Flashcards in Acute And Chronic Kidney Disease Deck (88):
What is AKI?
Abrupt decline in actual GFR (days to weeks)
Upset of ECF volume, electrolytes and acid-base balance
Accumulation of nitrogenous waste products
Why is AKI difficult to diagnose?
Doesn't present with a specific identifiable symptom
Measurements are not massively accurate either
What happens to serum creatinine as kidneys decline?
Kidney decline leads to increased serum creatinine
How do we define AKI through measurements?
Increased serum creatine > 26.5 micromoles/L within 48 hrs
Increased serum creatinine > 1.5 x their baseline in 7 days
Urine volume <0.5 ml/kg/h for 6 hours
Describe the staging of AKI
1 - 3 in increasing severity
1 = 1.5 - 2 times their baseline
2 = 2 - 3 times their baseline
3 = > 3 times their baseline
What are the types of AKI?
What are the causes of pre-renal AKI?
Blood supply compromised
Give some renal causes of AKI
Renal artery/vein occlusion
What does ATN stand for?
Acute tubular necrosis
What type of AKI are the vast majority?
90% of intrinsic renal causes of AKI are due to ...
Give some general causes of AKI
Describe how pre-renal problems cause AKI
Actual GFR reduced due to decreased renal blood flow
No cell drainage
Kidney works hard to restore blood flow
Increased reabsorption of salt and water (lots of aldosterone and ADH)
Responds to fluid resuscitation
Describe autoregulation of the kidneys
Keeps the kidneys between a minimum and maximum BP over which they can maintain a normal perfusion pressure
When hypertensive, these values shift to higher BPs (reset)
What is the SM response to decreased renal perfusion?
Vasodilation of afferent
Vasoconstriction of efferent
Why do NSAIDs make AKI worse?
Inhibition of production of prostaglandins
Cannot vasodilate in the arterioles of kidneys when required
Cannot regulate perfusion pressure
Why can ACEi make AKI worse?
Cannot vasoconstrict when need to
Give some causes of reduced ECF volume
Give some causes of impaired renal autoregulation
What are the causes of ATN?
Why is ATN a misnomer?
As there is generally no tubular necrosis
But cells are damaged
Damaged cells cannot reabsorbed salt and water efficiently
Or expel excess water
Aggressive fluid resuscitation risks fluid overload
Lost the ability to concentrate urine therefore urine comes out at the same rate no matter the volume of ECF
If dialysis is required, does the mortality of AKI increased or decreased?
Which parts of the nephron are most susceptible to hypoxia?
S3 of PCT
Thick ascending limb LOH
Describe damage in the kidneys due to nephrotoxins
Damage the epithelial cells lining the tubules and cause cell death and shedding into the lumen
Can be endogenous or exogenous
ATN more likely if reduced perfusion and a nephrotoxin
Give examples of endogenous nephrotoxins
In which treatment does urate build up?
Give some examples of exogenous nephrotoxins
Drugs (ACEi, aminoglycosides, NSAIDs)
Poisons (weedkillers, antifreeze)
How does rhabdomylosis cause ATN?
Muscular necrosis releases myoglobin 'crush injury'
In wars and natural disasters
Can occur in drug users and elderly when cannot move
Myoglobin is toxic to tubule cells and can also cause obstruction
Describe acute glomerulonephritis
Immune disease affecting the glomeruli
Can be primary or secondary
Give 2 types of rapidly progressing glomerulonephritis
Granulomatosis with polyangiitis
Crescenteric necrotising glomerulonephritis
Describe acute tubulo-interstitial nephritis
Caused by infection or toxins
Massive inflammatory infiltrate (lymphocytes)
What percentage of AKIs are post-renal causes?
What is the general mechanism for post-renal AKI?
Obstruction most block both kidneys or a single functioning kidney
Rise in intraluminal pressure
Dilation of renal pelvis
Decrease in renal function
Give some causes of post-renal AKI
Within lumen - stones, clots
Within wall - strictures (eg. Post-TB)
Pressure from outside - BPH, tumour, aortic aneurysm
Describe the serum changes common to all AKIs
What are the ECG changes of hyperkalaemia?
Tall T waves
Small/absent P waves
Increased P-R interval
Sine wave pattern
What do we check to see if the patient is volume depleted?
Reduced skin turgor
What do we assess when looking for fluid overload?
Describe the Hx of a patient will post-renal AKI
A single functioning kidney
Hx of stones
Hx of prostration or previous pelvic/abdo surgery
What should we examine for in post-renal AKI?
What is essential to do for every patient with AKI?
Blood, protein, leukocytes
What features of a urinanalysis of AKI when suggest intrinsic renal disease?
Blood and/or protein
How do we image AKI?
Ultrasound scan - obstruction
CXR - fluid overload, infection
Name some preventative methods for AKI
Identify risk factors
Monitor at risk patients
Ensure adequately hydrated
Detect early and identify cause
Give some of the susceptibilities for AKI
Give some exposure risk factors for AKI
What is the management for AKI?
Treat fluid overload - restrict Na+ and water
Treat hyperkalaemia with calcium gluconate, restriction of dietary K+, stop K+ sparing diuretics, ACEi etc, give dextrose and insulin, sodium bicarbonate
Treat acidosis - protein restrict, sodium bicarbonate
What are the indications that an AKI patient needs dialysis?
(All not responding to normal treatment)
Presence of dialysable nephrotoxin
Signs of uraemia
What is the prognosis for uncomplicated ATN?
Recovery in 2-3 weeks if no extra insults
What is the overall AKI mortality?
What is the normal GFR range?
90 - 120 ml/min
How many nephrons do we have and how many do we need to survive?
Need 40,000 approx (2%) to survive
What is chronic kidney disease?
Long term condition
Abnormal kidney function and/or structure
The irreversible and sometimes progressive loss of renal function over a period of months to years
What is the commonest cause of CKD?
Name some causes of CKD
Immunological - glomerulonephritis
Infection - pyelonephritis
Genetic - PCK, Alport
Obstruction and reflux nephropathy
Systemic disease - diabetes, myeloma
What is the common end point for the kidneys of many CKDs?
Small, shrunken kidney
With irregular outline
Lots of fibrous scarring
Who should be screened by CKD?
Ischaemic heart disease
Who is CKD more common in?
What is CKD classification based on?
Describe the stages of CKD
G4 < 15
Which measures of GFR are not very accurate?
> 60 GFR
Other than GFR, what other measurement can we look at?
Higher it gets = worsened condition
What are the stages of ACR?
A1 < 3
A2 3 - 30
A3 > 30
What percentage of the adult population have CKD 3 or worse?
Risk of death starts to increase when kidney function has declined by what percentage?
Even though no symptoms
What indicators what make us check kidney function?
Proteinuria and CKD together increase the risk of ...
Death by cardiovascular disease
More likely to need dialysis
What is the normal serum creatinine?
80 - 120 micromoles/L
What clearance markers can we use to represent eGFR?
What are the problems with using clearance markers to estimate GFR?
Require hospital stays
Collecting urine has bad compliance
Is the relationship between serum creatinine and GFR linear?
How much of your renal function can you lose before serum creatinine will change?
Creatinine concentration in serum is determined by:
Muscle mass (age, sex, race, exercise)
Why can't we use eGFR in AKI?
Can only use the eGFR formula if GFR is relatively stable
What can we look for in blood to indicate the cause of CKD?
Describe polycystic kidneys
Can become very large
Have CKD from the day they are born by definition but usually an issue until later in life
Acidosis can affect which organs?
Renal function decline further
Acidosis is not a problem until GFR is ...
How does CKD lead to anaemia?
Decreased production of EPO
Increased resistance to EPO (uraemic environment)
Reduced RBC lifespan
How do we treat anaemia from CKD?
Give EPO subcutaneous injections
How can CKD cause mineral and bone disorders?
Decreased GFR leads to increased serum phosphate and decreased serum calcium
Increased production of PTH
Decreased active vitamin D - decreased Ca2+ gut absorption
What types of renal osteodystrophy can occur?
Rugger jersey spine - sclerosis of end plates
Erosion to terminal phalanges
What are vertebral end plates?
The top and bottom portions of vertebral bodies that interface with vertebral discs
What other non-bone calcification can occur in CKD?
Small vessels in skin
What can we do to help prevent/delay CKD?
Treat proteinuria (ACEi)
When is renal replacement therapy usually needed? (GFR)
GFR = 8 - 10 ml/min