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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
What are the options for maintenance dialysis
Continuous ambulatory peritoneal dialysis Automated peritoneal dialysis Haemodialysis
26
What is peritoneal dialysis
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
27
What is haemodialysis
Usually 4 hours 3 days a week Tunnelled cuffed catheter/arterio-venous fistula
28
What are the features of nephritic syndrome
Haematuria Oliguria Proteinuria < 3.5 g/24 hrs Fluid retention Hypertension
29
What are the features of nephrotic syndrome
Peripheral oedema Proteinuria Serum albumin < 30 Hypercholesterolaemia Frothy urine Complication: higher risk of infection, VTE, progression to CKD, hypertension, hyperlipidaemia
30
What is glomerulonephritis
Conditions that cause inflammation of/around glomerulus and nephrons
31
What are the types of glomerulonephritis
Minimal change disease Focal segmental glomerulosclerosis Membranous glomerulonephritis IgA nephropathy Post-streptococcal glomerulonephritis Mesangiocapillary glomerulonephritis Rapid progressive glomerulonephritis Goodpasture syndrome
32
What is the general management for glomerulonephritis
Immunosuppression (steroids) Blood pressure control (ACE inhibitors or ARBs)
33
What is IgA nephropathy
Berger's disease Most common cause of primary glomerulonephritis Present in 20s
34
Membranous glomerulonephritis
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
What is post-streptococcal glomerulonephritis
Usually under 30s (often children 3 - 12) 1 - 3 weeks after streptococcal infection Usually make full recover
36
What is Goodpasture syndrome
Anti-GBM antibodies attack glomerulus and pulmonary basement membranes Get: glomerulonephritis, pulmonary haemorrhage
37
What is rapidly progressive glomerulonephritis
See 'crescentic glomerulonephritis' on histology Very acute illness Responds well to treatment Often secondary to Goodpasture syndrome
38
What is diabetic nephropathy
Most common cause of glomerular pathology or CKD Chronically high levels of glucose passing through glomerulus (get glomerular scarring) Have proteinuria
39
What investigations are needed for diabetic nephropathy
Diabetic patients should regularly be screened for nephropathy with albumin:creatinine and U&Es
40
What is the management for diabetic nephropathy
Optimise blood sugar levels and blood pressure (ACE inhibitors)
41
What is interstitial kidney disease
Inflammation of the space between cells and tubules in the kidney
42
What is acute interstitial nephritis
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
What is chronic tubulointerstitial nephritis
Chronic inflammation of tubules and interstitium Present with CKD Management: treat underlying cause, steroids
44
What is acute tubular necrosis
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
What are the causes of acute tubular necrosis
Ischaemia: shock, sepsis, dehydration Toxins: contrast, gentamycin, NSAIDs
46
What investigation is needed for acute tubular necrosis
Urinalysis ('muddy brown casts')
47
What is the management for acute tubular necrosis
Supportive management IV fluids Stop nephrotoxic medications Treat complications
48
What is renal tubular acidosis
Metabolic acidosis due to pathology in renal tubule Tubules: maintain normal pH 4 types
49
What is type 1 renal tubular acidosis
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
What is type 2 renal tubular acidosis
Pathology in proximal tubule (unable to reabsorb HCO3-) Causes: Fanconi's syndrome Treatment: oral bicarbonates Complications: hypokalaemia, metabolic acidosis, high urinary pH
51
What is type 3 renal tubular acidosis
Pathology in proximal and distal tubule (combination of types 1 and 2) Very rare
52
What is type 4 renal tubular acidosis
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
What is haemolytic uraemic syndrome
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
How might haemolytic uraemic syndrome present
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
What is the management for haemolytic uraemic syndrome
Supportive management: antihypertensives, blood transfusion, dialysis 10% mortality
56
What is rhabdomyolysis
Skeletal muscle breaks down, releases breakdown products into blood Apoptosis of myocytes releases: myoglobin (nephrotoxic), potassium, phosphate, creatine kinase
57
What are the causes of rhabdomyolysis
(Anything that causes significant damage to muscle cells) Prolonged immobility Rigorous exercise Crush injuries Seizures
58
How might rhabdomyolysis present
Muscle aches and pains Oedema Fatigue Constipation Red-brown urine
59
What investigations are needed for rhabdomyolysis
Creatinine kinase (rises for around 12 hours, remains elevated for 1-3 days, increased risk of AKI) Urine dipstick U&Es ECG
60
What is the management for rhabdomyolysis
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
What are the causes of hyperkalaemia
Conditions: AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome Medications: aldosterone antagonists (spironolactone), ACE inhibitors, ARBs, NSAIDs, potassium supplements
62
What investigations are needed for hyperkalaemia
U&Es ECG
63
What is the management for hyperkalaemia
Close ECG monitoring Insulin and dextrose infusion Calcium gluconate (stabilises cardiac muscles) Nebulised salbutamol Oral calcium resonium Sodium bicarbonate Dialysis
64
What is polycystic kidney disease
Kidney function impaired Also get hepatic cysts and cerebral aneurysms Can be autosomal dominant or autosomal recessive
65
How is polycystic kidney disease diagnosed
Ultrasound Genetic testing (autosomal dominant PKD-1/PKD-2,
66
Give an overview of autosomal dominant polycystic kidney disease
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
Give an overview of autosomal recessive polycystic kidney disease
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
What is the management for polycystic kidney disease
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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