Renal Medicine Flashcards

1
Q

What are the risk factors for developing a UTI? (8)

A
  1. Female
  2. Sexual intercourse
  3. Exposure to spermicide
  4. Pregnancy
  5. Menopause
  6. Immunosuppressed
  7. Urinary tract obstruction e.g. stones, catheter
  8. Urinary incontinence
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2
Q

What are the symptoms of UTI? (10)

A
  1. Dysuria
  2. Urgency
  3. Increased frequency
  4. Haematuria
  5. Suprapubic pain
  6. Fever
  7. Rigors
  8. Vomiting
  9. Loin-groin pain
  10. Oliguria (AKI)
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3
Q

If a patient presents with symptoms of a UTI but a urine dipstick if negative, what should you do?

A

Send off a mid-stream urine sample for MC&S (do this anyway if patient is male/child/pregnant/immunosuppressed)

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4
Q

What are the causes of sterile pyuria? (white cells in urine)

A
  1. Inadequately treated UTI
  2. Appendicitis
  3. Calculi
  4. Bladder tumour
  5. Polycystic kidney
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5
Q

What further investigations for UTI need to be arranged if the patient is male/child/failing to respond to normal treatment?

A
  1. USS
  2. CT KUB
  3. Cystocopy
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6
Q

What is the advice about prevention of UTIs?

A

Drink plenty of water

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7
Q

What is the 1st line treatment for UTI in women? (2)

A
  1. Nitrofurantoin 100mg modified-release twice a day for 3 days (if eGFR ≥45ml/minute) or
  2. Trimethoprim 200mg twice a day for 3 days (if low risk of resistance).
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8
Q

What is an AKI?

A

It is defined by a rapid reduction in kidney function leading to failure to maintain fluid, electrolyte and acid-base homeostasis.

  • Rise in creatinine >26umol/L in 48 hours
  • Rise in creatinine >1.5 x baseline
  • Urine output <0.5mL/kg/h for >6 consecutive hours
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9
Q

What are the risk factors for developing an AKI? (9)

A
  1. People aged >65
  2. History of AKI
  3. CKD
  4. Chronic conditions such as heart failure, liver disease, diabetes
  5. Sepsis
  6. Hypovolaemia
  7. Nephrotoxic drugs e.g. NSAIDs, ACEi, diuretics
  8. Cancer
  9. Immunocompromised
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10
Q

What are the complications of an AKI? (6)

A
  1. Hyperkalaemia
  2. Other electrolyte abnormalities - hyperphosphataemic, hyponatraemia, hypermagnesaemia, hypocalcaemia
  3. Metabolic acidosis
  4. Volume overload - peripheral/pulmonary oedema
  5. Uraemia - may require dialysis
  6. CKD
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11
Q

How many someone present with AKI? (4)

A
  1. N&V
  2. Diarrhoea
  3. Reduced urine output or changes in urine colour
  4. Confusion, fatigue, drowsiness
    - anyone with the risk factors previously mentioned e.g. CKD, heart failure, diabetes, sepsis, recently started on nephrotoxic drugs
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12
Q

How can you differentiate between AKI stage 1 - 3?

A

Stage 1 is creatinine >1.5x more than baseline
Stage 2 is creatinine >2x more than baseline
Stage 3 is creatinine >3x more than baseline

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13
Q

How should you manage someone with an AKI? (7)

A

Assess:

  1. Volume status
  2. Renal function and serum potassium level
  3. History to work out underlying cause
  4. Urine dipstick
  5. Stop nephrotoxic drugs
  6. Fluid replacement
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14
Q

What are the components of a fluid assessment? (6)

A
  1. Fluid intake and losses
  2. Peripheral perfusion (cap refill)
  3. HR/BP
  4. JVP
  5. Mucous membranes, skin turgor
  6. Peripheral oedema/pulmonary crackles
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15
Q

Why is a urine dipstick vital in the case of an AKI?

A

Can identify if there is infection and/or glomerular disease

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16
Q

What blood test might you consider doing and why if someone presents with AKI and back pain?

A

Paraprotein electrophoresis and immunoglobulins - chance it is multiple myeloma

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17
Q

What are the causes of CKD? (6)

A
  1. Diabetes
  2. Glomerular disease e.g. acute glomerulonephritis (typically if CKD follow strep upper UTI infection, but also from hep B, C and HIV)
  3. Hypertension
  4. Current or previous AKI
  5. Nephrotoxic drugs
  6. Multisystem diseases: SLE, myeloma
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18
Q

What are the markers of kidney damage, and what do they need to be in order for CKD to be diagnosed?

A
  1. Urinary albumin:creatinine ratio (ACR) >3mg/mol

2. eGFR <60ml/min/1.73m

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19
Q

How is accelerated progression of CKD defined?

A

A decrease in eGFR of more than 25% or a change in CKD category/stage within 12 months, OR a persistent decrease in eGFR of 15ml/min/1.73m within 12 months.

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20
Q

What is Alport’s syndrome?

A

A sex-linked recessive disease which typically causes haematuria

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21
Q

What are the complications of CKD? (8)

A
  1. AKI
  2. Hypertension and dyslipidaemia
  3. Cardiovascular: Ischaemic heart disease/peripheral disease, heart failure, stroke
  4. Renal anaemia
  5. Renal mineral and bone disorder
  6. Peripheral neuropathy and myopathy
  7. Malnutrition (end stage renal disease)
  8. Malignancy (end stage renal disease)
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22
Q

In addition to an eGFR of less than 60, and/or an ACR of more than 3mg/mmol, what else can aid diagnosis of CKD?

A

Persistent haematuria - two out of three urine dipsticks test positive (after exclusion of a UTI)

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23
Q

What are the general symptoms of CKD? (10)

A
  1. Lethargy
  2. Itch
  3. Breathlessness
  4. Cramps (often worse at night)
  5. Sleep disturbance
  6. Bone pain
  7. Loss of appetite
  8. Vomiting
  9. Weight loss
  10. Taste disturbance
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24
Q

What are the more specific symptoms of CKD? (4)

A

Change in urine output:

  1. Polyuria
  2. Oliguria
  3. Nocturia
  4. Anuria
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25
Q

What may be the signs on examination of progressive CKD? (10)

A
  1. Uraemic odour (ammonia-like smell)
  2. Pallor (renal anaemia)
  3. Cachexia and signs of malnutrition
  4. Dehydration
  5. Tachypnoea
  6. Cognitive impairment
  7. Palpable bilateral flank masses
  8. Palpable distended bladder
  9. Peripheral oedema (heart failure secondary to CKD)
  10. Frothy urine (may indicate proteinuria)
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26
Q

What investigations need to be arranged for someone with CKD? (5)

A
  1. eGFR
  2. Serum creatinine
  3. Early morning urine sample to measure ACR (sent off for microscopy, not urine dipstick as not sensitive enough for albumin levels)
  4. Urine dipstick for haematuria
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27
Q

What are the stages for CKD and what measurements do they use?

A

CKD is in stages 1-5 with a 3a and 3b. It is then ranked further based on urinary ACR into A1, A2 and A3.

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28
Q

What are the eGFR grades for each stage of CKD?

A
Stage 1 = >90
Stage 2 = 60-89
Stage 3a = 45-59
Stage 3b = 30-44
Stage 4 = 15-29
Stage 5 = <15 (kidney failure)
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29
Q

What do the ACR A1,2,3 grades relate to?

A
A1 = <3mg/mmol
A2 = 3-30mg/mmol
A3 = >30mg/mmol
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30
Q

In someone with CKD, what blood tests need to be monitored?

A
FBC (renal anaemia)
Serum calcium
Phosphate
Vitamin D
Parathyroid hormone 
(renal metabolic and bone disorders)
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31
Q

Which antihypertensive is first line for someone with CKD?

A

ACEi

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32
Q

What is the aim for blood pressure for people with CKD, dependent on their ACR?

A

ACR <70mg/mmol aim is <140/90

ACR >70mg/mmol aim is <130/80

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33
Q

If a person has diabetes, hypertension and CKD, what is the aim for their blood pressure?

A

<130/80mmHg

34
Q

What medications should everyone with CKD be on?

A

Statins and antiplatelets

35
Q

Glomerulonephritis simply refers to inflammation of the glomeruli and nephrons. What happens as a result of this inflammation? (3)

A
  1. Damage to the glomerulus restricts blood flow, leading to a compensatory rise in BP
  2. Damage to the filtration mechanism allows protein and blood to enter the urine
  3. Loss of usual filtration capacity leads to AKI
36
Q

What is seen in terms of blood pressure, urine dip and eGFR for nephrotic syndrome vs nephritic syndrome?

A

Nephrotic syndrome = normal/mildly raised BP, proteinuria >3.5g/day, normal/mildly reduced eGFR
Nephritic syndrome = moderate/severely raised BP, haematuria, moderate/severe eGFR

37
Q

In terms of nephrotic syndrome, what are the common primary causes? (4)

A
  1. Membranous nephropathy
  2. Minimal change
  3. Focal segment glomeruosclerosis (FSGS)
  4. Mesangiocapillary
38
Q

What are the common secondary causes of nephrotic syndrome? (4)

A
  1. Diabetes
  2. SLE
  3. Amyloid
  4. Hepatitis
39
Q

What are the primary causes of nephritic syndrome? (2)

A
  1. IgA nephropathy

2. Mesangiocapillary

40
Q

What are the secondary causes of nephritic syndrome? (5)

A
  1. Post-strep (normally URTI)
  2. Vasculitis
  3. SLE
  4. Anti-glomerular basement membrane disease
  5. Cryoglobulinaemia
41
Q

What are the different types of glomerulonephritis?

A
  1. IgA nephropathy
  2. Henoch-Schonlein purpura
  3. SLE
  4. Anti-glomerular basement membrane (GBM) disease
  5. Post-streptococcal GN
  6. Rapidly progressive GN
42
Q

What is the most common type of glomerulonephritis in the developed world?

A

IgA nephropathy

43
Q

IgA nephropathy is also known as what?

A

Berger’s disease

44
Q

Where does IgA nephropathy arise from - why do people get it?

A

It is an autoimmune renal disease arising from consequences of increased circulating levels of IgA1 with galactose-deficient hinge-region O-glycans.

45
Q

Four independent prognostic factors for progression to kidney disease from IgA nephropathy have been found on renal biopsy. What are they? (good luck with that)

A
  1. Mesangial hypercellularity score (estimate of the density of the mesangial cells around renal blood vessels)
  2. Segmental glomerulosclerosis
    3 Endocapillary hypercellularity
  3. Tubular atrophy/interstitial fibrosis
46
Q

IgA nephropathy is associated with a number of other disease. What are they? (7)

A
  1. HSP
  2. SLE
  3. Dermatits herpetiforms
  4. Ankylosing spondylitis
  5. Coeliac disease
  6. Hepatits and cirrhosis
  7. HIV
47
Q

How can IgA N present?

A

It is very variable, from microscopic haematuria to rapidly progressive glomerulonephritis.

  1. Gross haematuria usually associated with an URTI (less commonly gastroenteritis)
  2. Urine dipstick erythrocytes, casts and proteinuria
48
Q

What is rapidly progressive glomerulonephritis?

A

It is a term used to describe a rapid loss of renal function associated with formation of epithelial crescents in the majority of glomeruli (found on renal biopsy)

49
Q

What are the causes of rapidly progressive glomerulonephritis?

A
  1. Goodpasture’s syndrome
  2. Wegener’s granulomatosis
  3. SLE
  4. Microscopic polyarteritis
50
Q

What are the features of rapidly progressive glomerulonephritis?

A
  1. Nephritic syndrome - haematuria with red cell casts, proteinuria, hypertension and oliguria.
  2. Features specific to the underlying cause e.g. haemoptysis with Goodpasture’s
51
Q

cANKA is associated with what condition?

A

Wegeners granulomatosis (Granulomatosis with polyangiitis)

52
Q

What is found on renal biopsy for someone with Wegeners granulomatosis AKA granulomatosis with polyangiitis?

A

Crescenteric glomerulonephritis

53
Q

What is granulomatosis with polyangiitis?

A

It is a rare form of vasculitis. It is thought to be an autoimmune inflammatory process affecting epithelial cells. It is a multi-system disease which can affect many parts of the body, categories by the ELK classification.

54
Q

What is the ELK classification for granulomatosis with polyangiits (GPA)?

A

E - ENT
L - lungs
K - kidneys
- basically an inflammatory pattern of necrosis, granulomatous inflammation and vasculitis that occurs in the upper and lower respiratory tracts and kidneys

55
Q

Which antibody is positive in GPA?

A

c-ANCA

p-ANCA

56
Q

How can GPA present? (14…)

A
  1. Fever, malaise
  2. Night sweats
  3. Weakness
  4. Loss of appetite, weight loss
  5. Rhinorrhoea
  6. Sinusitis
  7. Facial pain
  8. Hoarseness
  9. Cough
  10. Dyspnoea
  11. Wheezing
  12. Chest pain
  13. Joint paints
  14. Hearing loss
57
Q

What are the drugs commonly used to treat GPA? (4)

A
  1. Corticosteroids
  2. Cyclophosphamide
  3. Rituximab
  4. Methotrexate
58
Q

Minimal change disease almost always presents with which syndrome; nephrotic or nephritic?

A

Nephrotic syndrome

59
Q

Which type of glomerulonephritis develops 1/2 days after an URTI?

A

IgA nephropathy

60
Q

IgA nephropathy typically causes which syndrome; nephrotic or nephritic?

A

Nephritic syndrome - with visible haematuria, proteinuria and hypertension

61
Q

Membranous glomerulonephritis typically causes which syndrome nephritic or nephrotic?

A

Nephrotic syndrome

62
Q

Membranous glomerulonephritis typically shows what TFT results?

A

Low total T4 levels

63
Q

What is the triad of nephrotic syndrome?

A
  1. Oedema
  2. Proteinuria
  3. Hypoalbuminaemia
64
Q

What is the triad of nephritic syndrome?

A
  1. Macroscopic haematuria
  2. Proteinuria
  3. Hypertension
65
Q

What are the causes of nephritic syndrome (but which don’t cause nephrotic syndrome) (3)

A
  1. IgA nephropathy
  2. Rapidly progressive GN
  3. Alport syndrome
66
Q

What are the causes of nephrotic syndrome (but which don’t cause nephritic syndrome? (5)

A
  1. Minimal change disease
  2. Membranous GN
  3. Focal segmental glomerulosclerosis (FSGS)
  4. Amyloidosis
  5. Diabetic nephropathy
67
Q

What are the things that can cause both nephrotic and nephritic syndrome? (3)

A
  1. Diffuse proliferative GN
  2. Membranoproliferative GN
  3. Post-streptococcal GN
68
Q

In someone with compartment syndrome who develops worsening renal function and muddy brown casts on microscopy, what is the most likely diagnosis?

A

Acute tubular necrosis

69
Q

What is found on histology of membranous glomerulonephritis? (3)

A
  1. Basement membrane thickening on light microscopy
  2. Subepithelial spikes on silver stain
  3. Positive immunohistochemistry for PLA2
70
Q

What treatment can be given to help vitamin D deficiency in a patient with severe renal impairment?

A

Alfacalcidol - there are several forms of vitamin D, but many require hydroxylation in the kidneys before its active. However alfacalcidol does not require hydroxylation.

71
Q

What are the clinical features of acute tubular necrosis?

A
  1. AKI - raised urea and creatinine, potassium

2. Muddy brown casts in urine

72
Q

What are the causes of a metabolic acidosis with a raised anion gap? (4)

A
  1. Lactate - shock, hypoxia
  2. Ketones - DKA, alcohol
  3. Urate - renal failure
  4. Acid poisoning - salicylates, methanol
73
Q

What are the causes of metabolic alkalosis? (6)

A
  1. Vomiting
  2. Diuretics
  3. Hypokalaemia
  4. Cushing’s syndrome
  5. Bartter’s syndrome
  6. Congenital adrenal hyperplasia
74
Q

What symptoms of minimal change disease cause?

A

Nephrotic syndrome symptoms - oedema, proteinuria, hypoalbuminaemia

75
Q

When does acute interstitial nephritis occur?

A

AIN is characterised by a triad of rash, fever and eosinophilia. AIN is commonly caused by antibiotic therapy and NSAIDs.
Often sterile pyuria and white cell casts are seen.

76
Q

What treatment can be given to help vitamin D deficiency in a patient with severe renal impairment?

A

Alfacalcidol - there are several forms of vitamin D, but many require hydroxylation in the kidneys before its active. However alfacalcidol does not require hydroxylation.

77
Q

Metabolic acidosis can be classified according to the anion gap - if it is normal or raised. What causes a metabolic acidosis with normal anion gap? (5)

A

(normal anion gap = hyperchloraemic metabolic acidosis)

  1. GI bicarbonate loss e.g. diarrhoea, fistula
  2. Renal tubular acidosis
  3. Drugs e.g. acetazolamide
  4. Ammonium chloride injection
  5. Addison’s disease
78
Q

What are the causes of a metabolic acidosis with a raised anion gap? (4)

A
  1. Lactate - shock, hypoxia
  2. Ketones - DKA, alcohol
  3. Urate - renal failure
  4. Acid poisoning - salicylates, methanol
79
Q

What are the causes of metabolic alkalosis? (6)

A
  1. Vomiting
  2. Diuretics
  3. Hypokalaemia
  4. Cushing’s syndrome
  5. Bartter’s syndrome
  6. Congenital adrenal hyperplasia
80
Q

When does acute tubular necrosis occur?

A

With prolonged renal ischaemia secondary to either continuing pre-renal injury or by direct toxicity due to nephrotoxins or sepsis

81
Q

When does acute interstitial nephritis occur?

A

AIN is characterised by a triad of rash, fever and eosinophilia. AIN is commonly caused by antibiotic therapy.
Often sterile pyuria and white cell casts are seen.

82
Q

What are the complications of nephrotic syndrome?

A

HIT
Hyperlipidaemia - DVT/PE/renal vein thrombosis
Infection (loss of immunoglobulin through urine)
Thromboembolism - loss of anti-thrombin III and protein C and S