RENAL Flashcards
(168 cards)
1
Q
What is HUS?
A
Haemolytic uraemia syndrome
Thrombosis in small blood vessels
2
Q
What is the triad of HUS?
A
• Haemolytic anaemia
• AKI
Thrombocytopenia
3
Q
How does HUS present?
A
Reduced urine output Haematuria Abdominal pain Lethargy Hypertension Bruising
4
Q
Who is most commonly affected by HUS?
A
Children
5
Q
What is typical HUS?
A
Secondary to E.coli infection
6
Q
What is primary HUS?
A
Caused by complement dysregulation
7
Q
What is STEC?
A
Shiga toxic-producing E.Coli
8
Q
What is the most common cause of HUS? Name three other causes.
A
E.coli (Shiga toxin) - 90% of cases in children
HIV
Pneumococcal infection
Rare: SLE, drugs, cancer
9
Q
Which two medications increase the risk of HUS?
A
Antibiotics
Anti-motility drugs (Loperamide)
10
Q
Which investigations should be done in HUS?
A
FBC - anaemia, thrombocytopenia
U&E - AKI
Stool culture - STEC infection, PCR for Shiga toxins
11
Q
What is the mortality rate of HUS?
A
10% - medical emergency
12
Q
How is HUS managed?
A
Supportive - self-limiting
Anti-hypertensives
Blood transfusions
Dialysis
13
Q
What percentage of patients will fully recover from HUS?
A
80%
14
Q
What is an AKI?
A
Acute kidney injury (AKI) is defined as an acute drop in kidney function. It is diagnosed by measuring the serum creatinine.
15
Q
What are the NICE criteria for AKI?
A
- Rise in creatinine of ≥ 25 micromol/L in 48 hours
- Rise in creatinine of ≥ 50% in 7 days
- Urine output of < 0.5ml/kg/hour for > 6 hours
16
Q
What are the three stages of AKI according to creatinine?
A
Stage 1 = ^1.5-1.9x baseline
Stage 2 = ^2-2.9x baseline
Stage 3 = >3x baseline
17
Q
What are the three stages of AKI according to urine production?
A
Stage 1 = <0.5ml/kg/hour >6 hours
Stage 2 = <0.5ml/kg/hour >12 hours
Stage 3 = <0.3ml/kg/hour >24 hours OR anuric for 12 hours
18
Q
What are the risk factors for AKI?
A
• Chronic kidney disease • 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
19
Q
What are the three types of AKI?
A
- Pre-renal - reducing renal perfusion (hypovolaemia/hypoperfusion)
- Intra-renal - damage to the kidney (ischaemia, sepsis, inflammation)
- Post-renal - outflow obstruction
20
Q
What is the most common cause of AKI?
A
Pre-renal
21
Q
What are the causes of pre-renal AKI?
A
- Dehydration
- Hypotension/shock (sepsis)
- Heart failure
22
Q
What are the causes of intra-renal AKI?
A
- Glomerulonephritis
- Interstitial nephritis
- Acute tubular necrosis
23
Q
What are the causes of post-renal AKI?
A
- Kidney stones
- Masses such as cancer in the abdomen or pelvis
- Ureter or urethral strictures
- Enlarged prostate or prostate cancer
24
Q
Name some drugs that will cause AKI.
A
Aminoglycosides
Amphotericin
Cytotoxic chemotherapy
Diuretics
Immunosuppressants
Lithium salts
NSAIDs/COX inhibitors
Radiocontrast media
Other
25
Name some pathological states that are nephrotoxic.
Hypoperfusion
Sepsis
Rhabdomyolysis
Hepatorenal syndrome
26
What is the best measure of renal function?
eGFR
27
When should creatinine clearance be used instead of eGFR to estimate renal function?
```
Elderly
Toxic drugs
Extremes of muscle mass
Drugs with narrow therapeutic window
DOACs
```
28
What will be seen on urinalysis in AKI?
- Leucocytes and nitrites suggest infection
- Protein and blood suggest acute nephritis (but can be positive in infection)
- Glucose suggests diabetes
29
What imaging might be needed in AKI?
US - particularly good for obstruction.
30
What is the approach to management of an AKI?
Prevent the injury and correct the underlying cause: avoid nephrotoxic medications.
- Fluid rehydration with IV fluids in pre-renal AKI
- Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
- Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
31
Which fluid should be prescribed in a patient with and AKI, hypovolaemia and metabolic acidosis?
Sodium bicarbonate 1.26%
32
Name 4 complications of AKI.
1. Hyperkalaemia - kidneys cannot filter excess potassium
2. Fluid overload - pulmonary oedema, heart failure
3. Metabolic acidosis - kidneys cannot produce bicarbonate
4. Uraemia - encephalopathy (confusion), pericarditis
33
How is pulmonary oedema treated in AKI?
Haemodialysis
34
What is acute tubular necrosis?
Damage and death of renal tubular epithelial cells
35
How does damage to the cells occur in ATN?
Secondary to ischaemia
| Directly due to toxins
36
How long does it take for renal tubular cells to recover?
7-21 days
37
Name 3 ischaemic causes of ATN.
Shock
Dehydration
Sepsis
38
Name 3 toxic causes of ATN.
```
NSAIDs
Contrast dyes
Aminoglycosides
Lithium
Heroin
```
39
What is seen on urinalysis in ATN?
Muddy brown casts - pathognomonic (only seen in ATN)
| Renal tubular epithelial cells
40
What is the management of ATN?
Supportive:
- Fluids
- Stop nephrotoxic medications
41
What are the causes of CKD?
```
Diabetes
HTN
Age-related decline
Glomerulonephritis
PKD
Drugs - NSAIDs, PPIs, lithium
```
42
Which drugs cause CKD?
NSAIDs
PPIs
Lithium
43
What are the risk factors for CKD?
Older age
HTN
Diabetes
Smoking
44
Which two parameters are used to classify CKD?
eGFR
| Albumin: creatinine ratio
45
How does CKD normally present?
Asymptomatic
```
Pruritis
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN
```
46
What investigations are done in CKD?
U&E
Urine dipstick
Renal US
47
How do you diagnose CKD?
2 x eGFR tests
| 3 months apart
48
What is the ACR? What result is significant?
Urine albumin: creatinine ratio
| >3mg/mmol
49
What is the G score?
Based on the eGFR (measure of glomerular filtration rate)
```
• G1 = eGFR >90
• G2 = eGFR 60-89
• G3a = eGFR 45-59
• G3b = eGFR 30-44
• G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)
```
50
What is the A score in CKD?
The A score is based on the albumin:creatinine ratio:
```
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol
```
51
What are the complications of CKD?
```
• Anaemia
• Renal bone disease
• Cardiovascular disease
• Peripheral neuropathy
Dialysis related problems
```
52
When should you refer a patient to a renal specialist in CKD?
• eGFR < 30
• ACR ≥ 70 mg/mmol
• Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
Uncontrolled hypertension despite ≥ 4 antihypertensives
53
What are the aims of management in CKD?
• Slow the progression of the disease
• Reduce the risk of cardiovascular disease
• Reduce the risk of complications
Treating complications
54
How can you slow the progression of CKD?
• Optimise diabetic control
• Optimise hypertensive control
Treat glomerulonephritis
55
How do you reduce the risk of complications in CKD?
• Exercise, maintain a healthy weight and stop smoking
• Special dietary advice about phosphate, sodium, potassium and water intake
Offer atorvastatin 20mg for primary prevention of cardiovascular disease
56
How do you treat anaemia caused by CKD?
Iron
| EPO
57
How do you treat HTN in CKD?
ACEi's offered to all patients:
• Diabetes plus ACR > 3mg/mmol
• Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol
58
How do you manage end stage renal failure?
- Dialysis in end stage renal failure
| - Renal transplant in end stage renal failure
59
What is allosensitisation?
Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.
60
What is CKD-MBD?
1. Osteomalacia (softening of bones)
2. Osteoporosis (brittle bones)
3. Osteosclerosis (hardening of bones)
61
What is seen on an XR of the spine in CKD-MBD?
“rugger jersey” spine
| sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)
62
How does CKD-MBD result in a secondary hyperparathyroidism?
parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone.
63
How is CKD-MBD managed?
- Active forms of vitamin D (alfacalcidol and calcitriol)
- Low phosphate diet
- Bisphosphonates can be used to treat osteoporosis
64
What is interstitial nephritis?
Inflammation of the cells surrounding the tubules within the kidney.
65
What are the two types of interstitial nephritis?
Acute interstitial nephritis
| Chronic tubulointerstitial nephritis
66
How does acute interstitial nephritis present?
AKI
HTN
(rash, fever or eosinophilia is hypersensitivity reaction)
67
Give three causes of acute interstitial nephritis.
Toxins
Infection
Hypersensitivity reaction
68
How do you treat acute interstitial nephritis?
treat underlying cause
| steroids
69
How does chronic tubulointerstitial nephritis present?
CKD
70
Give four causes of chronic tubulointerstitial nephritis
Autoimmune
Infectious
Iatrogenic
Granulomatous disease
71
What is the management of chronic tubulointerstitial nephritis?
treat underlying cause
| Steroids (under specialist supervision)
72
What is renal tubular acidosis (RTA)?
Metabolic acidosis due to pathology in the tubules of the kidney.
73
What is the normal function of the proximal and distal renal tubules?
Proximal - reabsorb bicarbonate back into the blood
| Distal - excrete H+ ions
74
How many types of RTA are there?
4
75
Which are the two most clinically relevant types of RTA?
1 and 4
76
What is the treatment for steroid resistant minimal change disease?
cyclophosphamide
77
What is the prognosis of minimal change disease?
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
78
What is the first-line management of minimal change disease?
```
PO prednisolone (80% of cases will respond)
Urgent outpatient review
```
79
What is the definition of hyperkalaemia? What is classified as severe?
>5.3mmol/L
| >6.5mmol/L
80
Give 6 causes of hyperkalaemia.
```
• Acute kidney injury
• Chronic kidney disease
• Rhabdomyolysis
• Adrenal insufficiency
• Tumour lysis syndrome
Drugs
```
81
Name 5 drugs that commonly cause hyperkalaemia?
```
• Aldosterone antagonists (spironolactone and eplerenone)
• ACE inhibitors
• Angiotensin II receptor blockers
• NSAIDs
Potassium supplements
```
82
What can cause a falsely elevated potassium level?
Haemolysis (lab may request another sample)
83
How does hyperkalaemia present?
```
Nausea
Muscle weakness
ECG changes
Ventricular fibrillation
Cardiac arrest
```
84
What are the ECG changes in hyperkalaemia?
• Tall peaked T waves
• Flattening or absence of P waves
Broad QRS complexes
85
What are the three aims of treatment in Hyperkalaemia?
Protect the heart
Lower serum potassium concentration
Remove excess potassium
86
What drug us used for cardio protection?
10ml calcium gluconate 10% solution, slow IV injection over 3-5 minutes
Titrate and adjust according to ECG
(mix with glucose 5% over 20 mins if taking digoxin)
87
How should you treat patients with a potassium of <6 mmol/L and otherwise stable renal function?
Diet
| Adjust medications
88
When do patients require urgent treatment for hyperkalaemia?
ECG changes
| >6.5mmol/L
89
What is first-line treatment for hyperkalaemia?
Insulin and dextrose
| Calcium gluconate
90
Which medication can be used to lower serum potassium?
Oral calcium resonium
91
What management might be needed in severe hyperkalaemia?
Dialysis
92
What is the definition of hypokalaemia?
<3.5mmol/L
93
Name some causes of hypokalaemia.
Internal distribution:
- Alkalosis
- ^insulin
- B-agonists
Excretion:
- Vomitting, diarrhoea
- RTA
- Diuretics, steroids
- Cushing's, Conn's syndrome
Inadequate intake:
- Inappropriate fluid management
94
Which drugs commonly cause hypokalaemia?
```
Laxatives
Glucocorticoid therapy
Insulin
Loop diuretics
Salbutamol
Antibacterial
Thiazide diuretics
Theophylline
```
95
What are the ECG changes in hypokalaemia?
```
• Flattened/inverted T waves
• Prominent U waves
• ST depression
• Long PR interval
Long QT interval
```
96
How does hypokalaemia present?
Often asymptomatic
```
Muscle weakness
Cramps
Fatigue
Constipation
Palpitations
```
97
How should low potassium be corrected?
1L IV sodium chloride 0.9% with 40 mmol KCl over 4 hours
potassium chloride 0.3% (1L is 40mmol of K)
IV potassium chloride 0.15% (1L is 20mmol of K)
98
What is the max dose of potassium that can be given IV in 1 hour?
10mmol
99
Which other electrolyte should be checked in hypokalaemia?
Mg - must be corrected for K to return to normal
100
What is glomerulonephritis?
an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron.
101
What are the two syndromes caused by glomerulonephritis?
Nephritic syndrome
| Nephrotic syndrome
102
What is glomerulosclerosis?
A pathological process of scarring of the tissue in the glomerulus.
Caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.
103
What is the most common cause of primary glomerulonephritis?
IgA nephropathy (AKA Berger’s disease)
104
What is Goodpasture's syndrome?
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes.
This causes glomerulonephritis and pulmonary haemorrhage.
105
How might a patient present with Goodpasture's syndrome?
Acute renal failure
| Haemoptysis
106
Which differential diagnoses should be considered in a patient presenting with acute renal failure and haemoptysis?
Goodpasture's syndrome
| Wegener's granulomatosis (granulomatosis with polyangiitis)
107
What investigations should be done in glomerulonephritis?
```
Urine dipstick
Light microscopy
Electron microscopy
Immunofluorescence
Bloods - Strep Ab's
```
108
What might be seen on a urine dipstick in glomerulonephritis?
Proteinuria
Haematuria
WBCs
109
What can be seen on light microscopy in glomerulonephritis?
Glomerular inflammation
| Sclerosis
110
What can be seen on electron microscopy in glomerulonephritis?
Effacement
111
How is glomerulonephritis generally treated?
- Immunosuppression (e.g. steroids)
- Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
112
Name a complication of glomerulonephritis?
Infection (due to loss of Ig in urine)
113
Which types of glomerular disease are likely to cause nephritic syndrome?
- IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
- Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
- Rapidly progressive glomerulonephritis
114
What are the features of nephritic syndrome?
```
• Abrupt onset
• Oedema +
• BP raised
• Proteinuria <3.5g/day
• Haematuria ++++
RBC casts
```
115
What is another name for IgA nephropathy?
Berger's disease
116
What is the peak age at presentation for IgA nephropathy?
20s
117
What is seen on histology in IgA nephropathy?
IgA deposits and glomerular mesangial proliferation
118
When do patients present with post-streptococcal glomerulonephritis?
1-3 weeks after infection
| <30 years
119
What type of hypersensitivity reaction causes post-streptococcal glomerulonephritis?
Type III
120
What is seen on histology in rapidly progressive glomerulonephritis?
Crescentic glomerulonephritis
121
What are the features of nephrotic syndrome?
```
• Insiduous onset
• Oedema ++++
• Normal BP
• Proteinuria >3.5g/day
• Hyperlipidaemia
Low albumin
```
122
Which types of glomerular disease are likely to cause nephrotic syndrome?
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
123
What is the most common cause of nephrotic syndrome in children? And adults?
```
Children = minimal change disease
Adults = focal segmental glomerulosclerosis
```
124
Which disease is associated with minimal change disease?
Hodgkin's lymphoma
125
What are the causes of focal segmental glomerulosclerosis?
Idiopathic
Sickle-cell disease
HIV
Heroin
HTN
126
What is seen on histology (immunofluorescence) in membranous glomerulonephritis?
IgG complement deposits on the basement membrane
127
What are the two types of PKD? Which is more common? Which is more severe?
autosomal dominant - common
| autosomal recessive - severe
128
Which two genes are responsible for autosomal dominant PKD?
PKD-1: chromosome 16 (85% of cases)
PKD-2: chromosome 4 (15% of cases)
129
Which gene are responsible for autosomal recessive PKD?
a gene on chromosome 6
130
When does autosomal dominant PKD present?
30-40 years
131
When does autosomal recessive PKD present?
In pregnancy with oligohydramnios (foetus does not produce enough urine)
Patients may require dialysis in the first few days of life
Usually have end-stage renal failure by adulthood
132
Name 5 extra-renal manifestations of autosomal PKD.
- Cerebral aneurysms
- Hepatic, splenic, pancreatic, ovarian and prostatic cysts
- Cardiac valve disease (mitral regurgitation)
- Colonic diverticula
- Aortic root dilatation
133
What is the screening investigation for ADPKD? Who should be screened?
Abdominal US
| Relatives of someone with ADPKD
134
What are the US criteria for patients with a positive family history of PKD?
- 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
135
What is shown in renal biopsy in ARPKD?
multiple cylindrical lesions at right angles to the cortical surface
136
What drug can be used to slow the development of cysts in autosomal dominant PKD?
Tolvaptan (vasopressin receptor antagonist)
137
What advice should be given to patients with PKD?
- Genetic counselling
- Avoid contact sports due to the risk of cyst rupture
- Avoid anti-inflammatory medications and anticoagulants
138
What monitoring is required in PKD?
• Kidney US
• Regular bloods to monitor renal function
• Regular blood pressure to monitor for hypertension
- MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history
139
How can the complications of PKD be managed?
- Antihypertensives for hypertension.
- Analgesia for renal colic related to stones or cysts.
- Antibiotics for infection. Drainage of infected cysts may be required.
- Dialysis for end-stage renal failure.
- Renal transplant for end-stage renal failure.
140
What are the complications of autosomal dominant PKD?
- Chronic loin pain
- Hypertension
- Cardiovascular disease
- Gross haematuria can occur with cyst rupture (this usually resolves within a few days
- Renal stones are more common in patients with PKD
- End-stage renal failure occurs at a mean age of 50 years
141
What is renal tubular acidosis (RTA)?
Metabolic acidosis due to pathology in the tubules of the kidney.
142
What is the normal function of the proximal and distal renal tubules?
Proximal - reabsorb bicarbonate back into the blood
Distal - excrete H+ ions
143
How many types of RTA are there?
4
144
Which are the two most clinically relevant types of RTA?
1 and 4
145
What are the causes of type I RTA?
```
• Genetic (autosomal dominant/recessive)
• Sjogren's syndrome
• SLE
• Primary biliary cirrhosis
• Hyperthyroidism
• Sickle-cell anaemia
Marfan's
```
146
What is found on a blood gas in RTA type I and type IV?
Type I:
- Hypokalaemia
- Metabolic acidosis
- High urinary pH
Type IV:
- Hyperkalaemia
- Hyperchloraemia
- Metabolic acidosis
- Low urinary pH
147
What is the treatment for type I RTA?
Bicarbonate PO
148
What is the treatment for RTA type IV?
Fludrocortisone
Sodium bicarbonate
Treat hyperkalaemia
149
What causes type IV RTA?
Reduced aldosterone:
- Adrenal insufficiency
- ACEi's
- Spironolactone
150
How many years does a renal transplant add to life expectancy?
10 years
151
How are donors matched?
HLA matching
152
Which chromosome are HLA types found?
6
153
How is a donor kidney transplanted into the recipient?
Old kidney remains in place
Donor kidney blood vessels are anastomosed with the patient's pelvic blood vessels
Kidney is anterior in the abdomen (can be palpated in the iliac fossa)
154
Where can a donor kidney be palpated?
Iliac fossa
155
Which incision is typically used?
Hockey-stick incision
156
What are the indications for renal transplantation?
End stage renal failure
157
Which three drugs are used for immunosuppression in renal transplant? Name three other immunosuppressants that can be used.
1. Tacrolimus
2. Mycophenolate
3. Prednisolone
Cyclosporine
Sirolimus
Azathioprine
158
What side effects do immunosuppressants cause?
Skin changes - seborrheic warts/skin cancers
Tremor - tacrolimus
Gum hypertrophy
Cushing's syndrome - steroids
159
What are the complications of a renal transplant?
Transplant related - rejection, failure, electrolyte imbalances
Immunosuppressant complications - ischaemic heart disease, T2DM, infections, non-Hodgkin lymphoma, skin cancer (particularly SCC)
160
What are the three types of transplant rejection?
Hyperacute (minutes to hours)
Acute (<6 months)
Chronic (>6 months)
161
What is the cause of hyperacute rejection? What type of reaction is it?
Pre-existing antibodies against ABO or HLA antigens
| Type II hypersensitivity reaction
162
How is a hyperacute rejection managed?
Removal of kidney
163
What are the causes of an acute rejection?
HLA mismatch
| CMV infection
164
How does an acute rejection present?
Usually asymptomatic
| Picked up by rising creatinine, pyuria and proteinuria
165
Why are patients with nephrotic syndrome predisposed to VTE?
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis.
166
What is the most common cause of peritionis secondary to peritoneal dialysis?
S.epidermis
167
What are the causes of a raised anion gap?
lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use
168
What are the causes of a normal anion gap metabolic acidosis?
```
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
```
