Renal Flashcards

1
Q

What is AKI and what are the criteria for diagnosis?

A

Acute drop in kidney function.

  1. Creatinine rise >25micromol/l in 48 hours
  2. Creatinine rise >50% in 7 days
  3. UO <0.5ml/kg/hr for >6 hours
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2
Q

Give 5 risk factors for AKI.

A
Chronic kidney disease
Surgery/infection
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment
Nephrotoxic medications such as NSAIDS and ACE inhibitors
Use of a contrast medium such as during CT scans
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3
Q

What are the pre-renal causes of AKI?

A

Most common. Inadequate perfusion due to:
Dehydration
Hypotension (shock)
Heart failure

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4
Q

What are the renal causes of AKI?

A

Intrinsic kidney disease leading to reduced blood filtration due to:
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

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5
Q

What are the post-renal causes of AKI?

A

Obstruction to outflow of urine from the kidney due to:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer

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6
Q

What would you see on urinalysis in infection?

A

Leucocytes and nitrites

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7
Q

What would you see on urinalysis in acute nephritis?

A

Protein and blood

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8
Q

What would you see on urinalysis in diabetes?

A

Glucose

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9
Q

What are the indications for ultrasound in AKI?

A

To look for obstruction. Not necessary if another cause found.

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10
Q

How is AKI managed?

A
Prevention - 
stop nephrotoxic medications eg NSAIDs
fluid balance especially in pre-renal
Relieve obstruction if post-renal
cause unknown or complications risk - get specialist advice
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11
Q

Give 4 complications of AKI.

A

Hyperkalaemia
Fluid overload –> HF, pulmonary oedema
Metabolic acidosis
Uraemia (high urea) - encephalopathy, pericarditis

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12
Q

Give 5 causes of CKD.

A
Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS, proton pump inhibitors and lithium
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13
Q

What is CKD?

A

Permanent and progressive decline in kidney function.

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14
Q

Give 5 risk factors for CKD.

A
Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys
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15
Q

How does CKD present?

A
Usually asymptomatic and diagnosed on routine testing
Itching
loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
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16
Q

How is CKD diagnosed and staged?

A
You need eGFR <60 or proteinuria.
Urine albumin creatinine ratio >3mg/mmol. This gives you an A score - 
(A1 = <3mg/mmol)
A2 = 3-30mg/mmol
A3 = >30mg/mmol
eGFR 2 tests 3 months apart, gives you a 'G score'
(G1 = >90 - not CKD)
G2 = 60-89 
G3a = 45-59
G3b = 30-44
G4 = 15-29
G5 = <15/ end stage
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17
Q

When is renal USS indicated in someone with reduced eGFR?

A

Accelerated CKD, haematuria, family history of polycystic kidneys, evidence of obstruction.

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18
Q

Give 5 complications of CKD.

A
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
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19
Q

What are the NICE indications to refer to a specialist in CKD?

A

eGFR <30 (G4/5)
ACR >70 mg/mmol (A3)
Accelerated progression - decrease in eGFR of 15, of 25%, or 15ml/min in 1 yr
htn despite 4 antihypertensives

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20
Q

How is CKD managed?

A

Can’t cure it but can:
slow progression by optimising control of diabetes and hypertension (ACEI) and treating glomerulonephirits;
reduce risk of complications with exercise, smoking cessation, specialised dietary advice and atorvastatin 20mg
and treat complications:
Sodium biarb for met acidosis
iron and epo for anaemia
vit D for bone disease
dialysis or transplant for end stage failure

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21
Q

How does CKD cause anaemia?

A

It is an anaemia of chronic disease.

Kidney usually produces EPO which stimulates RBC production. Kidney disease –> less EPO –> anaemia.

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22
Q

How is anaemia of CKD treated?

A

PO or IV iron
Erythropoietin.
Blood transfusions should be limited as they can cause allosensitisation, so transplanted organs are more likely to be rejected.

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23
Q

What is CKD-MBD?

A

Chronic kidney disease mineral and bone disorder, aka renal bone disease.
The kidney is also unable to convert vitamin D to its active form, which is needed to absorb calcium and regulate bone turnover. Reduced phosphate excretion by the kidneys leads to hyperphosphataemia, so the parathyroid glands excrete more PTH, leading to increased osteoclast activity, which cause calcium to leach from bones into blood.
The result is osteomalacia (softening), osteoporosis (reduced density) and osterosclerosis (hardening due to reaction from the osteoblasts)

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24
Q

What would you see on spine X ray in CKD-MBD?

A

Rugger jersey spine - osteomalacia in the centre of the vertebra, sclerosis at the ends, so looks stripy

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25
Q

How is renal bone disease managed?

A

Active vit D eg alfacalcidol, calcitriol
Low phosphate diet
Bisphosphonates for osteoporosis

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26
Q

Give 5 indications for acute dialysis in patients with a severe AKI.

A

Severe Acidosis that doesn’t respond to treatment
Electrolyte abnormalities eg severe, unresponsive hyperkalaemia
Intoxication (overdose of certain medications)
Severe and unresponsive pulmonary Oedema
Uraemia eg seizures, reduced consciousness

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27
Q

What are the indications for long term dialysis?

A

End stage renal failure (CKD stage 5 ie eGFR <15)

Acute indications continuing long term

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28
Q

What is peritoneal dialysis?

A

Uses the peritoneal membrane as a filtration membrane. Dialysis solution containing dextrose is added to the peritoneal cavity using a Tenckhoff catheter. Ultrafiltration occurs from the blood, across the peritoneal membrane, into the dialysis solution. The dialysis solution is then replaced, taking away the waste products.
It can be continuous ambulatory (change the fluid multiple times a day) or automated (overnight, a machine replaces the fluid overnight)

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29
Q

Give 5 complications of peritoneal dialysis.

A

Bacterial peritonitis - dextrose –> bacterial growth
Peritoneal sclerosis (thickening and scarring of the peritoneal membrane)
Ultrafiltration failure (patient absorbs the dextrose so the filtration gradient is reduced over time)
Weight gain due to absorbing the carbohydrate
Psychosocial effects

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30
Q

What is haemodialysis?

A

Blood is filtered by a haemodialysis machine. Requires good IV access using either a tunnelled cuffed catheter or AV fistula.

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31
Q

What is a tunnelled cuffed catheter?

A

Tube inserted into the subclavian or jugular vein with a tip that sits in the SVC or right atrium. Has a lumen for blood exiting (red) and entering (blue) the body. A Dacron cuff surrounds the catheter which promotes healing and adhesion of tissue to the cuff, making the catheter more permanent and providing a barrier to bacterial infection. They can stay in long term for regular haemodialysis. Complications are infection and clots in the catheter.

32
Q

How does an AV fistula work?

A

Artificial connection between an artery and a vein. Bypasses capillary system to blood can flow under high pressure from artery into vein, which provides permanent large easy access blood vessel with arterial flow. It is a surgical operation which takes 1-4 months to heal before use.
Can be radio-cephalic, brachio-cephalic etc.

33
Q

What should you look for on examination of an AV fistula?

A

Skin integrity
Aneurysms
Palpable thrill (vibration felt over the anastamosis)
Machinery murmur on auscultation

34
Q

What are the main complications of an AV fistula?

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome - inadequate blood flow to the limb distal to the fistula because the fistula is stealing the blood and diverting it to the venous system. This causes distal ischemia.
High output heart failure - rapid blood return to heart –> increased preload, hypertrophy, heart failure

35
Q

How are kidney donors and recipients matched?

A

Matched based on HLA type A, B and C on chromosome 6.

Don’t have to fully match, can be desensitised first, risk of transplant failing decreased if they match.

36
Q

Explain a renal transplant procedure.

A

Recipient keeps their own kidneys
Donor kidneys blood vessels anastamosed with patients pelvic vessels, usually external iliac vessels.
Donor kidney’s ureter anastamosed with patient’s bladder
Donor kidney placed anterior in abdomen so can usually be palpated in the iliac focca
Hockey stick incision typically used.

37
Q

What treatment is needed post renal transplant?

A

New kidney should function immediately.
Lifelong immunosuppression to reduce risk of transplant rejection, with tacrolimus, mycophenolate and prednisolone.
Sometimes cyclosporine, sirolimus and azathioprine used.
*cause skin changes (warts, cancer)

38
Q

Give a side-effect of cyclosporine.

A

Gym hypertrophy

39
Q

Give a side-effect of tacrolimus.

A

Tremor

40
Q

Give 3 complications of renal transplant.

A

Transplant rejection (hyperacute, acute and chronic)
Transplant failure
Electrolyte imbalances

41
Q

Give 3 complications of immunosuppressants in renal transplant.

A

Ischaemic heart disease
Type 2 diabetes (steroids)
Infections are more likely and more severe
Unusual infections can occur (PCP, CMV, PJP and TB)
Non-Hodgkin lymphoma
Skin cancer (particularly squamous cell carcinoma)

42
Q

What is nephritis? How is it different to nephritic syndrome?

A

Nephritis = Inflammation of the kidneys.
Nephritic syndrome = symptoms which fit with nephritis (kidney inflammation). No set criteria but usually includes haematuria, oliguria, light proteinuria, and fluid retention.

43
Q

What is nephrotic syndrome?

A

Peripheral oedema, proteinuria >3g.24h, serum albumin <25g/l, hypercholesterolaemia.
Set of signs, not a diagnosis. Usually caused by minimal change disease in children or focal segmental glomerulosclerosis in adults.

44
Q

What is glomerulonephritis? Give 3 types.

A

Any condition which causes inflammation of the glomerulus and nephron. Includes:
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
Mesangiocapillary glomerulonephritis
Rapidly progressive glomerulonephritis
Goodpasture Syndrome

45
Q

What is interstitial nephritis?

A

Inflammation between the cells and the tubules (interstitium) in the kidney. Includes acute interstitial nephritis and chronic tubulointerstitial nephritis.

46
Q

What is glomerulosclerosis?

A

Scarring of the tissue in the glomerulus eg caused by glomerulonephritis, obstructive uropathy, focal segmental glomerulosclerosis.

47
Q

How is glomerulonephritis treated?

A

Depends on cause but most types treated with immunosuppression (eg steroids) and antihypertensives eg ACE inhibitors/ARBs.

48
Q

What is the most common cause of nephrotic syndrome in children? How is it treated?

A

Minimal change disease. Usually idiopathic and treated with steroids.

49
Q

What is the most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis.

50
Q

What is the most common cause of primary glomerulonephritis, and usually occurs in 20-30 year olds?

A

Bergers disease aka IgA nephropathy. IgA deposits and glomerular mesangial proliferation.

51
Q

What is the most common cause of glomerulonephritis?

A

Membranous glomerulonephritis. Peak incidence in 20s and 60s, histology shows IgG and complement deposits on the basement membrane. Can be secondary to malignancy/RA/NSAIDS but usually idiopathic.

52
Q

What is the most likely cause of haematuria, oligouria and oedema in a 25 year old with a recent sore throat?

A

Post-strep glomerulonephritis (AKA diffuse proliferative glomerulonephritis).
Nephritic syndrome 1-3 weeks after strep, full recovery

53
Q

What is the most likely cause of acute kidney failure and haemoptysis? Give a differential.

A

Goodpasture syndrome - anti-GBM antibodies attack glomerulus and pulmonary basement membranes.
Differential: GPA - ANCA-associated vasculitis, wheeze, sinusitis, saddle shaped nose.

54
Q

What would you seen on histology in rapidly progressing glomerulonephritis secondary to goodpastures syndrome?

A

Crescentic glomerulonephritis.

55
Q

What is the most common cause of CKD in the UK?

A

Diabetic nephropathy.

56
Q

How does hyperglycaemia result in kidney failure?

A

High glucose passing through the kidney causes scarring (glomerulosclerosis). It becomes leaky so protein passes from blood to urine causing proteinurea.

57
Q

How is diabetic nephropathy screened for?

A

Albumin creatinine ratio
U+Es
regularly in people with diabetes

58
Q

How is diabetic nephropathy treated?

A

Optimise blood sugar and blood pressure

ACE inhibitors even if BP normal.

59
Q

What is interstitial kidney disease?

A

Inflammation of space between cells and tubules (interstitium) of the kidney. Includes acute interstitial nephritis and chronic tubulointerstitial nephritis.

60
Q

What is acute interstitial nephritis and how does it present?

A

Acute inflammation of the tubules and interstitium. Presents with AKI and hypertension. Usually caused by hypersensitivity reaction to drugs (NSAIDS, abx) or infection. May also get rash, fever and eosinophilia because of the hypersensitivity reaction.

61
Q

How do you manage interstitial kidney disease?

A

Treat underlying cause (eg stop NSAID/abx in AIN)

Steroids to reduce inflammation (more so in AIN than CTIN)

62
Q

What is chronic tubulointerstitial nephritis and how does it present?

A

Chronic inflammation of the tubules and interstitium. Can be AI, infectious, iatrogenic, granulomatous. Presents with CKD. Treat underlying cause.

63
Q

What is acute tubular necrosis and how does it present?

A

Damage and death of epithelial cells of renal tubules due to ischemia or toxins. Presents with AKI - most common cause.

64
Q

What would you see on urinalysis with ATN?

A

Muddy brown casts (pathognomonic), renal tubular epithelial cells that you’ve pissed out

65
Q

How do you manage ATN?

A

Fluids
Stop nephrotixic meds (NSAIDs, gentamycin, avoid contrast)
treat complications eg electrolyte imbalance
Epithelial cells should regenerate in 1-3 weeks

66
Q

What is renal tubular acidosis?

A

Metabolic acidosis due to pathology in the renal tubules. These usually balance H+ and HCO3 ions between blood and urine to maintain normal pH. There are 4 types each with different pathophysiology (1 and 4 most relevant).

67
Q

State which part of the kidney is affected by type 1 renal tubular acidosis and give 3 causes.

A
Distal tubule, unable to excrete H+ --> acidosis.
Genetic - AD/AR forms
SLE
Sjogren's 
PBC
Hyperthyroidism
Sickle cell anaemia
Marfan's
68
Q

How does type 1 RTA present?

A

Children - failure to thrive
Hyperventilation (resp compensation for metabolic acidosis)
CKD
Osteomalacia

Hypokalaemia
Urinary pH above 6 (high)

69
Q

How is t1 RTA managed?

A

Oral bicarbonate, this corrects other electrolyte imbalances.

70
Q

Which part of the kidney is affected by Type 2 renal tubular acidosis?

A

Proximal tubule unable to reabsorb bicarbonate from urine into blood –> piss out bicarb.
Hypokalaemia, met acidosis, urinary pH >6
treat with oral bicarb

71
Q

What causes type 2 renal tubular acidosis?

A

Fanconi’s syndrome usually.

72
Q

What is type 3 RTA?

A

Type 1+2 rta combined (proximal and distal tubule pathology)

73
Q

What is type 4 RTA?

A

Aldosterone usually causes potassium and hydrogen excretion in the urine. Reduced aldosterone –> distal tubule doesn’t excrete hydrogen or potassium ions leading to metabolic acidosis, high urinary pH and hyperkalaemia. Most common cause of RTA.

74
Q

What causes type 4 RTA?

A

Adrenal insufficiency
Drugs - ACEi, spironolactone
Systemic - SLE, diabetes, HIV

75
Q

How is type 4 RTA managed?

A

Fludrocortisone to replace aldosterone function
Sodium bicarb
Treat hyperkalaemia