity

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37
Q

How does anti-GBM disease present?

A
  • Haemoptysis
  • AKI/proteinuria/haematuria
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38
Q

What is the most common cause of refractory HTN?

A

Renal artery stenosis secondary to atherosclerosis

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39
Q

eGFR is an inaccurate in which patients?

A

Those with extreme muscle mass

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40
Q

What investigation is needed for patients with AKI of unknown aetiology?

A

US

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41
Q

Patients with HSP require what to monitor for renal involvement?

A

BP and urinalysis

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42
Q

Patient presents with grey/brown tinge to the skin along with history of CKD?

A

Urea build up within the blood

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43
Q

Management of lupus nephritis?

A

Cyclophosphamide and methylprednisolone

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44
Q

What are the indications for acute haemodyialysis?

A

AEIOU
Acidosis
Electrolyte disturbance e.g. hyperkalaemia
Intoxication i.e. drug overdose
Oedema
Uraemia symptoms e.g encephalopathy

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45
Q

What is causes of sterile pyuria (white cells in urine with negative culture)

A
  • Renal TB
  • Partially treated UTI
  • Drugs including NSAIDs, Abx
  • Urinary tract stones
  • Papillary necrosis
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46
Q

Schisotchtes on blood film?

A

Microangiopathic haemolytic anaemia -> HUS

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47
Q

Epithelial crescents in the glomeruli?

A

Rapidly progressing glomerulonephritis

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48
Q

What investigation should be done with all patients with AKI of unknown aetiology?

A

Renal US within 24 hours

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49
Q

Management of low urine output post surgery?

A

Fluid challenge - give bolus of NaCl

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50
Q

How should severe hyperkalaemia be managed?

A

Urgent discussion with nephrology/critical care

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51
Q

Pulmonary oedema with AKI needs what?

A

Haemodialysis

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52
Q

Cause of normal anion gap metabolic acidosis

A

Renal tubular acidosis

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53
Q

Causes of CKD

A

DM, Hypertension , glomerulonephritis, renovascular disease,
pyelonephritis, polycystic kidney disease, obstructive uropathy.

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54
Q

Signs of CKD on examination

A

purpura, bruising, brown discolouration of
nails, evidence of excoriation, peripheral oedema, hypertension,
pericardial rub, evidence o f pleural effusions, proximal myopathy,evidence of preparation for renal replacement therapy

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55
Q

How does haemodialysis work?

A

Blood and dialysis fluid flow either side of a semipermeable
membrane, molecules diffuse down their concentration gradients, plasma biochemistry changes to become more like the dialysis fluid.

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56
Q

What is the management of renal stones?

A

<5mm - wait and watch if asymptomatic
5mm - 10mm - Shockwave lithotripsy
10mm-20mm - Lithrotripsy / Ureteroscopy
>20mm - percutaneous nephrolithotomy

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57
Q

What is the management of ureteric stones?

A

If <10mm - shockwave lithotripsy +/- alpha blockers
If >10mm - Ureteroscopy

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58
Q

Which chromosome is affected in ADPKD?

A

16

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59
Q

Full house immunoflueoresence pattern on renal biopsy?

A

Lupus nephritis

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60
Q

How would Goodpastures present on biopsy?

A

Crescent formation and linear deposition of IgG antibodies across the glomerular basement membrane (anti-GBM antibodies)

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61
Q

What are C/I to renal biopsy?

A
  • HTN
  • CKD wit small kidneys
  • Abnormal coagulation studies
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62
Q

Dietary advice for nephrotic syndrome

A

Restrict salt intake, normal protein intake

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63
Q

AKI + Haemoptysis + Lung changes?

A

Think Goodpastures

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64
Q

What are causes of rhabdomyolysis?

A
  • Prolonged immobilisation
  • Crush injuries
  • Seizures
  • Post surgery
  • Medications such as statins
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65
Q

Period of hypotension followed by renal impairment with urinary casts

A

Acute tubular necrosis

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66
Q

How to calculate anion gap?

A

(sodium + potassium) - (bicarbonate + chloride)
Normal = 8-14

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67
Q

What are causes of normal anion gap metabolic acidosis?

A
  • Diarrhoea
  • Renal tubular acidosis
  • Addisons
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68
Q

What are causes of raised anion gap metabolic acidosis?

A
  • Shock
  • DKA/Alcohol
  • Acid poisoning e.g salicylates
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69
Q

How to work out pre, renal and post renal cause of AKI?

A

Urea / (creatinine(umol)/1000
Pre renal - >100
Renal/Normal - 40 - 100
Post renal - <40

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70
Q

What is in indication for chronic kidney disease over acute?

A

Hypocalcaemia

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71
Q

Acute interstitial nephritis vs acute tubular necrosis?

A

AIN is an inflammatory process so white cells will be in the urine whereas ATN is not therefore no white cells in urine

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72
Q

Tubulointerstitial nephritis with ueveitis?

A

usually young females; fever, weight loss and painful red eyes; urinalysis= +ve leukocytes and protein

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73
Q

Diarrhoea causes what?

A

Hypokalaemia metabolic acidosis

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74
Q

Eosinophilic casts are an indication of what?

A

Acute interstitial nephritis

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75
Q

What does proteinuria indicate in the context of AKI?

A

Intrinsic renal AKI cause

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76
Q

Anyone with severe hyperkalaemia / ECG changes for hyperkalaemia?

A

IV 10mls of 10% Calcium Gluconate
Insulin/Dextrose

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77
Q

What must be assessed in someone with bilateral calculi?

A

Renal function

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78
Q

HIV nephropathy causes what?

A

Focal segmental glomerulosclerosis -> causes nephrotic syndrome

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79
Q

Rapidly progressing glomerulonephritis is associated with what?

A

Goodpasture’s
GPA

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80
Q

What can invalidate an EGR?

A

Eating red meat

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81
Q

AKI values

A

Creatinine
Stage 1 - 1.5-1.9x baseline / Increased by 26 umol+ in 48hrs / urine output <0.5mls/kg >6 hours

Stage 2 - 2 - 2.9x baseline / urine output <0.5mls/kg >12 hours

Stage 3 - 3x baseline / urine output <0.3mls/kg >24 hours

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82
Q

What are the 4 variables in the MDRD equation to work out estimated EGFR in patients with CKD?

A

Creatinine
Age
Gender
Ethnicity

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83
Q

Addisons causes what?

A

Hyperkalaemic metabolic acidosis

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84
Q

Patients with CKD and ACR >30 should be started on what?

A

ACE + Statin

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85
Q

Hereditary haemochromatosis can cause what?

A

Cranial diabetes insipidus

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86
Q

fever + rash + renal dysfunction

A

Acute interstitial nephritis

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87
Q

Urine osmolality >500 + urine sodium < 20

A

Pre renal uraemia

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88
Q

Urine osmolality < 350 + urine sodium > 40

A

Acute tubular necrosis

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89
Q

Brown granular casts are a sign of what?

A

Acute tubular necrosis

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90
Q

What is the most common viral infection in solid organ transplant patients?

A

CMV

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91
Q

What is the treatment for acute clot retention in urethra?

A

Continuous bladder irrigation via a 3 way urethral catheter

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92
Q

What is a drug cause of nephrogenic diabetes insipidus?

A

Lithium - desensitizes the kidneys ability to respond to ADH in the collecting ducts

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93
Q

Granulomatosis with polyangiitis is associated with what?

A

Rapidly progressing glomerulonephritis

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94
Q

Young female patient with AKI after starting ACE?

A

Fibromuscular dysplasia

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95
Q

What is the daily maintenance fluids requirement?

A

25-30ml/kg/day

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96
Q

Haemodialysis can cause what?

A

A falsely low HbA1c

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97
Q

What is monitoring for ACE inhibitors?

A

Increase in creatinine up to 30% is acceptable
If K+ > 6 - stop ACE and switch to alternative

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98
Q

Why do you get kidney stones in PKD?

A

Cysts block collecting ducts leading to urinary stasis and stone formation

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99
Q

What part of nephron does RCC affect?

A

PCT

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100
Q

What are risk factors for RCC?

A
  • Smoking
  • Male
  • Increasing age
  • HTN
  • FH
  • Obesity
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101
Q

Symptoms of chronic renal failure?

A
  • Anaemia
  • Fatigue
  • Vomiting
  • Bone pain
  • SOB
  • Fluid overload
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102
Q

Complications of haemodialysis?

A
  • Hypotension
  • Thrombosis
  • Infection
  • Blockage
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103
Q

Complication of peritoneal dialysis?

A
  • Peritonitis
  • Obesity
  • Hernias
  • Loss of membrane function
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104
Q

Where does sodium reabsorption take place?

A

PCT

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105
Q

Anti-GBM has antibody against which type of collagen?

A

Type 4

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106
Q

What kind of reaction is IgA nephropathy?

A

Type 3

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107
Q

What can be given for calcium stones due to hypercalcicuria?

A
  • Potassium citrate
  • Thiazide diuretics (increase distal tubular reabsorption)
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108
Q

Most common cause of death in patients with CKD on harm-dialysis?

A

IHD

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109
Q

What is a complication UTI?

A

UTI in the presence of an abnormal urinary tract

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110
Q

What is the pathophysiology of IgA nephropathy?

A

IgA immune complex deposit in the mesangial cells

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111
Q

haemoptysis + haematuria

A

Think Good pastures

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112
Q

Sickness, headache, vomiting and drowsiness after haemodialysis?

A

Disequilibrium syndrome caused by rapid changes in plasma osmolality and cerebral oedema

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113
Q

Causes of raised CK?

A
  • Burns
  • Myositis
  • Seizures
  • Influenza
  • Duchennes muscular dystrophy
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114
Q

What gene is responsible for PKD?

A

PKD1

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115
Q

What are complications of PKD?

A
  • Renal failure
  • HTN
  • Renal calculi
  • Cyst infection
  • Hepatic cysts
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116
Q

What is screening of ADKPD for relatives?

A

Abdo US scan for first degree relatives

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117
Q

subepithelial ‘humps’ on electron microscopy

A

Post strep glomerulonephritis

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118
Q

A high urea can indicate what gastro pathology?

A

Upper GI bleed

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119
Q

What is a classic sign of renal artery stenosis?

A
  • Worsening renal function after starting an ACE
  • Refractory HTN
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120
Q

Which UTI medication can cause rise in creatinine?

A

Trimethoprim

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121
Q

What is a good marker prognosis in IgA nephropathy?

A

Macroscopic haematuria

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122
Q

Muddy brown casts

A

ATN

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123
Q

rash, eosinophilia and acute renal impairment

A

AIN

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124
Q

Most common component of renal stones?

A

Calcium oxalate

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125
Q

What is the most common cause of AKI?

A

Pre-renal causes

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126
Q

Management of acute upper urinary tract obstruction

A

Nephrostomy

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127
Q

fever, arthralgia, rash and eosinophilia in a setting of decreased renal function; HTN

A

Acute interstitial nephritis

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128
Q

When can a diagnosis of CKD be made?

A

When EGFR <60 on 2 tests which are 3 months apart

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129
Q

UTI + haematuria?

A

Must send MSU

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130
Q

Trimethoprim can cause a falsely low what?

A

eGFR

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131
Q

thickened glomerular basement membrane with IgG and C3 subepithelial deposits

A

Membranous nephropathy

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132
Q

Treatment of HTN in someone with IgA nephropathy?

A

ACE inhibitors

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133
Q

Headache and tremor can be signs of what?

A

Calcineurin inhibitors (tacrolimus) toxicity

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134
Q

Why are patients with nephrotic syndrome susceptible to clots?

A

Loss of antithrombin III and plasminogen via the kidneys

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135
Q

Periureteric fat stranding on CT KUB can indicate what?

A

Spontaneously passed calculus

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136
Q

Stag horn calculi are made of what?

A

Struvite (magnesium ammonium phosphate)

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137
Q

What is a vitamin D supplement which is used in end stage renal disease?

A

Alfacalcidol -> does not require activation in the kidneys

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138
Q

anti-MPO antibodies are indicative of what?

A

Microscopic polyangiitis

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139
Q

What are the types of renal tubular acidosis?

A

1 - inability to generate acid urine causing hypokalaemia (causes include RA, Sjogrens, SLE)
2 - decreased bicarb resorption causing hypokalaemia (causes include Wilsons)
4 - reduced aldosterone causing hyperkalaemia (causes include diabetes)

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140
Q

Crescent formation on biopsy with rapid decrease in EGFR?

A

Membranoproliferative glomerulonephritis

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141
Q

When is acute vs chronic rejection following transplant?

A

Acute - within first 6 months
Chronic - >6 months

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142
Q

Gold standard imaging for suspected renal cancer?

A

CT Abdo with contrast

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143
Q

Abx for UTI in egfr <45

A

Trimethoprim

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144
Q

What is the most common complication of haemodialysis?

A

Dialysis-induced hypotension

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145
Q

Worsening renal function with dark brown urine

A

ATN

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146
Q

Gentamicin can cause what?

A

ATN

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147
Q

What is calcitriol?

A

Active form of Vit D

148
Q

What is AKI?

A

spectrum of injury to kidneys that can result from a number of causes that may co-exist

149
Q

AKI is characterised by a sudden decline in…..

A

renal excretory function over hrs or days that can result in failure to maintain fluid, electrolyte and acid-base balance

150
Q

What is diagnosis of AKI and its staging based on?

A

Acute changes in serum creatinine and/or a reduction in urine output (oliguria)

151
Q

what is the word for a reduction in urine output?

152
Q

Causes of AKI?

A

pre-renal
intra-renal
post-renal

153
Q

Pre-renal causes of AKI?

A

Due to reduced perfusion of the kidneys and/or hypotension

154
Q

Intra-renal (intrinsic) causes of AKI?

A

Due to structural damage to the kidney

155
Q

Post-renal causes of AKI?

A

Due to acute urinary tract obstruction

156
Q

What people are at risk of AKI?

A
  • > 65yrs
  • Hx of AKI/urological obstruction
  • Hx CKD, HF, liver disease or DM
  • if reliant on others for fluid intake
  • pts with sepsis, hypovolaemia, hypotension, dehydration, reduced fluid intake, oliguria
  • specific drugs
157
Q

What are Cx of AKI? (depend on AKI severity and duration)

A

hyperkalaemia, metabolic acidosis, fluid overload, uraemia, CKD

158
Q

When should AKI be suspected?

A

acute illness with D&V; acute illness with AKI RFs; illness & CKD/urological disease; AKI warning test result based on creatinine change.

159
Q

CP of AKI?

A

N, V, D or suspected dehydration, reduced urine output or changes to urine colour, confusion, fatigue, drowsiness

160
Q

When can a diagnosis of AKI be made?

A

if one of the following:
1) A rise in serum creatinine of 26 micromol/L or greater within 48 hours

2) A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days

3) A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours.

161
Q

A diagnosis of AKI can be made if there is a rise in serum creatinine of … within 48hrs

A

26 micromol/L or greater

162
Q

A diagnosis of AKI can be made if there is a ….% or greater rise in serum creatinine in past 7d

163
Q

A diagnosis of AKI can be made if there is a fall in urine output to less than…. for more than 6hrs?

A

0.5mL/kg/hr

164
Q

How to assess a person with AKI?

A
  • fluid intake, UO, meds
  • volume status and signs of urological obstruction
  • renal function & serum potassium.
  • urine dip: underlying cause and renal disease
  • U&Es= Na, K, urea, creatinine
165
Q

When to urgently admit someone to hospital or same day referral with AKI?

A

if AKI stage 3, severe cause or Cx or no identifiable cause

166
Q

Mx of AKI

A

TUC: advise fluid balance, temporarily stop/reduce specific meds; monitor serum creatinine regularly

167
Q

What follow up should be done for a pt with AKI?

A
  • referral to nephrology if CKD
  • monitor renal function regularly= development or progression of CKD
  • review need for specific meds
168
Q

What can cause a false positive result in creatinine in pt with suspected AKI?

A

recently treated with trimethoprim or recently been pregnant

169
Q

AKI: urine dip with negaitive urinalysis?

A

indicates pre-renal or drug cause

170
Q

AKI what to analyse on urine dip?

A

blood, protein, leucocytes, nitrites and glucose

171
Q

AKI: urine dip with +ve protien and blood?

A

may suggest glomerular disease if no evidence of UTI or trauma due to catherisation

172
Q

AKI: urine dip showing increased white cells?

A

non-specific but typically infection (common) or interstitial nephritis

173
Q

Examples of pre-renal causes of AKI?

A
  • hypovolaemia 2 to D/V
  • renal artery stenosis
174
Q

Examples of intrinsic causes of AKI?

A
  • drugs
  • glomerulonephritis
  • acute tubular necrosis (ATN)
    acute interstitial nephritis (AIN), respectively
  • rhabdomyolysis
  • tumour lysis syndrome
175
Q

Examples of post-renal causes of AKI?

A
  • kidney stone in ureter or bladder
  • BPH
  • external compression of the ureter
176
Q

When is renal replacement therapy eg. haemodialysis used for AKI?

A

When not responding to Mx of Cx eg. hyperkalaemia, pulmonary oedema, acidosis or uraemia (eg. pericarditis, encephalopathy)

177
Q

What do the kidneys do in prerenal uraemia?

A

hold on to sodium to preserve volume

178
Q

What is autosomal dominant polycystic kidney disease (ADPKD)?

A

Inherited cause of kidney disease, 2 types: PKD1 and PKD2.

179
Q

PKD1 codes for what? Chromosome?

A

Codes for polycystin-1
Chromosome 16.

180
Q

PKD2 codes for what? Chromosome?

A

Polycystin-2.
Chromosome 4.

181
Q

ADPKD 1 vs ADPKD 2?

A

T1 more common and presents with renal failure earlier.

182
Q

Screening Ix for relatives for ADPKD?

183
Q

USS diagnostic criteria (in pts with +ve family history for ADPKD)?

A
  • two cysts, unilateral or bilateral, if aged < 30 years
  • two cysts in both kidneys if aged 30-59 years
  • four cysts in both kidneys if aged > 60 years
184
Q

Mx for ADPKD?

A

Tolvaptan to slow progression of cyst development and renal insufficiency

185
Q

When is tolvaptan used in ADPKD?

A
  • they have chronic kidney disease stage 2 or 3 at the start of treatment
  • there is evidence of rapidly progressing disease and
  • the company provides it with the discount agreed in the patient access scheme.
186
Q

Tolvaptan drug classification?

A

vasopressin receptor 2 antagonist

187
Q

Definition of CKD?

A

Abnormalities in kidney structure or function (or both) present for >3m with associated health implications.

188
Q

CKD should be diagnosed in people with what present for min 3m?

A
  • GFR <60 mL/min/1.73 m2 on at least two occasions separated by a period of at least 90 days (with or without markers of kidney damage).
  • Markers of kidney damage such as urinary albumin:creatinine ratio (ACR) >3 mg/mmol, urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology, structural abnormalities detected by imaging, and a history of kidney transplantation.
189
Q

CKD should be diagnosed in people if the GFR is less than… on at least 2 occasions separated by a period of at least 90 days (with or without markers of kidney damage)

A

<60mL/min/1.73m2

190
Q

CKD should be diagnosed in people with markers of kidney damage present for min of 3m. What are some markers of kidney damage?

A
  • urinary albumin:creatinine ratio (AR) >3mg/mmol
  • urine sediment abnorm
  • electrolyte & other abnorm due to tubular disorders
  • abnorm histology
  • structural abnorm detected. by imaging
  • Hx of kidney transplant
191
Q

CKD is classified using what?

A

eGFR and ACR

192
Q

Causes and RFs for CKD and its progression?

A

HTN, DM, CVD, AKI, nephrotoxic drugs, obstructive uropathy

193
Q

Cx of CKD (increases with disease progression)

A

AKI, HTN, CVD, renal anaemia, renal mineral and bone disorder, end-stage renal disease (ESRD), mortality

194
Q

CKD should be suspected in people with what?

A
  • RFs
  • CP
  • incidental finding of raised serum creatinine and/or eGFR of <60 or other markers of kidney damage
195
Q

Inital Ix if CKD is suspected?

A
  • serum creatinine and eGFR
  • early morning measure ACR
  • urine dip ?haematuria
  • BMI, BP, HbA1c, lip profile for ?cvd RFs
  • renal tract USS if indicated
196
Q

CKD: indications for renal tract USS?

A

FHx polycystic kidney disease, suspected urinary tract stones or obstruction

197
Q

If CKD is confirmed, what monitoring for disease progression should be done?

A
  • eGFR and urine ACR
  • FBC: exclude renal anaemia
  • serum Ca, K, Vit D, PTH : exclude renal metabolic and bone disorders
    (depends of severity of CKD)
198
Q

When should you refer to nephrology in pts with CKD?

A
  • 5yr risk needing renal replacement therapy >5%
  • accelerated progression
  • ACR 70 or more unless have DM
  • ACR 30 or more + persistent haematuria (after excluding UTI)
  • uncontrolled HTN
  • rare or genetic cause
  • suspected renal artery stenosis
  • suspected Cx of CKD
199
Q

How to measure ACR?

A

early morning urine sample

200
Q

Mx in primary care for CKD

A
  • manage RFs
  • offer ARB
  • offer atorvastatatin 20mg and antiplatelet
  • consider SGLT-2 inhibitor eg. dapagliflozin (give to everyone with DM)
201
Q

Patients with CKD must be immunised with what vaccines?

A

Influenza and pneumococcal disease

202
Q

CP of CKD

A
  • Lethergy, itch, breathlessness, cramps (worse at night), sleep disturbance, bone pain, poor appetitie, weight loss, N&V, taste disturbance (end stage).
  • Polyuria, nocturia.
  • Cachexia, cognitive impairment.
  • dehydratation/hypovolaemia
  • dyspnoea
  • frothy urine
  • flank mass (cysts/ ?ca)
  • pallor (renal anaemia)
  • palpable distended bladder
  • ammonia-like smell of breath (end stage)
  • peripheral oedema
203
Q

CKD: what may frothy urine suggest?

A

Proteinuria

204
Q

CKD: what may palpable distended bladder suggest?

A

obstructive uropathy

205
Q

CKD: what may peripheral oedema be due to?

A

renal sodium retention, hypoalbuminaemia or HF

206
Q

Unexplained chronic renal impairment is an indicator for what condition?

207
Q

What is associated with increased risk of adverse outcomes in CKD?

A

Increased ACR or
Decreased GFR or
Increased ACR and Decreased GFR in combination

208
Q

Nephrotoxic drugs?

A

NSAIDs
PPI
ACE in
ARB
bisphosphonates
diuretics
lithim
methotrexate
aminoglycosides
ciclosporin

209
Q

Type of anaemia most common in patients with GFR <35?

A

Reduced erythripoietin levels- normochromic normocytic anaemia

210
Q

Causes of anaemia in renal failure?

A
  • reduced erythopoietin levels
  • reduced absorption of iron
  • reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • anorexia/nause due to uraemia
  • reduced cell survival (esp in haemodialysis)
  • blood loss due to capillary fragility and poor platelet function
  • stress ulceration leading to chronic blood loss
211
Q

Anaemia in CKD predisposes to the development of what?

A

L ventricular hypertrophy

212
Q

CKS is associated with a decrease in production of what?

A

Erythropoietin- hormone produced by kidneys that stimulates erythropoiesis in bone marrow. So less RBC production.

213
Q

2 reasons why there can be reduced iron absorption in CKD?

A
  • hepcidin levels increased due to inflamm and reduced renal clearance, leads to decreased iron absorption from gut
  • metabolic acidosis (common in CKD) can ihibit converson of ferric iron to absorbable form ferrous iron in duodenum
214
Q

Target Hb in pt with CKD?

215
Q

What should be done prior to administration of erythropoiesis-stimulating agents (ESA)?

A

Determination and optimisation of iron status

216
Q

What patients with CKD should be offered oral ion?

A

Pts not on ESAs or haemodialysis. If Hb levels not reached withinin 3m, switch to IV iron

217
Q

What patients with CKD generally require IV iron?

A

Pts on ESAs or haemodialysis

218
Q

When should ESAs be used in pts with CKD?

A

Eg. erythropoietin and darbepoetin. In those who are ‘likely to benefit in terms of QOL and physical function’

219
Q

Basic problems in CKD that can lead to bone disease?

A
  • low vit D
  • high phosphate
  • low Ca
  • secondary hyperparathyroidism (low Ca, high phos, low vit D)
220
Q

why do you get low vit D in CKD?

A

1-alpha hydroxylation normally occurs in kidneys

221
Q

Clinical manifestations of bone disease in CKD?

A
  • osteitis fibrosa cystica (hyperparathyroid bone disease)
  • adynamic
  • osteomalacia
  • osteosclerosis
  • osteoporosis
222
Q

What is adynamic in CKD?

A

Reduction in cellular activity (both osteoblasts and clasts) in bone. May be due to over treatment with vit D.

223
Q

Common causes of CKD?

A

diabetic nephropathy; chronic glomerulonephritis; chronic pyelonephritis; HTN; adult PKD

224
Q

CKD: what does the Modificaation of Diet in Renal Disease (MDRD) equation used to help estimate eGFR uses what variables?

A

serum creatinine, age, gender, ethnicity

225
Q

What factors may affect eGFR?

A

pregnancy; muscle mass (amputees, body-builders); eating red meat 12hr prior to sample taken

226
Q

CKD stages?

A

Stage 1) eGFR >90ml/min
2) 60-90
3a) 45-59
3b) 30-44
4) 15-29
5) <15

227
Q

What does CKD stage 5 mean?

A

Established kidney failure- dialysis/kidney transplant may be needed

228
Q

Main features of CKD if symptomatic (late-stage disease)

A

oedema (ankle swelling, weight gain), polyuria, lethargy, pruritus, anorexia (weight loss), insomnia, N&V, HTN

229
Q

Why may pts with CKD get pruritus?

A

secondary to uraemia

230
Q

What level of decrease in eGFR or rise in creatinine is acceptable in pts with CKD taking ACE inhibitors for HTN?

A

decrease in eGFR up to 25% or rise in creatinine up to 30% (any rise should prompt monitoring)

231
Q

Why is a small fall in glomerular filtration pressure (GFR) and rise in creatine be expected when taking ACE inhibitors in CKD?

A

these drugs tend to reduce filtration pressure

232
Q

What is a useful anti-hypertensive in pts with CKD (as well as ACE inh), particularly if GFR <45?

A

Furosemide. Added benefit of lowering serum potassium but if pt at risk of dehydration eg. gastroenteritis then consider temp stop.

233
Q

Why can pts with CKD get high phosphate?

A

kidneys normally excrete phosphatew

234
Q

Why can pts get osteomalacia in CKD?

A

high phosphate levels ‘drags’ calcium from bones

235
Q

Why can pts have low calcium in CKD?

A

due to lack of vit D, high phosphate

236
Q

Why can pts get secondary hyperparathyroidism in CKD?

A

due to low Ca, high phosphate and low vit D

237
Q

Aim of bone disease Mx in CKD?

A

reduce phosphate and parathyroid hormone levels

238
Q

Mx of bone disease in CKD?

A

1st- reduce dietary intake of phosphate

  • phosphate binders
  • vit D eg. alfacalcidol, calcitriol
  • parathyroidectomy may be needed in some cases
239
Q

How do phosphate binders eg. sevelamer work in bone disease management in CKD?

A
  • non-calcium based binder
  • binds to dietary phosphate and prevents its absorption
  • also can reduce uric acid levels and improve lipid profiles
240
Q

What is an important marker for CKD and esp diabetic nephropathy?

A

Proteinuria

241
Q

What do you use in patients with proteinuria?

A

albumin:creatinine ratio (ACR) ?CKD

242
Q

How to take an albumin:creatinine ratio?

A

first-pass morning urine specimen

243
Q

What if ACR is 3-70mg/mmol?

A

Confirm by a subsequent early morning sample. If 70+ then don’t need a repeat sample.

244
Q

What value for ACR is regarded as clinically important proeinuria?

A

3mg/mmol or more

245
Q

NICE recommends referral to nephrologist for proteinuria if what?

A
  • ACR 70 or more unless known to be caused by diabetes
  • ACR 30 or more with persistent haematuria after excluding UTI
  • ACR 3-29 with persistent haematuria + RFs e. decreasing eGFR or CVD
246
Q

Persistent haematuria?

A

2/3 dip show 1+ or more of blood

247
Q

Mx for proteinuria in CKD?

A
  • ACE inhibitors (if HTN and ACR >30 or if ACR >70 regardless of BP)
  • could consider SGLT-2 inhibitors
248
Q

Why may SGLT-2 inhibitors be beneficial for proteinuria in CKD?

A

act by blocking reabsorption of glucose in proximal tubule- -> lowers renal glucose threshold -> glycosuria.
by blocking the cotransporter, also reduce Na reabsorption -> natruresis reduced intravascular volume and BP and increased delivery of Na to macula densa -> normalises tubuloglomerular feedback and reduces intraglomerular pressure.

249
Q

Nephrotic syndrome?

A

When basement membrane in glomerulus becomes highly permeable to protein, allowing proteins to leak from blood into urine.

250
Q

What age is nephrotic syndrome most common?

251
Q

What does nephrotic syndrome present with?

A

frothy urine, generalised oedema and pallor

252
Q

Nephrotic syndrome triad?

A
  • proteinuria (>3+ on dip) causing
  • hypoalbuminaemia (<30g/L) and
  • oedema
253
Q

Other features of nephrotic syndrome?

A
  • deranged lipid profile, high cholesterol, triglycerides and low density lipoproteins
  • HTN
  • hyper-coagulability
254
Q

Causes of nephrotic syndrome?

A
  • minimal change disease (90% in children <10yrs)
  • secondary to intrinsic kidney disease
  • secondary to underlying systemic illness: Henoch schonlein purpura (HSP), diabetes, HIV, hepatitis, malaria
255
Q

Nephrotic syndrome can occur secondary to intrinsic kidney disease, give 3 examples

A
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranoproliferative glomerulonephritis
256
Q

2-5yr old child with oedema, proteinuria and low albumin?

A

Minimal change disease causing nephrotic syndrome

257
Q

Mx of nephrotic syndrome?

A
  • high dose steroids eg. pred
  • low salt diet
  • diuretics for oedema
  • albumin infusions if severe hypoal
  • Abx prophylaxis in severe cases
258
Q

How long are high dose steroids given for nephrotic syndrome?

A

4w then gradually weaned over next 8w. 80% will relapse at some point and need more.

259
Q

In nephrotic syndrome what Mx can be used in steroid resistant children?

A

ACE inhibitors and immunosuppressants eg. cyclosporine

260
Q

Cx of nephrotic syndrome?

A

Hypovolaemia, thrombosis, infection, acute or chronic renal failure, relapse.

261
Q

Minimal change disease?

A

Nearly always presents as nephrotic syndrome. Most common cause of nephrotic syndrome (90% of children under 10yrs).

262
Q

Causes of minimal change disease?

A
  • most idiopathic
  • drugs eg. NSAIDs, rifampicin
  • hodgkin’s lymphoma, thymoma
  • infectious mononucleosis

eg. NSAIDs -> minimal change disease -> nephrotic syndrome

263
Q

Pathophysiology of minimal change disease?

A

T-cell and cytokine-mediated damage to glomerular BM -> polyanion loss -> reduction of electrostatic charge -> increased glomerular permeability to serum albumin

264
Q

Features of minimal change disease?

A
  • nephrotic syndrome
  • normotension
  • highly selective proteinuria
265
Q

Why do you get highly selective proteinuria in minimal change disease?

A

only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

266
Q

Minimal change disease: features on renal biopsy?

A
  • normal glomeruli on light microscopy
  • electron microscopy shows fusion of podocytes and effacement of foot processes
267
Q

Mx of minimal change disease?

A

Oral corticosteroids (80%) steroid responsive.
- steroid-resistant: cyclophosphamide

268
Q

Is relapse common in minimal change disease?

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

269
Q

Nephritic syndrome?

A

Nephritis +
- Haematuria
- Oliguria
- Proteinuria (but <3g per 24hrs)
- Fluid retention

270
Q

Nephritis?

A

Inflammation in kidenys

271
Q

Glomerulonephritis?

A

Inflammation of glomeruli. Describes the pathology that occurs in various diseases rather than being a disease.

272
Q

What does the glomerulus do?

A

First part of the nephron. Filters fluid out of the capillaries and into renal tubule.

273
Q

Mx for glomerulonephritis?

A
  • diagnosis: renal biopsy for histology
  • Mx: suportive care (HTN Mx, dialysis if severe) and immunosuppression eg. corticosteroids
274
Q

Most common cause of primary glomerulonephritis?

A

IgA nephropathy (Berger’s disease)

275
Q

Pt in 20s with haematuria; histology shows IgA deposits and mesangial proliferation.

A

IgA nephropathy causing glomerulonephritis.

276
Q

What do mesangial cells do?

A

found in centre of glomerulus and help support capillaries + other functions

277
Q

Membranous nephropathy?

A

Deposits of immune complexes in glomerular basement membrane, causing thickening and malfunctioning of the membrane and proteinuria.

278
Q

What does histology show in membranous nephropathy?

A

IgG and complement deposits on basement membrane

279
Q

Membranous nephropathy is a key cause of what in adults?

A

Nephrotic syndrome

280
Q

What are the causes of membranous nephropathy?

A
  • Majority idiopathy
  • 2 to malginancy, SLE, or drugs eg. NSAIDs

eg. malignancy -> membranous nephropathy -> nephrotic syndrome

281
Q

Membranioproliferative glomerulonephritis (or mesangiocapillary glom…)?

A

typically pts <30yrs, involves immune complex deposits and mesangial proliferation

282
Q

Post-streptococcal glomerulonephritis?

A

pts <30yrs; presents 1-3w after strep infection (eg. tonsillitis or impetigo); pts usually make full recovery

283
Q

Rapidly progressive glomerulonephritis (or cresentic glom…)?

A

Acute severe illness but tends to respond well to treatment. Histology= glomerular crescents.

284
Q

Goodpasture syndrome (anti-glomerular base membrane (anti-GBM) disease) causes what?

A

Anti-GBM antibodies attack glomerulus and pulmonary basement membranes. Causes glomerulonephritis and pulmonary haemorrhage

285
Q

Pt in their 20s or 60s with acute kidney failure and haemoptysis?

A

Goodpastures

286
Q

Systemic diseases that cause glomerulonephritis?

A

HSP, vasculitis (microscopic polyangiitis or granulomatosis with polyangiitis) , lupus nephritis

287
Q

Pt with AKI and haemoptysis, consider which conditions based on different antibodies?

A

Anti-GBM = Goodpastures

p-ANCA (MPO antibodies)= microscopic polyangiitis

c-ANCA (PR3 antibodies)= granulomatosis with polyangiitis

288
Q

Causes of nephritic syndrome?

A
  • IgA nephropathy
  • Post-strep glomerulonephritis
  • Goodpastures
  • Membranoproliferative glomerulonephritis
  • HSP. hepatitis, vasculitis, mononucleosis, measles, mumps
  • Alport syndrome
289
Q

Deep vein thrombosis?

A

Formation of thrombus (clot) in deep vein, usually legs, which partially or completely obstructs blood flow

290
Q

Intrinsic RFs for DVT?

A

history, cancer, >60, overweight, male, HF, thrombophilia, inflam disorders eg. IBD, vasculitis

291
Q

Extrinsic RFs?

A
  • immbolity eg. recent surgery, wheelchair use
  • travel
  • signif trauma or direct trauma to vein eg. IV catheter
  • HRT
  • pregnancy and post-partum
  • dehydration
292
Q

Cx of DVT?

293
Q

CP DVT

A
  • pain, pallor, paralysis, paraesthesia, pulseless and perishingly cold
  • redness, warmth, vein distension, localised pain and swelling in calf, oedema
294
Q

Determine likelihood of DVT?

A

Well’s score

295
Q

Initial Ix for DVT?

A
  • clinical exam: assess leg and thigh swelling (circum 10cm below tibial tuberosity and compare with other leg; if diff >3cm then high prob)
  • DVT Wells score
296
Q

Ix for pt likely to have DVT based on Wells score?

A
  • proximal leg vein USS with results available within 4hrs; if can’t be done within 4hrs of being requested then:
  • D-dimer testing, interim therapeutic anticoag and USS within 24hrs
297
Q

Ix for pt unlikely to have DVT based on Wells score?

A
  • bloods for D-dimer with results within 4hrs
  • if +ve then do same Ix if Well’s was likely (USS)
  • if -ve then alternative diagnosis
  • if results not available within 4hrs= interim anticoag whilst waiting
298
Q

DVT Mx?

A
  • Anticoagulants in secondary care
299
Q

What will pts on discharge after having DVT need?

A

maintenance treatment with oral anticoag for at least 3m

300
Q

When is DVT Wells risk score likely?

A

2 points or more

301
Q

When is DVT Wells risk score unlikely?

A

1 point or less

302
Q

Interim therapeutic anticoag for DVT?

A

DOAC: Apixaban or rivaroxaban

if not suitable then LMWH 5d followed by dabigatran OR LMWH + vit K antagonist 5d

303
Q

What baseline bloods are needed for people starting interim anticoag therapy for DVT? (don’t wait on results before starting)

A

FBC, renal and hepatic function, PT, activated partial thromboplastin time (APTT)

304
Q

Ensure people with an unprovoked DVT are investigated for what?

A

cancer and thrombophilia

305
Q

Warfarin INR target (eg. for DVT long term Mx)?

A

2.5, or within 2-3

306
Q

Contraindications to starting maintenance treatment with anticoag for DVT following acute treatment?

A

Pregnancy or cancer

307
Q

Maintenance Mx for DVT?

A

Warfarin, apixaban or ravroxaban (if DVT provoked then 3m, if unprovoked then 6m)

308
Q

CP of dehydration

A

Dry mucous membranes, loss of skin turgor, sunken eyes.
Severe= tachycardia, hypotension, delirium.

309
Q

Fluid resuscitation?

A

fluid bolus 500ml crystalloid over less than 15 mins (0.9% saline or Hartmann’s)

310
Q

Examples of crystalloid fluids?

A

Saline 0.9%, Hartmann’s

311
Q

Examples of colloid fluids?

A

Albumin, dextran, blood

312
Q

Crystalloid vs colloid fluids?

A

Crystalloids: small molecules, cheap, immediate fluid resus but may increase oedema.
Colloid= larger molecules, cost more, risk of allergic reactions and kidney failure

313
Q

Electrolyte concs in plasma

A

Na+ = 135-145
Cl- = 98-105
HCO3- = 22-28
Glucose = N/A

314
Q

Electrolyte conc in 0.9% saline?

A

Na+ = 154
Cl- = 154
K+ = N/A
HCO3- = N/A
Glucose = N/A

315
Q

Electrolyte concs in 5% glucose?

A

Na+ = N/A
Cl- = N/A
K+ = N/A
HCO3- = N/A
Glucose = 50g

316
Q

Electrolyte concs of 0.18% saline with 4% glucose

A

Na+ = 30
Cl- = 30
K+ = N/A
HCO3- = N/A
Glucose = 40g

317
Q

Electrolyte concs of Hartmann’s solution?

A

Na+ = 131
Cl- = 111
K+ = 5
HCO3- = 29
Glucose = N/A

318
Q

What happens if large volumes of 0.9% saline are used?

A

increased risk of hyperchloraemic metabolic acidosis

319
Q

What pts should Hartmann’s be not used in?

A

Those with hyperkalaemia as contains potassium

320
Q

In nephrotic syndrome, why is pt predisposed to thrombosis?

A

loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels= thrombosis

321
Q

Most common type of renal stone

A

Calcium oxalate

322
Q

RFs for calcium oxalate renal stones

A

Hypercalciuria; hyperoxaluria; hyppercitraturia.

323
Q

Other types of renal stones?

A

cystine, uric acid, calcium phosphate, struvite

324
Q

pH of urine?

A

Variation throughout day (5-7).
Falls after eating as purine metabolism produces uric acid.
Then becomes more alkaline (alkaline tide)

325
Q

When a stone is not available for analysis, what may be used to help determine which stone was present?

A

pH of urine

326
Q

Urine acidity with different renal stones?

A

Calcium phosphate= Normal- alkaline >5.5

Calcium oxalate= Variable 6

Uric acid= Acid 5.5

Struvate= Alkaline >7.2

Cystine= Normal 6.5

327
Q

Renal/ureteric colic?

A

acute and severe loin pain caused when urinary stone moves from kidney or obstructs flow of urine

328
Q

CP of renal colic

A
  • severe unilateral abdo pain from loin/flank to groin (labia in women/ groin or testicle in men)
  • pain lasts mins-hrs with spasms then after dull ache
  • N & V
  • haematuria
  • dysuria, urinary frequency and straining
  • restless
329
Q

Exclude what if ?renal colic

A

appendicitis and diverticulitis

330
Q

RFs for renal colic

A

chronic dehydration, FHx, GI conditions eg. Crohn’s, medications (eg. protease inhibitors)

331
Q

Cx of renal colic

A

urinary tract obstruction (hesitancy, intermittent urinary stream) and UTI (fever, sweats)

332
Q

Immediate hospital admission for pt with renal colic if what symptoms?

A
  • in shock/systemic infection eg. fever, sweats
  • increased risk of AKI eg. CKD, transplanted kidney or bilateral stones suspected
  • dehydrated and can’t take oral fluids due to vomiting
  • uncertain about diagnosis
333
Q

Ix for suspected renal colic

A
  • urine dip ?haematuria/infection
  • urgent low-dose non-contract CT KUB within 24hrs (USS if child or pregnant)
334
Q

Mx for renal colic

A
  • analgesia: NSAIDs or IV paracetamol
    -watch and wait, medical expulsive therapy or surgery
335
Q

What does Mx of urinary stones depend on?

A

size, severity of symptoms, location (renal or ureteric), age

336
Q

Increasing fluid intake, reducing salt intake (rec 2-6g/day), avoiding carbonated drinks, maintaining normal calcium intake all reduce the risk of recurrence of what?

A

renal/ureteric colic/stones

337
Q

Reduce risk of recurrence of renal/ureteric colic/stones

A
  • lifestyle and dietary advice
  • consider potassium citrate if recurrence of stones that are >50% calcium oxalate
  • thiazide if recurrence of stones >50% calcium oxalate & hypercalciuria, after restricting Na+ intake to <6g a day
338
Q

When is watchful waiting advised for renal/ureteric stones?

A

stone <5mm and asymptomatic

339
Q

Medical expulsive therapy for renal/ureteric stones?

A

with distal ureteric stones <10mm

use of alpha-blocker to facilitate sponstaneous stone passage under observation

340
Q

Surgery for renal/ureteric stones?

A

within 48hrs or readmission if pain ongoing or stone unlikely to pass

either: shockwave therapy; percutaneous nephrolithotomy, ureteroscopy or open surgery.

341
Q

What metabolic Ix are recommended for people with renal or ureteric stones?

A

Serum calcium and stone analysis ?cystinuria, uric acid stones and primary hyperparathyroidism

342
Q

Stones what size usually pass spontaneously?

343
Q

Drugs that promote calcium stones (RF)?

A

loop diuretics, steroids, acetazolamide, theophylline

344
Q

How do thiazides prevent calcium stones?

A

increase distal tubular calcium resorption

345
Q

How do calcium oxalate stones appear on radiograph?

A

opaque, 40% frequency

346
Q

Commonest cause of glomerulonephritis?

A

IgA nephropathy (aka Berger’s disease)

347
Q

Macroscopic haematuria in young people following an URTI- think?

A

IgA nephropathy

348
Q

Conditions associated with IgA nephropathy?

A

alcoholic cirrhosis; coeliac/dermatitis herpetiformis; Henoch-Schonlein purpura

349
Q

IgA nephropathy thought to be caused by what?

A

mesangial deposition of IgA immune complexes; pathological overlap with HSP

350
Q

Histology of IgA nephropathy

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

351
Q

Differentiate between IgA nephropathy and post-streo glomerulonephritis?

A
  • IgA= develops 1-2 days after URTI, macroscopic haematuria, young males
  • Post-strep= 1-2w after URTI, main symptom is proteinuria (haematuria can occur); low complement levels
352
Q

IgA nephropathy Mx: isolated haematuria, no/ <500-100mg/day proteinuria and normal eGFR?

A

no Mx needed, follow-up to check renal function

353
Q

IgA nephropathy Mx: persistent proteinuria >500-1000/day and a normal or slightly reduced eGFR?

A

inital: ACE inhibitors

354
Q

IgA nephropathy Mx: active disease (falling GFR) or failure to respond to ACE inhibitors?

A

immunosuppression with corticosteroids

355
Q

Markers of good prognosis in IgA nephropathy?

A

frank haematuria

356
Q

Markers of poor prognosis in IgA nephropathy?

A

male, proteinuria (esp >2g/day), HTN, smoking, hyperlipid, ACE genotype DD

357
Q

25% of pts with IgA nephropathy develop what?

358
Q

Renal cell cancer (hypernephroma) arises from what?

A

Proximal renal tubular epithelium

359
Q

Most common histological subtype of renal cell cancer (hypernephroma)?

A

clear cell (75-85%) tumours

360
Q

RFs for renal cell cancer (hypernephroma)?

A

middle-aged men; smoking; von Hippel-Lindau syndrome; tuberous sclerosis.

361
Q

Classic triad for renal cell cancer (hypernephroma)?

A

haematuria, loin pain, abdo mass

362
Q

Other features apart from the triad for renal cell cancer (hyper nephroma)?

A
  • pyrexia of unknown origin
  • varicocele (most L sided; caused by tumour compressing veins)
  • stauffer syndrome
  • 25% have mets at presentation
  • endocrine effects
363
Q

Endocrine effects of renal cell cancer?

A
  • may secrete erythropoietin (polycythaemia)
  • parathyroid hormone related protein (hypercalcaemia), renin
  • ACHT
364
Q

Stauffer syndrome?

A

paraneoplastic disorder associated with renal cell ca; presents as cholestasis/hepatosplenomegaly; though to be 2 to increased IL-6 levels

365
Q

T1-T4 for renal cell cancer?

A

T1= ≤ 7 cm and confined to the kidney
T2= > 7 cm and confined to the kidney
T3= extends into major veins or perinephric tissues but not into ipsilateral adrenal gland and not beyond Gerota’s fascia
T4= invades beyond Gerota’s fascia (incl contiguous extension into the ipsilateral adrenal gland)

366
Q

Mx for renal cell cancer?

A
  • confined disease: partial (T1) or total nephrectomy
  • alpha-interferon and interleukin-2= reduce tumour size & mets
  • receptor tyrosine kinase inhibitors eg. sorafenib

FINALS (37 decks)

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