Renal Flashcards
what is an acute kidney injury (AKI)? how is it measured?
- an acute drop in kidney function
- serum creatinine
NICE criteria to diagnose an AKI?
- rise in creatinine of 20 micromol/L or more in 2 days (48 hours)
- rise in creatinine of 50% or more in 7 days
- urine output of less than 0.5ml/kg/h for over 6 hours
what is normal urine output?
0.5ml per kg per hour
risk factors for developing an AKI?
- chronic disease: CKD, HF, DM, liver disease
- old age (>65)
- cognitive impairment
- drugs (NSAIDs, ACE-i)
- contrast used in CT scans
how can the causes of AKI be classified? which is most common?
- pre-renal (most common)
- renal
- post-renal
examples of pre-renal causes of AKI?
- dehydration
- hypotension (shock)
- HF
describe the pathophysiology of pre-renal AKI
- pathology causing reduced blood flow to the kidneys
- less blood gets filtered through them
describe the pathophysiology of renal AKI
- intrinsic disease of the kidney
- makes it less able to filter blood
examples of renal causes of AKI?
- glomerulonephritis
- interstitial nephritis
- acute tubular necrosis
describe the pathophysiology of post-renal AKI
an obstruction to outflow causes urine to build up in the kidney and reduce kidney function
examples of post-renal causes of AKI?
- kidney stones
- Ca of abdomen / pelvis
- ureter / urethral strictures
- enlarged prostate (BPE)
- Ca of prostate
investigations in AKI?
- urinalysis
- USS of urinary tract (?obstruction)
what might urinalysis show in AKI?
depends on underlying cause:
- leukocytes and nitrites (infection)
- protein and blood (acute tubular necrosis, infection)
- glucose (diabetes)
how can AKI be prevented?
- avoid nephrotoxic meds where possible
- ensure adequate fluids are given
management of AKI?
treat underlying cause:
- fluid rehydration (IV)
- stop NSAIDs / antihypertensives
- relieve obstruction (e.g. catheter to get past an enlarged prostate)
if severe without clear cause, refer to renal
complications of AKI?
- hyperkalaemia
- fluid overload, HF, pulmonary oedema
- metabolic acidosis
- uraemia
which 2 complications could uraemia (secondary to AKI) cause?
- pericarditis
- encephalopathy
what is CKD?
permanent and progressive reduction in kidney function
causes / risk factors of CKD?
- DM
- HTN
- age-related decline
- glomerulonephritis
- polycystic kidney disease
- drugs
drug causes of CKD?
- NSAIDs
- PPIs
- lithium
presentation of CKD?
- may be asymptomatic
- pruritus
- reduced appetite, nausea
- oedema
- muscle cramps
- peripheral neuropathy
- pallor
- HTN
investigations for CKD?
- eGFR
- urine albumin : creatinine ratio (ACR)
- urine dipstick
- renal USS
how must eGFR be done in order to diagnose CKD?
2 tests done 3m apart
what is a significant urine ACR reading in CKD? what does this mean?
- 3mg/mmol or more
- indicates proteinuria
what might urine dipstick show in CKD? why is this important?
- haematuria
- could be bladder Ca, investigate!!!!
which CKD patients should be offered renal USS?
- accelerated disease
- haematuria
- FHx of polycystic kidney disease
- evidence of obstruction
how is CKD staged?
G score for each eGFR:
- G1 = >90
- G2 = 60-89
- G3a = 45-59
- G3b = 30-44
- G4 = 15-29
- G5 = <15 (end-stage renal failure)
what is A score in CKD?
score based on the albumin : creatinine ratio
how is CKD diagnosed?
at LEAST eGFR <60, OR proteinuria
complications of CKD?
- anaemia
- bone disease
- CVD
- peripheral neuropathy
- dialysis-related problems
when does a CKD patient need a renal referral?
- eGFR <30
- ACR 70mg/mmol or more
- accelerated disease
- uncontrolled HTN despite 4 or more any-hypertensives
in CKD, what is classed as “accelerated disease”?
one of the following: - eGFR drops by 15 - eGFR drops by 20% - eGFR drops by 15ml/min all within 1 year
how can the progression of CKD be slowed?
- optimise DM and HTN control
- treat glomerulonephritis
how can complications be reduced in CKD?
- exercise to maintain healthy weight
- stop smoking
- special dietary advice on phosphate, sodium, potassium and water intake
- atorvastatin 20mg for CVD prevention
how are complications in CKD treated?
- PO sodium bicarbonate (metabolic acidosis)
- iron and erythropoietin (anaemia)
- vit D (bone disease)
- dialysis / transplant for ESRF
first line drug for HTN in CKD? target BP?
- ACE-i
- <140/90
which electrolyte needs to be monitored closely in someone with CKD and on an ACE-i?
- serum K+
- hyperkalaemia can result from both of these
how does CKD cause anaemia?
healthy kidney cells should produce erythropoietin but they don’t in CKD
How should the iron deficiency in CKD be treated?
- erythropoietin
- IV iron used in dialysis patients
which bone diseases can arise from CKD?
- osteomalacia (softening)
- osteoporosis (brittle)
- ostesclerosis (hardening)
X-ray changes seen in CKD bone disease?
- “rugger jersey”
- sclerosis on both ends of vertebra
- osteomalacia in the middle
how does CKD cause secondary hyperparathyroidism?
the parathyroid glands respond to the low Ca by secreting more PTH
management of renal bone disease in CKD?
- active forms of vit D (alfacalcidol, calcitriol)
- low phosphate diet
- bisphosphates if osteoporotic
AEIOU: indications for acute dialysis in AKI patients
- Acidosis (severe, refractory)
- Electrolytes (severe hyperkalaemia)
- Intoxication (drug OD)
- Oedema (severe, pulmonary)
- Uraemic symptoms
features of uraemia indicating dialysis?
- seizures
- reduced consciousness
2 indications for long-term dialysis?
- ESRF (CKD stage 5)
- any acute indications continuing long-term
what are the 3 main types of dialysis?
- continuous ambulatory peritoneal dialysis
- automated peritoneal dialysis
- haemodialysis
which factors are taken into account when choosing a method for dialysis?
- patient preference
- comorbidities
- individual risks of each type
which factors are taken into account when choosing a method for dialysis?
- patient preference
- comorbidities
- individual risks of each type
complications of peritoneal dialysis?
- bacterial peritonitis
- peritoneal sclerosis
- ultrafiltration failure
- weight gain
- psychosocial effects
which 2 methods are there to access blood flow in order to carry out haemodialysis?
- tunnelled cuff catheter
- AV fistula
complications of an AV fistula?
- aneurysm
- infection
- thrombosis
- stenosis
- STEAL syndrome
- high output heart failure
what is STEAL syndrome?
inadequate blood flow to limb distal to AV fistula (it literally STEALS the blood rip)
describe the scar left by a renal transplant
hockey stick scar over ipsilateral iliac fossa
describe the scar left by a renal transplant
hockey stick scar over ipsilateral iliac fossa
what is the immunosuppressant regime used after a kidney transplant? hint: there are 3
- tacrolimus
- mycophenolate
- prednisolone
how long is the immunosuppressant regime continued for after a renal transplant?
lifelong
complications of a renal transplant?
- transplant rejection
- transplant failure
- electrolyte imbalances
- any complications relating to immunosuppressant therapy
features of nephritic syndrome?
- haematuria
- oliguria
- proteinuria
- fluid retention
features of nephrotic syndrome?
- peripheral oedema
- proteinuria (>3g/day)
- frothy urine
- low serum albumin
- hypercholesterolaemia
define glomerulonephritis
an umbrella term used to describe any condition which causes inflammation of the glomerulus
define interstitial nephritis. what are the 2 main diagnoses?
- inflammation between the cells and tubules of the nephron
- acute interstitial nephritis
- chronic tubulointerstitial nephritis
define glomerulosclerosis
- scarring of the glomerulus tissue
list 3 causes of glomerulosclerosis
- glomerulonephritis
- obstructive uropathy
- focal segmental glomerulosclerosis
management of glomerulonephritis?
- steroids
- ACE-i / ARB
complications of untreated nephrotic syndrome?
- thrombosis
- HTN
- high cholesterol
most common cause of nephrotic syndrome in children?
minimal change disease
most common cause of nephrotic syndrome in adults?
focal segmental glomerulosclerosis
what is IgA nephropathy?
- Berger’s disease
- most common cause of primary glomerulonephritis
when does IgA nephropathy typically present?
in 20s
what is seen on histology in IgA nephropathy?
- IgA deposits
- glomerular mesangial proliferation
what is the most common type of glomerulonephritis overall?
membranous glomerulonephritis
how does post-strep GN present?
- patient <30 years old
- weeks after a strep infection
- nephritic syndrome presentation
- full recovery
which streptococcal infections could be followed by post-strep GN?
- tonsillitis
- impetigo
key feature of diabetic nephropathy?
proteinuria
how is diabetic nephropathy prevented?
it is screened for using albumin:creatinine ratio (ACR) and UEs
management of diabetic nephropathy?
- optimise BMs and BP
- ACE-i is antihypertensive of choice
- start even if they have a normal BP
how does acute interstitial nephritis present?
delayed onset, 2-40 days after drug trigger:
- AKI
- HTN
- rash
- fever
- eosinophilia
- transient arthralgia in some
causes of acute interstitial nephritis?
infection but mostly drugs:
- ABx
- NSAIDs
- diuretics
- rifampicin
- allopurinol
- PPIs
management of acute interstitial nephritis?
- remove underlying cause
- steroids
pathophysiology of acute tubular necrosis?
ischaemia / toxins causing death of epithelial cells of the renal tubules
causes of acute tubular necrosis? (hint: split into ischaemic and nephrotoxic)
ischaemic:
- shock
- sepsis
- dehydration
nephrotoxic:
- radiology contrast dye
- gentamicin
- NSAIDs
- lithium
- statins
- ACE-i, ARBs
- heroin
investigation and findings in acute tubular necrosis?
urinalysis shows “muddy brown casts”
management of acute tubular necrosis? hint: same as other AKIs
- supportive
- IV fluid resus
- stop / remove any nephrotoxins
- haemofiltration / haemodialysis if severe
pathophysiology of type 1 renal tubular acidosis?
- pathology of distal tubule making it unable to excrete hydrogen ions
- results in acidosis
causes of type 1 renal tubular acidosis?
- genetic
- SLE
- sjogren’s syndrome
- PBC
- hyperthyroidism
- sickle cell anaemia
- marfan syndrome
how does type 1 renal tubular acidosis present?
- FTT in children
- hyperventilation (compensatory)
- CKD
- osteomalacia
investigation findings in renal tubular acidosis (type 1 and type 2)?
- low K+
- metabolic acidosis
- urinary pH >6 (high)
management of renal tubular acidosis (types 1 and 2)?
PO bicarbonate
pathophysiology of type 2 renal tubular acidosis?
pathology of proximal tubule making it unable to reabsorb bicarbonate
main cause of type 2 renal tubular acidosis?
fanconi syndrome
which group of people is fanconi syndrome most associated with?
Ashkenazi Jews
features of fanconi syndrome?
- cafe au lait spots
- triangular face
- microcephaly
- absent radii bones
what causes type 4 renal tubular acidosis?
low aldosterone
investigation findings in type 4 renal tubular acidosis?
- high K+
- high Cl-
- metabolic acidosis
- low urinary pH (due to low ammonia production)
most common type of renal tubular acidosis?
type 4
causes of type 4 renal tubular acidosis? hint: these all lower aldosterone levels
- adrenal insufficiency
- ACE-i
- spironolactone
- SLE
- DM
- HIV
what is haemolytic uraemic syndrome (HUS)? what causes this?
- thrombosis in all the small vessels throughout the body
- caused by shiga toxin
management of type 4 renal tubular acidosis?
- fludrocortisone (mineralocorticoid, so mimics aldosterone)
- sodium bicarbonate
- treat hyperkalaemia (IV insulin w/ glucose + calcium gluconate)
what is haemolytic uraemic syndrome (HUS)? what causes this?
- thrombosis in all the small vessels around the body
- caused by shiga toxin
features of HUS? hint: classic triad
- haemolytic anaemia
- AKI
- thrombocytopenia
where does the shiga toxin come from?
either E. coli or shigella infection
presentation of HUS?
- E. coli gastroenteritis (bloody diarrhoea)
- reduced UO
- haematuria (dark brown)
- abdo pain
- lethargy, irritability
- confusion
- HTN
- bruising
management of HUS?
- medical emergency!
- anti-hypertensives
- blood transfusions
- dialysis
prognosis of HUS?
- 10% mortality rate
- approx 75% make a full recovery
what do muscle cells release when they die? (features of rhabdomyolysis)
- myoglobin (myoglobinurea)
- potassium
- phosphate
- creatinine kinase (raised CK)
complication of potassium release from rhabdomylosis?
- high K+
- increased risk of arrhythmias
- cardiac arrest
causes of rhabdomyolysis?
- prolonged immobility
- extremely rigorous exercise
- crush injuries
- seizures
presentation of rhabdomyolysis?
- muscle aches / pains
- oedema
- fatigue
- confusion (esp in elderly)
- red-brown urine
investigations and findings in rhabdomyolysis?
- CK (raised, remains high for 1-3 days)
- urine dipstick (positive for blood due to myoglobin)
- UEs (AKI, hyperkalaemia)
- ECG (hyperkalemia changes)
management of rhabdomyolysis?
- IV fluids
- IV sodium bicarbonate
- IV mannitol (raises GFR)
- treat hyperkalaemia
main complication of hyperkalaemia?
- arrhythmias
- particularly VF
causes of hyperkalaemia?
- AKI
- CKD
- rhabdomyolysis
- adrenal insufficiency
- tumour lysis syndrome
- drugs
drug causes of hyperkalaemia?
- spironolactone
- ACE-i, ARBs
- NSAIDs
- potassium supplements
what can cause a falsely raised potassium in a blood test?
haemolysis of the sample
ECG signs in hyperkalaemia?
- tall tented T waves
- flat / absent P waves
- broad QRS complexes
management of acute hyperkalaemia?
- close ECG monitoring
- IV insulin and dextrose infusion
- IV calcium gluconate
management of less urgent hyperkalaemia?
- nebulised salbutamol
- IV fluids
- PO calcium resonium
- IV / PO sodium bicarbonate
- dialysis
at what level of K+ does hyperkalaemia need to be managed urgently?
- > 6mmol/L with ECG changes, OR:
- >6.5 mmol/L regardless of ECG
what is polycystic kidney disease (PKD)? what does it cause?
genetic condition where the kidneys develop fluid-filled cysts
which other organs can have cysts in them in PKD?
- liver
- spleen
- pancreas
- ovaries
- prostate
extrarenal findings in ADPKD?
- cysts in liver, pancreas, spleen
- cerebral aneurysms
- mitral regurg (from mitral valve prolapse)
- colonic diverticula
- aortic root dilatation
what is the mode of inheritance of PKD?
- there are both autosomal dominant and recessive forms
- autosomal dominant (ADPKD) is more common
how is PKD diagnosed?
- USS of kidneys
- genetic testing
which genes are associated with autosomal dominant PKD?
- PKD-1 (chrom 16), majority
- PKD-2 (chrom 4)
complications of PKD?
- chronic loin pain
- HTN
- CVD
- gross haematuria
- renal stones
- ESRF aged 50
management of PKD?
- tolvaptan
- manage the complications
- genetic counselling
- avoid contact sports
- regular USS to monitor cysts
how does autosomal recessive PKD (ARPKD) present?
- oligohydramnios in pregnancy
- underdeveloped lungs, resp failure shortly after birth
- flat nasal bridge
- low set ears
- ESRF before reaching adulthood
renal features of ADPKD?
- flank pain
- renal dysfunction
- HTN
- haematuria
- microalbuminuria
most common complication of dialysis?
dialysis-induced hypotension
criteria for stage 1 AKI?
either:
- Cr >1.5x baseline
- UO <0.5ml/kg/hr for 6h
criteria for stage 2 AKI?
either:
- Cr >2x baseline
- UO <0.5ml/kg/hr for 12h
criteria for stage 3 AKI?
any of these:
- Cr >3x baseline
- Cr >354
- UO <0.3ml/kg/hr for 24h
- anuria for 12h
which other conditions are associated with focal segmental glomerular sclerosis?
- IgA nephropathy (berger’s disease)
- HIV
- sickle cell disease
first line renal replacement therapy in ESRF? why is this preferred?
- peritoneal dialysis
- does not require AV fistula
- can be done at home
which variables are taken into account to calculate eGFR?
- age
- sex
- Cr
- weight
