Renal Flashcards
What are the 6 functions of the kidney?
- regulation of extracellular fluid volume and BP
- regulation of blood osmolarity
- maintenance of ion balance
- homeostatic regulation of plasma pH
- excretion metabolic + other wastes
- hormone activity
What is creatinine?
- undergoes complete glomerular filtration with very little reabsorption and so is a useful indicator of GFR
- the metabolic waste product of creatine metabolism in muscles
- measured by lab tests
What is the cockroft and gault formula?
(140 - age) x weight (kg) x F
serum creatinine
F = 1.04 (female) 1.23 (male)
What are the 2 pros of cockroft and gault?
- easy to calculate in practice
- in use for many years
What are the 2 cons of cockroft and gault?
- based on limited variables
- increasing rates of obesity meaning weight is no longer accurate of muscle mass
What is the 1 pro of MDRD?
- better estimate than C+G
What are the 2 cons of MDRD?
- more difficult in practice
- not routinely used in clinical practice
What are the 2 pros of CKD-EPI?
- best estimate of GFR
- version available using cystatin C for patients with loss of muscle mass
What is the 1 con of CKD-EPI?
- complex to calculate
What is AKI?
Acute kidney injury - a sudden reduction in function which is often asymptomatic
What are the 5 signs and symptoms of AKI?
- acidosis
- oedema
- reduced urine output
- hyperkalaemia
- toxicity of medicines with narrow therapeutic window
What are the 6 risk factors of AKI?
- CKD
- HF
- liver disease
- diabetes
- oliguria
- neurological impairment
What are the 4 ways that AKI managed?
- treat the cause
- optimise meds
- maintain good hydration
- RRT
What are the 4 ways that AKI can be prevented in hospitals?
- ACEi/ARBs should be discontinued on the day of admin of bowel preparations and withheld for 72 hours
- diuretics should be discontinued on the day pf admin of oral and bowel preparation and witheld for 24 hrs
- ACEi/ARBs should be withheld peri-operatively
- monitor fluid balance
What are the 2 ways that AKI can be prevented in community?
monitoring of:
- conditions leading to dehydration
- drugs with nephrotoxic potential
What are the critical care acuity levels 0-3?
0 - needs met through normal ward care
1 - patients at risk of deterioration
2 - patients requiring detailed observation, including support for a single failing organ system
3 - patients requiring advanced respiratory support or basic support with at least two failing organ systems
Who comes to critical care?
Post-operative:
- Elective surgical patients (prolonged or major surgery such as laparotomy)
- Emergency
Serious short term condition
- Cardiac arrest -> likely requiring intubation; temperature management (cooling); blood pressure support
- Overdose / poisoning
Serious infections: sepsis or severe pneumonia
Shock: circulatory or septic
Trauma
Pancreatitis
Renal failure requiring renal replacement therapy (RRT)
Severe neurological conditions
- Guilliain-Barré
How can you quickly assess a patient in the ICU?
Can the patient talk to you
Organ failure
- Are they on a ventilator
- How many syringes have they got running
- Look at the monitor (The more on the monitor the sicker the patient)
- Are they on the filter
What tubes have they got in
- NG (Free drainage or for administration; is there a bag on the end or spigotted)
- NJ
- Do they have parenteral nutrition
- Drains / Urine output (Are they bleeding?)
What is the ICU alphabet?
A - airways
B - breathing
C - circulation
D - delirium
E - electrolytes
F - fluids
G - gastro
H - haemotology
I - infection
L - lines
M - medicines
N - nutrition
What is the definition of CKD?
Abnormalities of kidney function or structure present for more than 3months, with implications for health
What are the 5 stages of CKD?
stage - eGFR
1 - >90
2 - 60-89
3A - 45-59
3B - 30-44
4 - 15-29
5 - <15
How is absorption altered in a CKD patient?
May result in increase or decrease in bioavailability
Reduced transporter availability for uptake from GIT
Reduced enzymatic metabolism in intestinal enterocytes
How is distribution altered in a CKD patient?
Oedema; volume of distribution may increase
Hypoalbuminaemia; reduced protein binding leads to a greater free fraction of the drug
Increased free fraction can increase clearance and/or distribution
How is metabolism altered in a CKD patient?
Decreased drug metabolism via CYP enzymes
Increased free drug (due to reduced protein binding) so higher metabolism
Decreased metabolic functions; enzymes are inhibited by uraemic toxins
How is excretion altered in a CKD patient?
Decreased rate of glomerular filtration
Decrease rate of active secretion
What are the 4 risks in practice of treating CKD patients?
- Risk of increased side effects and toxicity (secondary to changes in PK) (opioid analgesics)
- Risk of ineffectiveness (nitrofurantoin to treat urinary tract infection)
- Risk of exacerbating impacts of CKD (spironolactone and hyperkalaemia risk)
- Risk of causing worsening renal function (NSAIDs)
What are the 8 causes of CKD?
- Diabetes: 30-40% of end-stage renal disease
- Hypertension
- Glomerulonephritis – inflammation of the structures of the kidney
- Polycystic Kidney disease and other inherited diseases
- Genetic malformations
- Lupus and other immune conditions
- Obstructions
- Repeated Urinary Infections
What are the implications of impaired homeostatic function?
Acid-base balance -> Low pH; metabolic acidosis
Fluid balance -> oedema, hypertension
Electrolyte balance -> Hypernatraemia, Hyperkalaemia
What are the implications of impaired endocrine function?
- Reduced erythropoietin production -> Anaemia
- Reduced vitamin D activation -> Renal bone disease
- Reduced renin production -> Blood pressure control, Increased cardiovascular risk
What are the implications of impaired filtration + excretion function?
- Reduced excretion of water-soluble toxic substances and waste products -> Cramps and restless leg syndrome, Nausea, Stress ulceration
- Reduced excretion of medications -> increased side effects
What are the 8 key signs and symptoms of CKD?
Itch
Restless legs
Cramps
Fractures
Frothy Urine
Thirst
Difficulty concentrating
Reduced urine output
What are the 3 complications associated with CKD that require immediate management?
Fluid overload
Hyperkalaemia
Metabolic acidosis
What are the 5 complications associated with CKD that require long-term management?
Renal bone disease and related hyperparathyroidism
Renal anaemia
Cardiovascular risk reduction
Symptom control of pruritus, cramps etc
Medicines optimisation
How is metabolic acidosis treated?
Refer to specialist care – renal specialist, critical care
Intravenous sodium bicarbonate as per local protocol
Dialysis
How is fluid overload managed?
Urine output falls as CKD progresses leading to build-up of fluid
This becomes dangerous if it accumulates on the lungs = pulmonary oedema
Management options:
Fluid restriction
Diuretics; loop, thiazide, potassium-sparing
Dialysis
How is hyperkalaemia managed?
Aims: prevent cardiac arrhythmias by lowering serum potassium levels and stabilising the cardiac tissues.
To stabilise the cardiac tissue (if ECG changes are present)
Give calcium gluconate 10ml of 10% IV by slow IV Bolus. Repeat until ECG normalises, then:
To reduce serum potassium (increase uptake into cells)
Give 50mL of 50% Glucose with 10 units of Actrapid insulin over 10minutes
Consider giving 10-20mg of nebulised salbutamol
To reduce potassium absorption
Dietary potassium binders; sodium zirconium cyclosilicate, calcium resonium
Dietary restriction
How can hyperkalaemia be prevented?
Reduce potassium intake in the diet
Review medications pre-disposing to hyperkalaemia
Potassium-sparing; ACE inhibitor/ARB, LMWH, aldosterone antagonist
Potassium-containing; macrogols
Reducing excretion; nephrotoxics, ACEis, NSAIDs
What are the implications of renal bone disease?
Damaged kidneys must work harder to remove phosphorus from your body. Buildup of phosphorus is associated with less calcium in your blood and with the release of PTH by your parathyroid glands. PTH moves calcium out of your bones and into your blood causing major loss of calcium in bones
What are the 3 other implications of renal bone disease?
Calciphylaxis – deposition of calcium and phosphate in other parts of the body
Soft tissue calcification – leading to painful necrotic ulcers
Peripheral vascular calcification
Cardiovascular calcification; vessels or valves
What are phosphate binders?
Calcium based phosphate binders are first line for renal bone disease
Calcium binds to phosphate in the gut and prevents absorption of dietary phosphate
Must be taken with meals
Calcium acetate is licensed, first-line option
Second line is non-calcium phosphate binders
Use if the patient has hypercalcemia or if calcium-based binders are not tolerated
How is renal disease treatment monitored?
Successful drug therapy aims to reduce fracture risk and soft tissue calcification
Vitamin D and phosphate binders are long-term treatments which gradually correct blood results
Phosphate, calcium and parathyroid hormone levels should be monitored to optimise therapy
Adjustments are generally made at 4-12 weekly intervals to allow time for response
What are the normal blood ranges for phosphate, calcium and PTH?
Phosphate
Normal range 0.8-1.5mmol/L (May vary by location)
Corrected Calcium
Normal range 2.20-2.60mmol/L
Parathyroid Hormone
Normal Range 1.1-6.9pmol/L
How can CKD cause anaemia
The kidneys are the main site of erythropoietin production
Erythropoietin is the growth factor that promotes red blood cell formation and release of reticulocytes from the bone marrow
In patients with CKD erythropoietin levels fail to increase in response to normal stimuli, leading to anaemia
How is anaemia treatment monitored?
Monitor response and adjust dose to maintain Hb 100-120g/L
Avoid Hb level >120g/L as this has been associated with adverse effects including:
Cardiovascular events
Loss of dialysis access
Hypertension
Continue to monitor iron levels and replace to maintain ferritin 200-500micrograms/L
Note that ESA therapy is less effective in the presence of inflammation and/or infection amongst other conditions
Why are RAAS system antagonists in CKD important?
RAAS antagonists (ACEi and ARB) help to protect the kidneys and preserve function in CKD
Useful for reducing protein loss in urine due to CKD
It is vital to identify whether or not a patient has AKI or CKD:
In AKI we withhold ACEi/ARB
In CKD we continue ACEi/ARB
