CHEMPATH: Acute kidney injury and chronic kidney disease Flashcards
Compare and contrast AKI vs CKD.
AKI:
- Abrupt decline in GFR
- Potentially reversible
- Treatment targeted to precise diagnosis and reversal of disease
CKD:
- Longstanding decline in GFR
- Irreversible
- Treatment targeted to prevention of complications of CKD and limitation of progression
What are the functions of the kidney?
- Excretion of water-soluble waste
- Water balance
- Electrolyte balance
- Acid-base homeostasis
- Endocrine functions - EPO, RAS, Vit D
What are the different stages of AKI according to KIDGO?
AKI Stage 1:
- sCr : x1.5- 1.9 the reference OR rise of ≥26 µmol/L
- UO: <0.5ml/kg/hr for 6-12 hrs
AKI Stage 2:
- sCr : x2.0-2.9 the reference
- UO: <0.5ml/kg/hr for _>_12hrs
AKI Stage 3:
- sCr : x≥3 the reference OR or rise of ≥354 µmol/L
- UO: <0.3ml/kg/hr for _>_24hrs OR anuria for _>_12 hours
Define AKI.
A rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis, defined as any of the following:
- sCR increase of _>_26.5umol/L within 2 days
- sCr _>_x1.5 the baseline, known to have occurred in the last 2 weeks
- urine volume <0.5ml/kg/hr
What are the three categories of AKI causes?
- pre-renal
- intrinsic renal
- post-renal
What is the aetiology of pre-renal AKI?
Reduced renal perfusion –>
- generalised reduction in tissue perfusion
- OR selective renal ischaemia
Pre-renal AKI occurs when normal adaptive mechanisms (RAS) fail to maintain renal perfusion
Summarise RAS response to reduced circulating volume.
- Activation of central baroreceptors
- Activation of RAS
- Release of vasopressin
- Activation of sympathetic system
- Vasoconstriction, increased cardiac output, renal sodium retention
What are the clinical causes of pre-renal AKI?
- True volume depletion
- Hypotension
- Oedematous states – fluids not in the right compartment because fluid is mostly in the interstitium
- Selective renal ischaemia
- Drugs affecting glomerular blood flow
What does this show?
Renal artery stenosis to the left kidney
Which class of drugs may predispose patients to developing pre-renal AKI? Explain each.
- A.NSAIDs
- B.Calcineurin inhibitors
- C.ACEi or ARBs
- D.Diuretics
- E.All of the above
All of the above
- NSAIDs - decrease afferent arteriolar dilatation
- Calcineurin inhibitors - decrease afferent arteriolar dilatation
- ACEi or ARBs - decrease efferent arteriolar constriction
- Diuretics – affect tubular function, decrease preload
Is AKI the same as ATN?
No, ATN occurs when prolonged insult leads to ischaemic injury i.e. prolonged AKI –> ATN
Pre-Renal AKI is not associated with structural renal damage and responds immediately to restoration of circulating volume whereas ATN does not respond.
A 68 year old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys. What is the likely cause of his AKI?
- A.Right-sided kidney stone
- B.Left ureteric transitional cell carcinoma
- C.Membranous glomerulonephropathy
- D.Benign prostatic hypertrophy
- E.Amyloid
D.Benign prostatic hypertrophy
What are the post-renal causes of AKI?
- (Intra-renal obstruction)
- Ureteric obstruction (bilateral)
- Prostatic / Urethral obstruction
- Blocked urinary catheter
What is the pathophysiology of post-renal AKI?
- Obstruction results in increased tubular pressure
- Immediate decline in GFR
- GFR is normally dependent on hydraulic pressure gradient
What are the renal complications of prolonged obstructive uropathy?
- Glomerular ischaemia
- Tubular damage
- Long term interstitial scarring
What are the renal causes of AKI?
Abnormality in any part of the nephron:
- Vascular Disease e.g. vasculitis
- Glomerular Disease e.g. glomerulonephritis
- Tubular Disease e.g. ATN
- Interstitial Disease e.g. analgesic nephropathy
What are 5 causes of direct tubular injury causing renal AKI?
Ischaemia (most common)
Endogenous toxins
- Myoglobin
- Immunoglobulins e.g. Myeloma
Exogenous toxins - contrast, drugs
- Aminoglycosides
- Amphotericin
- Acyclovir
Rhabdomyolysis
A 40 year old female presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?
- A.NSAIDs
- B.Systemic vasculitis
- C.Amyloidosis
- D.Tumour lysis syndrome following chemotherapy for lymphoma
- E.Myeloma
Systemic vasculitis
Give 2 examples of how immune dysfunction can cause renal AKI.
- Glomerulonephritis
- Vasculitis
Give 2 examples of how infiltration/abnormal protein deposition can cause renal AKI.
- Amyloidosis
- Lymphoma
- Myeloma-related renal disease
What are the top 5 causes of in-hospital AKI?
- Decreased renal perfusion
- Medications
- Radiographic contrast media
- Postoperative
- Sepsis
Source: In-hospital AKI. Nash 2002
What is the prognosis with AKI?
Only ~39% have a complete recovery and 19% die
What two measures do we use to define severity of acute kidney injury?
Serum creatinine
Urine output (or eGFR)
What are the 4 phases of healing in AKI?
- Haemostasis
- Inflammation
- Proliferation
- Remodeling
When there is an imbalance between scarring and remodelling, scar tissue will cause chronic disease.
What are the stages of CKD? What factors are considered?
GFR is measured
Other than GFR, what can be used to predict prognosis in CKD?
ACR (albumin:Cr ratio)
What are the most common causes of CKD?
- Diabetes
- Atherosclerotic renal disease
- Hypertension
- Chronic Glomerulonephritis
- Infective or obstructive uropathy
- Polycystic kidney disease
What are the 4 main complications of CKD?
Progressive failure of homeostatic function i.e. acidosis + hyperkalaemia
Progressive failure of hormonal function i.e. anaemia + renal bone disease
Cardiovascular disease i.e. vascular calcification + uraemic cardiomyopathy
Uraemia and Death
Why does renal acidosis occur in CKD? What are the consequences of this? How is this treated?
There is failure of renal excretion of protons.
Consequences:
- Muscle and protein degradation
- Osteopenia due to mobilization of bone calcium
- Cardiac dysfunction
Tx: oral sodium bicarbonate
Regarding hyperkalaemia, which of the following is true?
- A.It can lead to ECG changes such as peaked p waves and flattened t waves.
- B.In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.
- C.NSAIDs can lower potassium levels
- D.Hyperaldosteronism is a common cause
- E.All of the above
B..In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.
NB:
- ECG – flattened p waves and peaked T waves should be seen
- NSAIDs – can increase K
- Hyperaldosteronism (Conn’s) - lowers K
List 3 medications which can cause hyperkalaemia.
- ACEi
- Spironolactone
- ’Potassium-sparing’ diuretics
What abnormality is shown?
Hyperkalaemia
Why does anaemia occur in CKD?
Progressive decline in EPO producing cells with loss of renal parenchyma (usually when GFR<30mL/min) –> normochromic, normocytic anaemia
Important to exclude other common causes:
- Iron deficiency
- B12 and/or folate deficiency
What medications can be used to manage anaemia in CKD?
Erythropoiesis-stimulating agents (ESAs):
- Erythropoietin alfa (Eprex)
- Erythropoietin beta (NeoRecormon)
- Darbopoietin (Aranesp)
Your patient with CKD has been started on an ESA but does not respond. What could be the cause?
- A.Iron deficiency
- B.TB
- C.Malignancy
- D.B12 and folate deficiency
- E.Hyper-parathyroidism
- F.Any of the above
F.Any of the above
List 4 types of renal bone disease.
- Osteitis fibrosa
- Osteomalacia
- Adynamic bone disease
- Mixed osteodystrophy
May occur together
What is the aetiology of hyperparathyroidism in CKD?
- Phosphate retention
- Low Vit D levels due to lack of 1-α-hydroxylase
What is osteitis fibrosa?
Osteoclastic resorption of calcified bone and replacement by fibrous tissue due to hyperparathyroidism
What is osteomalacia?
Insufficient mineralization of bone osteoid due to lack of vitamin D (due to lack of 1-alpha-hydroxylation in kidney)
What is the cause of adynamic bone disease?
Excessive iatrogenic suppression of PTH in CKD –> low bone turnover and reduced osteoid
What are the three main treatments for renal bone disease?
- Phosphate control - dietary reduction + phosphate binders
- Vit D receptor activators – give 1-alpha calcidol + paricalcitol (vit D analogue)
- Direct PTH suppression - Cinacalcet
What is cardiovascular disease characterised by in CKD?
Renal vascular lesions are frequently characterised by heavily calcified plaques, rather than traditional lipid-rich atheroma
What are the three phases of uraemic cardiomyopathy?
- Left ventricle (LV) hypertrophy
- LV dilatation
- LV dysfunction
The following are contraindications to transplantation: true or false?
- HIV positive –
- Any malignant disease –
- BMI >30 –
- Active Sepsis –
- Aged above 65 years -
- HIV positive – FALSE
- Any malignant disease – FALSE
- BMI >30 – FALSE
- Active Sepsis – TRUE
- Aged above 65 years - FALSE
What are the two types of dialysis?
Haemodialysis
Peritoneal dialysis
