AKI and CKD Flashcards
what is Glomerular Filtration Rate (GFR)
the rate at which the glomerulus is filtering the blood to form the filtrate
Males 90-140 ml/min
Females 80-125ml/min
how do you estimate GFR?
To be able to measure GFR we need a substance that is:
- completely filtered
- not re-absorbed
- not secreted
- not metabolised by the nephron
(10ml of solution in blood - collect urine and there is 10ml)
Inulin fits this profile (100% gets filtered) BUT it requires an infusion into the blood therefore not practical - it takes a long time
In practice – creatinine clearance is measured
what is creatinine?
what is it produced by?
It is a chemical waste molecule that is generated from muscle metabolism
Produced from creatine, a molecule of major importance for energy production in muscles
Released into the circulation at a constant rate
Removed from the circulation by filtration and excreted in urine
Why is it important to check blood creatinine levels?
Measurement of creatinine concentration is used to:
- Determine sufficiency of kidney function - Determine severity of kidney damage - Monitor progression of kidney disease
Kidneys maintain blood creatinine at a specific levels
If creatinine levels in the blood are rising it could indicated that the kidneys are not functioning to their full ability to clear the creatinine
Problems with kidney function may lead to: Loss of nutrients from the body Failure to remove toxins Affect drug treatments Affect blood pressure
what is creatinine clearance
It is a value which indicates the volume of creatinine (in millilitres) removed by the kidneys over a period of time (per minute)
how is creatinine clearance measured?
24 hour urine collection = not practical
In practice: blood is taken from the patient. This is measuring the amount of creatinine in the blood plasma.
The higher the level of creatinine in the blood, the slower the kidneys are working = low creatinine clearance (mL/min)
How can creatinine clearance be calculated?
Cockcroft & Gault equation:
```
CrCl = F(140-age) x weight / Serum Creatinine
F = 1.04 in females, F = 1.23 in males
Units = ml/min
~~~
difference between eGFR and creatinine clearance
eGFR = estimated glomerlus filtration rate = which is measured via blood tests in labs = this has a chance of over estimating renal function
when does creatinine clearance have to be calculated
DOACs Nephrotoxic drugs > 75 years Extremes of muscle mass Drugs that are ++renally excreted Narrow therapeutic index drugs
how can serum creatinine be affected?
1) The amount of muscle tissue you have
- Men tend to have higher levels of blood creatinine because they have more skeletal muscle tissues than women
2) High protein in diet
3) Exercise, particularly if muscle building
4) Any injuries involving damage to the muscles
- e.g. severe burns or conditions resulting in acute muscle wastage
5) Malnutrition leading to dramatic weight loss
what is acute kidney injury (AKI)
AKI is NOT a disease but is the result of another clinical problem
AKI should be regarded as a spectrum of injury that may progress to organ failure
AKI occurs most commonly in patients who are at risk, who either are acutely ill or have had major surgery
what is acute kidney injury (AKI)
AKI is NOT a disease but is the result of another clinical problem
AKI should be regarded as a spectrum of injury that may progress to organ failure
AKI occurs most commonly in patients who are at risk, who either are acutely ill or have had major surgery
what are the risk factors of AKI?
Age >75 years Previous AKI Pre-existing CKD (eGFR <60ml/kg/1.73m2) Heart failure Atherosclerotic peripheral vascular disease (PVD) Diabetes mellitus Liver disease Debility and dementia
what are triggers for AKI
Sepsis or infection
Hypotension (Mean arterial pressure <65 mmHg, systolic pressure <90 mmHg)
Hypovolaemia (dehydration, bleeding)
Nephrotoxic medications e.g. gentamicin, NSAIDs, iodinated contrast
Anti-hypertensives e.g. ACE inhibitors, loop diuretics
what are the three classifications of AKI
Pre renal - inadequate perfusion - not enough blood at sufficient pressure to allow filtering
renal - cellular damage/ intrinsic - damage to the cells that makes filtering mechanisms possible
post renal - obstruction - urine unable to drain adequately - system ‘backed up’
Pre - renal
mechanism
causes
mechanism - Blood flow to the kidney reduced i.e. decreased perfusion. If not managed it can cause ischaemic injury.
cause :
- Intravascular volume depletion e.g. diarrhoea, vomiting or haemorrhage
- Decreased arterial pressure e.g. heart failure or sepsis
- Nephrotoxic medications e.g. ACEIs, ARBs, NSAIDs
- Kidney function typically returns to baseline after volume status established or nephrotoxic
medication discontinued
post renal AKI
mechanism
causes
mechanism - Obstruction to outflow from the kidneys.
causes:
Causes waste (urine) to build up in the kidneys
Common causes include:
- kidney stones: mainly occurs in the ureters but may also develop in the urethra
- benign prostatic hyperplasia (BPH)
- CNS disorders that may affect outflow such as stroke, multiple sclerosis, spinal cord injury,
- blood clots in the ureters or urethra
- cancer of the prostate, cervix or colon
- nephrotoxic medications
Renal/ intrinsic AKI
mechanism
causes
mechanism:
Damage to the functional tissues of the kidney
causes:
Can be categorised by the component of the kidney that is affected e.g.
- Glomerular: glomerulonephritis
- Tubular: acute tubular necrosis; rhabdomyolysis; myeloma
- Interstitial: interstitial nephritis
Acute tubular necrosis (ATN) is most common in hospitalised patients
In contrast to pre-renal causes, ATN does not improve with adequate repletion of intravascular volume
May resolve over time but temporary renal replacement therapy (i.e. dialysis) may be required
Common cause is usually ischaemic (prolonged hypotension) or due to nephrotoxic drugs
what is the management for pre-renal AKI
hydration with IV fluids
what is the management for post-renal AKI
refer patient to a urologist
what is the management for intrinsic?
treat the damage…if treatable!
what are other management options for AKI ( in terms of medication)
Hold all nephrotoxic medications
Adjust doses of all other medications that are prescribed
what are possible further complications of AKI?
Hyperkalaemia high potassium levels in blood
Metabolic acidosis blood is too acidic; pH <7.25
Fluid overload peripheral and/or pulmonary oedema
Uraemic encephalopathy high urea levels in the blood
what is the management of hyperkalemia?
AKI causes concentration of potassium in the blood stream to increase
Can have very severe consequences, in particular altering electrophysiology leading to cardiac arrhythmias
Acute treatment with Insulin or Salbutamol causes a shift of potassium from the blood stream into cells
Dietary potassium should be restricted
If potassium persistently high, patients may need to undergo urgent dialysis
what is the management of acidosis?
In AKI acidosis occurs as the kidneys are no longer able to excrete H+ ions
This rise causes the blood to become acidic
Solution to neutralise the pH of the blood
IV Sodium bicarbonate is given and often these patients are admitted to HDU/ITU
what is the management of odema?
In AKI oedema occurs as the kidneys are no longer able remove water or sodium as efficiently
Give a loop diuretic e.g. furosemide; often needs to be given IV at a high dose
Monitor serum creatinine as there is a risk of worsening pre-renal AKI through dehydration
Not all patients will be responsive
If persistently fluid overloaded, patients may need to undergo urgent dialysis
what is the management of uraemic encephalothopy
In AKI uraemia occurs as the kidneys are no longer able remove urea as efficiently
Urea is toxic and able to cross the blood brain barrier causing encephalopathy
Encephalopathy can range in severity from mild confusion to coma
Patients with uraemic encephalopathy must undergo urgent renal replacement therapy (dialysis) to remove the toxic urea from the blood
what are nephrotoxic medications
Medications with nephrotoxic potential which must be reviewed in patients with AKI (or those at risk of AKI) include: ACEIs ARBs NSAIDs Diuretics Aminoglycosides Iodinated contrast agents
what does the afferent and efferent arterioles do when there is low blood pressure.
deliver more blood to glomerlus and prevent blood from leaving the glomerlus
keep blood in glomerlus to improve perfusion
When renal perfusion is low (i.e. decreased blood pressure) the body does the following in the blood vessels of the glomerulus:
- vasoconstricts the efferent blood vessels - vasodilates the afferent blood vessels
what does prostaglandins do?
produced by macular densa cells
causes vasodilation of the affarent arteriole
what does angiotensin 2 do?
vasoconstriction of the efferent arteriole
-concentrates the blood in the glomerlus
what does NSAIDs do?
in regards to AKI
inhibit prostaglandins - prevents vasodilation of the afferent arteriole = preventing maximum blood entering the glomerlus
what does ACEi do?
in regards to AKI?
inhibits conversion of angiotensin I to angiotensin II
causes vasoconstriction on the efferent arteriole
to increase resistance of the blood leaving the glomerulus - more concentrate blood in the glomerulus
preventing reperfusion
Paradoxically, ACEIs are also renoprotective but can cross over into being nephrotoxic - patients with stable kidney even if they have kidney disease
poor renal function but is stable = fine to continue acei
acute kidney problem = stop acei
things to bear in mind before starting medications for people with AKI
Do not initiate in patients that are at a higher risk of AKI always consider risk Vs benefit
Hold drugs if patient is pre-op
Discontinue drugs immediately if patient has an AKI
what is chronic kidney disease?
“abnormalities of kidney function or structure present for more than 3 months, with implications for health”
Common, frequently unrecognised and often exists with other conditions e.g. CV disease or diabetes
200-9/10 £1.5billion (1.3% of NHS spend)
2% of the above was for renal replacement therapy
~30% of people with advanced kidney disease are referred late to nephrology, causing increased mortality and morbidity
Risk increases with age
Asymptomatic
what are the risk factors of CKD?
Diabetes mellitus Hypertension Cardiovascular disease Hypercholesterolaemia Obesity Metabolic syndrome Age and race AKI Malignancy Family history of CKD Kidney stones Infections like Hep C and HIB Autoimmune disease
Long-term & regular use of nephrotoxic medications e.g. NSAIDs or lithium
Glomerulonephritis: kidney inflammation
Polycystic Kidney Disease: an inherited condition where growth called cysts develop in the kidneys
Blockages in the flow of urine: recurrent kidney stones or an enlarged prostate
how does diagnosing CKD work?
Diagnosing CKD is done according to the classifications however there are certain prompts or findings that will lead to checking the GFR. These can be:
Persistent microalbuminuria
Persistent proteinuria
Persistent haematuria (after excluding other causes)
OR, it could be as a result of imaging e.g.
Ultrasound or biopsy
what are clinical complications of CKD
There are multiple complications with CKD result in the majority of renal patients being on long-term medications: Chronic anaemia Hypertension Hypercalcaemia Hyperphosphataemia Chronic vitamin D deficiency Pulmonary oedema Acidosis
Other clinical complications include: Renal osteodystrophy Hyperparathyroidism resulting in bone changes Uraemic encephalopathy Peripheral neuropathy Coagulopathy
