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Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is AKI

A

Acute drop in kidney function

Diagnosed by measuring serum creatinine

Increased morbidity and mortality

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2
Q

What is the NICE criteria for AKI

A

Rise in creatinine in .25 micromol/L in 48 hrs

Rise in creatinine of > 50% in 7 days

Urine output of < 0.5 ml/kg/hr for > 6 hrs

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3
Q

What are the risk factors for AKI

A

Consider in anyone with an acute illness or having surgery

CKD

Heart failure

Diabetes

Liver disease

Sepsis

> 65

Cognitive impairment

Nephrotoxic drugs (NSAISs, ACE inhibitors, antibiotics)

Use of contrast

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4
Q

What are the pre-renal causes of AKI

A

Most common cause of AKI

Due to inadequate blood supply to kidneys

Dehydration

Hypotension (shock)

Heart failure

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5
Q

What are the renal causes of AKI

A

Glomerulonephritis

Intestinal nephritis

Acute tubular necrosis

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6
Q

What are the post-renal causes of AKI

A

Obstruction of outflow of urine (backpressure to kidneys, obstructive uropathy)

Kidney stones

Masses

Ureter/urethral strictures

Enlarged prostate/prostate cancer

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7
Q

What investigations are needed for AKI

A

Urinalysis (leukocytes and nitrates, proteins, blood, glucose)

Ultrasound of urinary tract

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8
Q

What is the management for AKI

A

Avoid/stop nephrotoxic drugs

Adequate fluid intake/fluid rehydration

Relieve obstruction

May need dialysis

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9
Q

What are the indications for renal replacement therapy

A

Hyperkalaemia due to medical therapy

Metabolic acidosis due to medical therapy

Fluid overload due to diuretics

Uraemic pericarditis

Uraemic encephalopathy (vomiting, confusion, drowsiness, reduced consciousness)

Intoxications (lithium, methanol)

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10
Q

What are the complications of AKI

A

Hyperkalaemia

Fluid overload

Heart failure

Pulmonary oedema

Metabolic acidosis

Uraemia (encephalopathy, pericarditis)

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11
Q

What is CKD

A

Chronic reduction in kidney function

Usually permanent and progressive

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12
Q

What are the causes of CKD

A

Diabetes

Hypertension

Age-related decline

Glomerulonephritis

Polycystic kidney disease

Medications (NSAIDs, PPIs, lithium)

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13
Q

What are the risk factors for CKD

A

Increasing age

Hypertension

Diabetes

Smoking

Nephrotoxic drugs

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14
Q

How might CKD present

A

Usually asymptomatic

Pruritus

Loss of appetite

Nausea

Oedema

Muscle cramps

Peripheral neuropathy

Pallor

Hypertension

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15
Q

What investigations are needed in CKD

A

U&Es (measure eGFR, 2 tests 3 months apart)

Proteinuria (urine albumin:creatinine, > 3 mg/mmol is significant)

Haematuria (urine dip, investigate for malignancy)

Renal ultrasound (if have accelerated CKD, haematuria, family history of polycystic kidney disease, evidence of obstruction)

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16
Q

What are the stages of CKD

A

G score (based on eGFR):
- G1: > 90
- G2: 60 - 89
- G3: 45 - 59
- G4: 15 - 29
- G5: < 15 (end stage renal failure)

A score (based on albumin:creatine):
- A1: < 3 mg/mmol
- A2: 3 - 30 mg/mmol
- A3: > 30 mg/mmol

Need to have at least eGFR < 60 or proteinuria to have CKD

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17
Q

What are the complications of CKD

A

Anaemia

Renal bone disease

Cardiovascular disease

Peripheral neuropathy

Dialysis-related problems

Hyperparathyroidism

Hypertension

Malnutrition

Dyslipidaemia

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18
Q

What are the NICE guidelines for referral to a specialist in CKD

A

eGFR < 30

ACR > 70 mg/mmol

Accelerated progression (eGFR decrease by 15 (or 25%) in 1 year)

Uncontrolled hypertension (despite using > 4 antihypertensives)

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19
Q

What is the management for CKD

A

Treat underlying cause

Slow progression (optimise diabetes/hypertension, treat glomerulonephritis, monitor bloods)

Reduce risk of cardiovascular disease (statins, control BP, improve diabetic control, lifestyle modifications)

Reduce risk of complications (exercise, weight loss, smoking cessation, reduce salt, atorvastatin)

Treat complications

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20
Q

How is hypertension treated in CKD

A

ACE inhibitors (1st line for CKD)

Target < 140/90

Monitor serum potassium (CKD and ACE inhibitors cause hyperkalaemia)

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21
Q

What is anaemia of CKD

A

CKD causes from in EPO

Management: exogenous EPO, blood transfusions

Treat iron deficiency before giving EPO

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22
Q

What is renal bone disease

A

Features: osteomalacia, osteoporosis, osteosclerosis

X-ray changes (‘rugger jersey spine’

Management: vit D supplements, low phosphate diet, bisphosphonates

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23
Q

What are the indications for acute dialysis

A

AEIOU

Acidosis (severe and not responding to treatment)

Electrolyte abnormalities (severe and unresponsive hyperkalaemia)

Intoxication (overdose)

Oedema (severe and unresponsive pulmonary oedema)

Uraemia (seizures, reduced consciousness)

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24
Q

What are the indications for long term dialysis

A

End stage renal disease (CKD stage 5)

If any of the acute indications continue long term

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25
Q

What are the options for maintenance dialysis

A

Continuous ambulatory peritoneal dialysis

Automated peritoneal dialysis

Haemodialysis

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26
Q

What is peritoneal dialysis

A

Use peritoneal membrane as filtration membrane

Dialysis solution (dextrose) added to peritoneal cavity

Ultrafiltration occurs from blood

Involves a tenckhoff catheter

Continuous ambulatory peritoneal dialysis/automated dialysis

Complications: bacterial peritonitis, peritoneal sclerosis, ultrafiltration failure, weight gain, psychological effects, hydrothorax

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27
Q

What is haemodialysis

A

Usually 4 hours 3 days a week

Tunnelled cuffed catheter/arterio-venous fistula

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28
Q

What are the features of nephritic syndrome

A

Haematuria

Oliguria

Proteinuria < 3.5 g/24 hrs

Fluid retention

Hypertension

29
Q

What are the features of nephrotic syndrome

A

Peripheral oedema

Proteinuria

Serum albumin < 30

Hypercholesterolaemia

Frothy urine

Complication: higher risk of infection, VTE, progression to CKD, hypertension, hyperlipidaemia

30
Q

What is glomerulonephritis

A

Conditions that cause inflammation of/around glomerulus and nephrons

31
Q

What are the types of glomerulonephritis

A

Minimal change disease

Focal segmental glomerulosclerosis

Membranous glomerulonephritis

IgA nephropathy

Post-streptococcal glomerulonephritis

Mesangiocapillary glomerulonephritis

Rapid progressive glomerulonephritis

Goodpasture syndrome

32
Q

What is the general management for glomerulonephritis

A

Immunosuppression (steroids)

Blood pressure control (ACE inhibitors or ARBs)

33
Q

What is IgA nephropathy

A

Berger’s disease

Most common cause of primary glomerulonephritis

Present in 20s

34
Q

Membranous glomerulonephritis

A

Most common type of glomerulonephritis

Peaks in 20s and 60s

Get IgG and complement deposits on basement membrane

70% idiopathic

Can be secondary to: malignancy, rheumatoid disorders, drugs (NSAIDs)

35
Q

What is post-streptococcal glomerulonephritis

A

Usually under 30s (often children 3 - 12)

1 - 3 weeks after streptococcal infection

Usually make full recover

36
Q

What is Goodpasture syndrome

A

Anti-GBM antibodies attack glomerulus and pulmonary basement membranes

Get: glomerulonephritis, pulmonary haemorrhage

37
Q

What is rapidly progressive glomerulonephritis

A

See ‘crescentic glomerulonephritis’ on histology

Very acute illness

Responds well to treatment

Often secondary to Goodpasture syndrome

38
Q

What is diabetic nephropathy

A

Most common cause of glomerular pathology or CKD

Chronically high levels of glucose passing through glomerulus (get glomerular scarring)

Have proteinuria

39
Q

What investigations are needed for diabetic nephropathy

A

Diabetic patients should regularly be screened for nephropathy with albumin:creatinine and U&Es

40
Q

What is the management for diabetic nephropathy

A

Optimise blood sugar levels and blood pressure (ACE inhibitors)

41
Q

What is interstitial kidney disease

A

Inflammation of the space between cells and tubules in the kidney

42
Q

What is acute interstitial nephritis

A

On presentation: AKI, hypertension, features of hypersensitivity reaction (rash, fever, eosinophilia)

Acute inflammation of tubules and interstitium

Usually due to hypersensitivity to drugs/infection

Management: treat underlying cause, steroids

43
Q

What is chronic tubulointerstitial nephritis

A

Chronic inflammation of tubules and interstitium

Present with CKD

Management: treat underlying cause, steroids

44
Q

What is acute tubular necrosis

A

Necrosis of epithelial cells of renal tubules

Most common cause of AKI

Damage due to ischaemia/toxins

Reversible (epithelial cells can regenerate, 7-12 days to recovery)

45
Q

What are the causes of acute tubular necrosis

A

Ischaemia: shock, sepsis, dehydration

Toxins: contrast, gentamycin, NSAIDs

46
Q

What investigation is needed for acute tubular necrosis

A

Urinalysis (‘muddy brown casts’)

47
Q

What is the management for acute tubular necrosis

A

Supportive management

IV fluids

Stop nephrotoxic medications

Treat complications

48
Q

What is renal tubular acidosis

A

Metabolic acidosis due to pathology in renal tubule

Tubules: maintain normal pH

4 types

49
Q

What is type 1 renal tubular acidosis

A

Pathology in distal tubule (unable to excrete H+)

Causes: genetic, SLE, Sjogren’s syndrome, primary biliary cirrhosis, hyperthyroidism, sickle cell anaemia, Marfan’s syndrome

Presentation: failure to thrive in children, hyperventilation (compensate for metabolic acidosis), CKD, bone disease

Treatment: oral bicarbonates (correct electrolyte imbalance)

Complications: hypokalaemia, metabolic acidosis, high urinary pH

50
Q

What is type 2 renal tubular acidosis

A

Pathology in proximal tubule (unable to reabsorb HCO3-)

Causes: Fanconi’s syndrome

Treatment: oral bicarbonates

Complications: hypokalaemia, metabolic acidosis, high urinary pH

51
Q

What is type 3 renal tubular acidosis

A

Pathology in proximal and distal tubule (combination of types 1 and 2)

Very rare

52
Q

What is type 4 renal tubular acidosis

A

Due to reduced aldosterone

Causes: adrenal insufficiency, medications (ACE inhibitors, spironolactone), SLE, diabetes, HIV

Treatment: fludrocortisone, sodium bicarbonate

Complications: hyperkalaemia, high chloride, metabolic acidosis, low urinary pH

53
Q

What is haemolytic uraemic syndrome

A

Thrombosis in small blood vessels throughout body

Usually triggered by shiga toxin (E coli 0157)

Clots: consume platelets, cut up RBCs as they pass

54
Q

How might haemolytic uraemic syndrome present

A

Classic triad: haemolytic anaemia, AKI, thrombocytopenia

Initially get GI symptoms (bloody diarrhoea)

Around day 5, develop HUS: reduced urine output, haematuria, abdominal pain, lethargy and irritability, confusion, hypertension, bruising

55
Q

What is the management for haemolytic uraemic syndrome

A

Supportive management: antihypertensives, blood transfusion, dialysis

10% mortality

56
Q

What is rhabdomyolysis

A

Skeletal muscle breaks down, releases breakdown products into blood

Apoptosis of myocytes releases: myoglobin (nephrotoxic), potassium, phosphate, creatine kinase

57
Q

What are the causes of rhabdomyolysis

A

(Anything that causes significant damage to muscle cells)

Prolonged immobility

Rigorous exercise

Crush injuries

Seizures

58
Q

How might rhabdomyolysis present

A

Muscle aches and pains

Oedema

Fatigue

Constipation

Red-brown urine

59
Q

What investigations are needed for rhabdomyolysis

A

Creatinine kinase (rises for around 12 hours, remains elevated for 1-3 days, increased risk of AKI)

Urine dipstick

U&Es

ECG

60
Q

What is the management for rhabdomyolysis

A

IV fluids (rehydration, filtration of breakdown products)

IV sodium bicarbonate (reduces toxicity of myoglobin)

IV mannitol (increases GFR, flush out breakdown products, reduces oedema)

Treat complications

61
Q

What are the causes of hyperkalaemia

A

Conditions: AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome

Medications: aldosterone antagonists (spironolactone), ACE inhibitors, ARBs, NSAIDs, potassium supplements

62
Q

What investigations are needed for hyperkalaemia

A

U&Es

ECG

63
Q

What is the management for hyperkalaemia

A

Close ECG monitoring

Insulin and dextrose infusion

Calcium gluconate (stabilises cardiac muscles)

Nebulised salbutamol

Oral calcium resonium

Sodium bicarbonate

Dialysis

64
Q

What is polycystic kidney disease

A

Kidney function impaired

Also get hepatic cysts and cerebral aneurysms

Can be autosomal dominant or autosomal recessive

65
Q

How is polycystic kidney disease diagnosed

A

Ultrasound

Genetic testing (autosomal dominant PKD-1/PKD-2,

66
Q

Give an overview of autosomal dominant polycystic kidney disease

A

Extra-renal manifestations: cerebral aneurysms, hepatic/splenic/pancreatic/ovarian cysts, mitral regurge, colonic diverticula, aortic root dilation

Complications: chronic loin pain, hypertension, cardiovascular disease, gross haematuria, renal stones, end-stage renal failure

67
Q

Give an overview of autosomal recessive polycystic kidney disease

A

Rarer, more severe

Often presents with pregnancy (oligohydramnios)

Features: underdevelopment of lungs (respiratory failure just after birth), dysmorphic features (underdeveloped ear cartilage, low set ears, flat nasal bridge)

68
Q

What is the management for polycystic kidney disease

A

Tolvaptan (vasopressin receptor antagonist, slows development of cysts)

Supportive: antihypertensives, analgesia, antibiotics, dialysis, renal transplant

Other steps: genetic counselling, avoid contact sports, regular ultrasounds, regular bloods, regular BP monitoring, MR angiogram

Medicine (9 decks)

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