Renal Flashcards
1
Q
How is AKI diagnosed?
A
Serum creatinine levels
2
Q
What is the diagnostic criteria for AKI?
A
Rise in creatinine > 25micromol/L in 48h
Rise in creatinine > 50% in 7d
Urine output < 0.5ml/kg/h over 6h
3
Q
List risk factors for AKI
A
> 65y
Sepsis
CKD
HF
Diabetes
Liver disease
Cognitive impairment- Decreased fluid intake
Medications (NSAIDs, gentamicin, diuretics and ACE-is)
Radiocontrast agents (CT scans)
4
Q
List pre-renal causes of renal impairment
A
Insufficient blood supply to kidneys reducing filtration of blood
- Dehydration
- Shock (septic or acute blood loss)
- HF
5
Q
List renal causes of renal impairment
A
Intrinsic disease in kidneys
- Acute tubular necrosis
- Glomerulonephritis
- Acute interstitial nephritis
- HUS
- Rhabdomyolysis
6
Q
List post-renal causes of renal impairment
A
Obstruction to outflow of urine
- Kidney stones
- Tumours
- Strictures of ureters or urethra
- BPH
- Neurogenic bladder
7
Q
What is acute tubular necrosis?
A
Damage and death of epithelial cells of renal tubules
8
Q
What are the causes of acute tubular necrosis?
A
Ischaemia due to hypoperfusion (dehydration, shock, HF)
Nephrotoxins (gentamicin, radiocontrast, cisplatin)
9
Q
What is seen on urinalysis in acute tubular necrosis?
A
Muddy brown casts
Renal tubular epithelial cells
10
Q
What is the prognosis of acute tubular necrosis?
A
Epithelial cells regenerate = Reversible
Recovery in 1-3wks
11
Q
What does urinalysis +ve for protein and blood suggest?
A
Acute nephritis
12
Q
How to test for obstructive cause of AKI
A
US
13
Q
Outline management of AKI
A
IV fluids
Withhold meds that worsen condition- NSAIDs, ACE-is
Withhold meds that may accumulate with reduced renal function- Metformin and opiates
Catheter if obstruction
Dialysis if severe
14
Q
List complications of AKI
A
Fluid overload, HF, pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia (high urea)- Can lead to encephalopathy and pericarditis
15
Q
Define CKD
A
Chronic reduction in kidney function sustained over 3mths- Permanent and progressive
16
Q
List causes of CKD
A
Diabetes
HTN
Meds- NSAIDs or lithium
Glomerulonephritis
PKD
17
Q
Outline presentation of CKD
A
Fatigue
Pallor (anaemia)
Foamy urine (protein)
Nausea
Loss of appetite
Pruritis
Oedema
HTN
Peripheral neuropathy
18
Q
What is eGFR based on?
A
Serum creatinine
Age
Gender
19
Q
What is GFR?
A
Rate at which fluid is filtered from blood into Bowman’s capsule
20
Q
How do you quantify proteinuria?
A
Urine albumin : Creatinine ratio (ACR)
21
Q
Outline diagnostic criteria of CKD
A
eGFR sustained below 60mL/min/1.73m2
Urine ACR sustained above 3mg/mmol
22
Q
Outline G score
A
Based on eGFR- Marker of CKD
- G1>90
- G2 60-89
- G3a 45-59
- G3b 30-44
23
Q
Outline A stage
A
Based on ACR- Marker of CKD
- A1 <3mg/mmol
- A2 3-30mg/mmol
- A3 >30mg/mmol
24
Q
What is accelerated progression in CKD?
A
Sustained decline in eGFR within 1yr of either 25% or 15mL/min/1.73m2
25
List complications of CKD
Anaemia
Renal bone disease
CVD
Peripheral neuropathy
End stage kidney disease
26
List criteria for referral to renal specialist
eGFR<30mL/min/1.73m2
Urine ACR > 70mg/mmol
Accelerated progression
5yr risk of requiring dialysis >5%
Uncontrolled HTN despite 4+ antihypertensives
27
List medications that slow disease progression of CKD
ACE-i/ARBs
SGLT-2 inhibitor (dapagliflozin)
28
List medications that reduce the risk of complications of CKD
Exercise, maintain healthy weight, avoid smoking
Atorvastatin 20mg for primary prevention CVD
29
List medications that manage complications of CKD
Oral sodium bicarbonate- Metabolic acidosis
Iron and erythropoietin- Anaemia
Vit D, low phosphate diet, phosphate binders- Renal bone disease
30
Why does anaemia occur in CKD?
Kidneys produce EPO (produces RBCs)
CKD= Lower EPO and RBC production
Normocytic, normochromic anaemia
31
What is renal bone disease?
CKD- Mineral bone disorder
High serum phosphate
Low Vit D
Low serum calcium
32
Why does renal bone disease occur?
Reduced phosphate excretion by diseased kidneys results in high serum phosphate
Kidneys metabolise vit D to activate, normally allows calcium absorption in intestines and reabsorbed in kidneys- Responsible for regulating bone turnover and promoting bone reabsorption
Parathyroid glands react to low serum calcium and high serum phosphate by excreting more PTH- Secondary hyperparathyroidism
PTH stimulates osteoclast activity, increasing calcium absorption from bone
33
Why does osteomalacia occur?
Increased turnonver of bones without adequate calcium supply
34
Why does osteosclerosis occur?
Osteoblasts respond by increasing activity to math the osteoclasts, create new tissue in bone
Low calcium level means new bone not properly mineralised
35
Outline management of renal bone disease
Low phosphate diet
Phosphate binders
Active forms of Vit D (alfacalcidol and calcitriol)
Ensuring adequate calcium intake
36
When are ACE-is offered to patients with CKD?
Diabetes + urine ACR >3mg/mmol
HTN + urine ACR >30mg/mmol
All patients with urine ACR >70mg/mmol
37
What in particular needs monitoring in patients with CKD taking ACE-is?
Serum potassium- Risk of hyperkalaemia
38
What is the criteria for offering SGLT-2 inhibitors to patients with CKD?
Dapagliflozin
Offered- Diabetes plus urine ACR >30mg/mmol
Considered- Diabetes plus urine ACR 3-30mg/mmol
Non-diabetic with ACR >22.6mg/mmol
39
What is a rugger jersey spine?
Finding on spinal X-ray involving sclerosis of both ends of each vertebral body (denser white) and osteomalacia in centre (less white)
40
What is dialysis and when is it used?
Performs filtration tasks of kidneys artificially
Used in end-stage renal failure or complications of acute AKI
Removes excess fluids, solutes and waste products
41
What are the indications for short-term dialysis?
A- Acidosis (severe and not responding to treatment)
E- Electrolyte abnormalities (treatment resistant hyperkalaemia)
I- Intoxication
O- Oedema (severe and unresponsive pulmonary oedema)
U- Uraemia symptoms (seizures, reduced consciousness)
42
Outline haemodialysis
4h/d, 3d/wk
Blood taken out of body passed through machine, passes along semipermeable membranes inside machine
Solutes filter out of blood into dialysate and conc. gradient causes water and solutes to leave blood
Anticoagulation with citrate and heparin prevents blood clotting in machine
43
What are the long term access options for haemodialysis?
Tunnelled cuffed catheter (tube in subclavian or jugular vein with tip in SVC or RA)- Has 2 lumens- Red (blood exiting) and blue (blood entering)
Arteriovenous fistula (artificial connection between artery and vein, bypasssing capillary system)- Requires 4-16wks after surgery till it can be used
44
What are the main complications of a tunnelled cuffed catheter?
Infection
Blood clots
45
What are the main complications of an AV fistula?
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output HF
46
Where can a fistula be placed for haemodialysis?
Radiocephalic- Wrist- Radial artery to cephalic vein
Brachiocephalic- Antecubital fossa- Brachial artery to celhalic vein
Brachiobasilic- Upper arm- Less common
47
What are the features of a fistula on examination?
Check skin integrity
Aneurysms
Palpable thrill (fine vibration over anastomosis)
Machinery murmur on auscultation over fistula
48
List complications of AV fistulas
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output HF
49
What is STEAL syndrome?
Inadequate blood flow to limb distal to fistula
AV fistula steals blood from rest of limb- Blood diverted away from part of limb it was supposed to supply= Ischaemia
50
What is high-output HF?
Caused by blood flowing quickly from arterial to venous system through AV fistula
Rapid return of blood to heart= Increased pre-load= Hypertrophy of heart muscle and HF
51
What is a key rule regarding fistulas?
Never take blood from a fistula= Risk of damage
52
Outline the complications of peritoneal dialysis
Bacterial peritonitis
Peritoneal sclerosis- Thickening and scarring of peritoneal membrane
Ultrafiltration failure- Dextrose absorbed, reducing filtration gradient= Less effective
Weight gain- Due to absorption of dextrose
Psychosocial impairment
53
What is peritoneal dialysis?
Uses peritoneal membrane to filter blood
Dextrose added to peritoneal cavity
Ultrafiltration occurs from blood, accross peritoneal membrane, into dialysis solution
Dialysis solution replaced, taking away waste products
54
What is the tube used in peritoneal dialysis called?
Tenckhoff catheter
55
What is continuous ambulatory peritoneal dialysis (CAPD)?
Dialysis solution always in peritoneal cavity- Various regimes for changing solution (eg: 2L solution replaced 4x daily)
56
What is automated dialysis?
Type of peritoneal dialysis
Machine continuously replaces dialysis fluid for 8-10h overnight
57
What is the potential prognosis of a kidney transplant in end-stage renal failure?
10yrs compared to dialysis and significantly improves QoL
58
How is donor matching done?
Matched based on human leukocyte antigen (HLA) type A, B and C on Chr 6
Don't have to fully match, but closer is better
59
Outline the basics of a kidney transplant procedure
Leave patient's kidneys in place
Donor kidney blood vessels anastomosed with pelvic vessels- Usually external iliac vessels
Ureter of donor kidney anastomosed directly with bladder
Donor kidney placed anteriorly in abdomen and can be palpated in iliac fossa area
Hockey stick incision used
60
What is expected post-renal transplant?
New kidney will function immediately
Basiliximab- Monoclonal antibody- Targets IL2 receptor on T cells- 2 doses given after surgery to prevent acute rejection
Require life-long immunosuppression- Combination of tacrolimus, mycophenolate, ciclosporin, azathioprine, prednisolone
61
What are the SEs of immunosuppresants?
Cause seborrhoeic warts and skin cancers
Tacrolimus- Tremor
Ciclosporin- Gum hypertrophy
Steroids- Features of Cushing's syndrome
62
List the potential complications of transplant
Transplant rejection
Transplant failure
Electrolyte imbalances
63
List complications related to immunosuppressants
Ischaemic heart disease
T2D (steroids)
Infections more likely/severe/involve unusual pathogens
Non-Hodgkin lymphoma
Skin cancer (SCC)
64
List unusual infections that can occur secondary to immunosuppressant meds
Pneumocystis jiroveci pneumonia (PCP/PJP)
Cytomegalovirus (CMV)
TB
65
What is glomerulonephritis?
Inflammation of the glomeruli in the kidneys
Glomerulus= 1st part of nephron- Filters fluid out of capillaries and into renal tubule
Describes pathology that occurs in various diseases- Treat underlying cause
66
What is nephritic syndrome?
Group of features that occur with nephritis
Haematuria- Microscopic/macroscopic
Oliguria- Sig. reduced urine output
Proteinuria- But <3g/24h (higher suggests nephrotic syndrome)
Fluid retention
67
What is nephritis?
Inflammation of kidneys
Descriptive term, not a diagnosis
68
What are the features of nephrotic syndrome?
Proteinuria (>3g/24h)- Frothy urine
Low serum albumin (<25g/l)
Peripheral oedema
Hypercholesterolaemia
69
What is nephrotic syndrome?
Basement membrane in glomerulus becomes highly permeable, resulting in significant proteinuria
70
What does nephrotic syndrome predispose patients to?
Thrombosis
HTN
High cholesterol
71
What is the most common cause of nephrotic syndrome in children?
Minimal change disease- Usually idiopathic and treated successfully with steroids
72
What are the main causes of nephrotic syndrome in adults?
Membranous nephropathy
Focal segmental glomerulosclerosis
73
What are the less common causes of nephrotic syndrome?
Membranoproliferative glomerulonephritis
Henoch-Schonlein Purpura (HSP)
Diabetes
Infection (eg: HIV)
74
Outline IgA nephropathy
Most common cause of primary glomerulonephritis
Patient- 20s presenting with haematuria
75
What is seen on histology of IgA nephropathy?
IgA deposits and mesangial proliferation (found in centre of gomerulus and help support capillaries)
76
Outline membranous nephropathy
Involves deposits of immune complexes in glomerular basement membrane- Causes thickening and malfunctioning of membrane and proteinuria
77
What is seen on histology of membranous nephropathy?
IgG and complement deposits on basement membrane
78
What are the causes of membranous nephropathy?
Majority idiopathic (70%)
Can be secondary to malignancy/SLE/drugs (eg: NSAIDs)
79
Outline membranoproliferative glomerulonephritis
Affects patients <30y
Involves immune complex deposits and mesangial proliferation
80
Outline post-streptococcal glomerulonephritis
Affects patients <30y
Presents 1-3wks after streptococcal infection (eg: Tonsillitis/impetigo)
Usually make full recovery
81
Outline rapidly progressive glomerulonephritis
Acute severe illness- Responds well to treatment
82
What is seen on histology of rapidly progressive glomerulonephritis?
Glomerular crescents
83
What is Goodpasture syndrome?
Anti-glomerular basement membrane (anti-GBM) disease
Anti-GBM antibodies attack glomerulus and pulmonary basement membranes
84
What does Goodpasture syndrome cause?
Glomerulonephritis
Pulmonary haemorrhage
85
What is the typical presentation of Goodpasture syndrome?
Patients in 20s or 60s with acute kidney failure and haemoptysis (coughing up blood)
86
List systemic diseases that can cause glomerulonephritis
HSP
Vasculitis (microscopic polyangiitis or granulomatosis with polyangiitis)
Lupus nephritis (associated with SLE)
87
AKI, haemoptysis and anti-GBM antibodies
Goodpasture syndrome
88
AKI, haemoptysis and p-ANCA/MPO antibodies
Microscopic polyangiitis
89
AKI, haemoptysis, c-ANCA/PR3 antibodies
Granulomatosis with polyangiitis
90
Outline management of glomerulonephritis
Supportive care (HTN management and dialysis if severe)
Immunosuppression (corticosteroids)
91
What is renal tubular acidosis?
Involves metabolic acidosis due to pathology in tubules of kidneys
Tubules balance hydrogen and bicarbonate ions between blood and urine to maintain normal pH
92
Outline Type 1 renal tubular acidosis
Distal tubule cannot excrete hydrogen ions
High urinary pH
Low serum potassium
HYPOKALAEMIA
93
Outline type 2 renal tubular acidosis
Proximal tubule cannot reabsorb bicarbonate
High urinary pH
Low serum potassium
94
Outline type 4 renal tubular acidosis
Low aldosterone/impaired aldosterone function
Low urinary pH
High serum potassium
HYPERKALAEMIA
95
What is the result of type 1 RTA (distal RTA)?
High urinary pH due to absence of H+
Metabolic acidosis due to retained H+ in blood
Hypokalaemia due to failure of H+ and potassium exchange (H+/K+ ATPase)
96
What can cause distal RTA (type 1)?
Genetic
SLE
Sjogren's syndrome
PBC
Hyperthyroidism
SCA
Marfans
97
How does type 1 RTA present?
Failure to thrive in children
Recurrent UTIs (due to alkaline urine)
Bone disease (rickets or osteomalacia)
Muscle weakness
Arrhythmias (due to hypokalaemia)
98
How is Type 1 RTA managed?
Oral bicarbonate- Corrects acidosis and electrolyte imbalances
99
What is the result of Type 2 renal tubular acidosis?
High urinary pH due to excess bicarbonate in urine
Metabolic acidosis due to inadequate bicarbonate in blood
Hypokalaemia due to urinary loss of potassium along with bicarbonate
100
What are the key causes of Type 2 renal tubular acidosis?
Inherited
Multiple myeloma
Fanconi's syndrome
101
How is type 2 renal tubular acidosis managed?
Oral bicarbonate
102
What is the role of aldosterone?
Stimulates sodium reabsorption and potassium and hydrogen ion excretion in distal tubules
Low aldosterone/impaired aldosterone function leads to insufficient potassium and hydrogen excretion
103
What is the role of ammonia?
Produced in distal tubules
Balances excretion of hydrogen ions
Is a base and buffers hydrogen ions, preventing urine becoming too acidotic
104
What is the result of type 4 renal tubular acidosis?
Hyperkalaemia due to retained potassium in blood
Metabolic acidosis due to retained hydrogen ions in blood
Low urinary pH- Hyperkalaemia suppresses ammonia= Urine acidotic
105
What causes low aldosterone/low aldosterone activity?
Adrenal insufficiency
Diabetic nephropathy
Meds (ACE-is, spironolactone, eplerenone)
(Type 4 RTA)
106
Outline management of type 4 renal tubular acidosis
Aldosterone deficiency- Fludrocortisone (mineralocorticoid)
Oral bicarbonate
Treatment of hyperkalaemia
107
What is haemolytic uraemic syndrome (HUS)?
Thrombosis in small blood vessels throughout body- Triggered by Shiga toxins (E. coli or Shigella)
Most common in children following an episode of gastroenteritis
108
What increases the risk of HUS?
Use of antibiotics and antimotility meds (eg: Loperamide) used to treat gastroenteritis
109
Outline the classic triad of HUS
Microangiopathic haemolytic anaemia
AKI
Thrombocytopenia (low platelets)
110
Outline management of HUS
Stool culture
EMERGENCY- Requires hospital admission and supportive management
Hypovolaemia- IV fluids
Treat HTN
Severe anaemia- Blood transfusion
Severe renal failure- Haemodialysis
111
Outline presentation of HUS
Diarrhoea 1st symptom- Turns bloody within 3d- 1wk after diarrhoea onset, features of HUS develop:
Fever
Abdo pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
HTN
Bruising
Jaundice (due to haemolysis)
Confusion
112
What is the result of formation of blood clots in HUS?
Blood clots consume platelets, leading to thrombocytopenia
Blood flow through kidney affected by thrombi and damaged RBCs= AKI
113
What is microangiopathic haemolytic anaemia (MAHA)?
Occurs in HUS
Destruction of RBCs (haemolysis) due to small vessels- Tiny thrombi partially obstruct small blood vessels and churn RBCs as pass through= Rupture
114
What is rhabdomyolysis?
Skeletal muscle breakdown and release into blood:
Myoglobin
Potassium
Phosphate
Creatine kinase
Myocytes undergo apoptosis
115
What is the result of rhabdomyolysis?
Potassium- Most immediately dangerous breakdown product- Hyperkalaemia- Cardiac arrhythmias/cardiac arrest
Myoglobin- Toxic to kidneys (AKI)
116
What are the complications of rhabdomyolysis?
Compartment syndrome
Disseminated intravascular coagulation
117
List causes of rhabdomyolysis
Prolonged immobility- Frail patients who fall and spend time on floor before being found
Extremely rigorous exercise- Beyond person's fitness level
Crush injuries
Seizures
Statins
118
List signs and symptoms of rhabdomyolysis
Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)
119
Outline investigations of rhabdomyolysis
Creatine kinase (CK)- >150 U/L- Typically rises in first 12h, remains elevated for 1-3d, then gradually falls- Higher CK = Greater risk of kidney injury
Myoglobinuria- Red-brown- Dip positive for blood
U&Es- AKI and hyperkalaemia
ECGs- Hyperkalaemia
120
Outline management of rhabdomyolysis
IV fluids- Corrects hypovolaemia and encourages filtration of breakdown products
Treat complications
121
What is the main complication of hyperkalaemia?
Cardiac arrhythmias- VF- Cardiac arrest
122
What are the values of normal serum potassium and hyperkalaemia?
Normal- 3.5-5.3
Mild- 5.4-6
Moderate- 6-6.5
Severe- Over 6.5
123
List causes of hyperkalaemia
AKI
CKD (stage 4/5)
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
124
List medications that can cause hyperkalaemia
Aldosterone antagonists (spironolactone)
ACE-is (ramipril)
ARBs (candesartan)
NSAIDs (naproxen)
125
What is a cause of falsely elevated potassium (pseudohyperkalaemia)?
Haemolysis during sample
126
Outline ECG changes in hyperkalaemia
Tall peaked T waves
Flattening or absence of P waves
Prolonged PR interval
Broad QRS complexes
127
Outline management of hyperkalaemia <6.5mmol/L w/o ECG changes
Treat underlying cause- AKI and stop certain meds
128
When do patients with hyperkalaemia require urgent treatment?
ECG changes
Serum potassium >6.5mmol/L
129
Outline mainstay treatment of severe hyperkalaemia
Insulin- Drives potassium from ECS to ICS
Dextrose infusion- Prevents hypoglycaemia on insulin
Calcium gluconate- Stabilises cardiac muscle cells and reduces risk of arrhythmias
130
Outline options for lowering serum potassium in hyperkalaemia
Nebulised salbutamol- Temporarily drives potassium into cells
Oral calcium resonium- Reduces potassium absorption in GI tract (slow and causes constipation)
Sodium bicarbonate- Used in acidotic patients on renal advice- Drives potassium into cells as corrects acidosis
Haemodialysis- Required in severe/persistent cases
131
What is polycystic kidney disease (PKD)?
Genetic condition
Healthy kidney tissue replaced with many fluid-filled cysts
Enlarged kidneys may be palpable on exam
Leads to renal failure
132
What is the inheritance of PKD?
Autosomal dominant most common (ADPKD):
PKD1 gene on Chr16 (85% cases)
PKD2 gene on Chr4 (15% cases)
ARPKD
133
List the extra-renal manifestations of ADPKD
Cerebral aneurysms
Hepatic/splenic/pancreatic/ovarian/prostatic cysts
Mitral regurgitation
Colonic diverticula
134
List complications of ADPKD
Chronic loin/flank pain
HTN
Gross haematuria- Can occur with cyst rupture (usually resolves within a few days)
Recurrent UTIs
renal stones
End-stage renal failure- Mean age 50y
135
Outline autosomal recessive PKD
Mutation in Polycystic kidney and hepatic disease 1 (PKHD1) gene on Chr6
More rare and severe than ADPKD
Often picked up on antenatal scans with oligohydramnios (reduced amniotic fluid volume due to reduced urine output)
Oligohydramnios- Leads to underdevelopment of fetal lungs (pulmonary hypoplasia) and resp. failure shortly after birth
May require haemodialysis within 1st few days of life
May have dysmorphic features- Underdeveloped ear cartilage, low-set ears, flat nasal bridge
End-stage renal failure usually occurs before reaching adulthood
136
How is PKD diagnosed?
US
Genetic testing
137
Outline management of PKD
Tolvaptan- Slow development of cysts and progression of renal failure in autosomal dominant PKD
Antihypertensives (ACE-Is)
Analgesia
ABs (UTIs or cyst infections)
Drainage of symptomatic
Dialysis/renal transplant- End-stage renal failure
Genetic counselling
Avoid contact sports due to risk of cyst rupture
Avoid NSAIDs and anticoagulants
MR angiography- Screen for cerebral aneurysms
