Chronic Kidney Diseae And Renal Failures Flashcards
What homeostatic functions do the kidneys have? (3)
- Electrolyte balance
- Acid-base balance
- Volume homeostasis
What happens to homeostatic functions on kidney disease
- Potassium increases
- Phosphate increases
- Bicarbonate decreases
- pH decreases (metabolic acidosis)
- Salt and water imbalance
What excretory functions do the kidneys have? (5)
- Nitrogenous waste
- Hormones
- Peptides
- ‘Middle sized molecules’ molecular weight of (2-5000 da)
- Salt and water
What happens to the excretory functions in kidney disease 3
- Increase in urea
- Increase in creatinine
- Decrease in insulin requirement (due to low insulin clearance so more stays in system)
What endocrine functions do the kidneys have? (2)
- Erythropoietin
- 1-alpha hydroxylase for vitamin D
What happens to the endocrine functions in kidney disease
- Decrease in calcium
- Anaemia
- Increase in parathyroid hormone (to compensate for low calcium)
What glucose metabolism functions do the kidneys have? (2)
- Gluconeogenesis
- Insulin clearance
In kidney disease, what is there an increased overall risk of?
Increase in cardio disease
How does rate of deterioration affect clinical presentation?
- If rate of deterioration is slow, body is very good at adapting e.g. some patients present with urea of 50 (which for a normal person is really bad) but their body is used to it since it’s developed over years so they don’t feel unwell
- Acute renal failure presents quicker because body hasn’t adapted
Give 1 example of how the cause of kidney failure can dictate the clinical presentation
you have Goodpasture’s disease where body makes antibodies against glomerular basement membrane, you might present with haemoptysis (lung involvement of Goodpasture’s since antibodies are made against lung too) and then you do blood test and find renal failure in the patient too
Or
If you have skin rash (purpura) and do blood test and find they have renal failure
How does hypovalaemia present
- Low bp
- Reduced capillary refill
- JVP not visible
- No pulmonary oedema
Why would a pt be tachypnoiec with normal oxygen and clear lungs on auscultation
Respiratory compensation
Kussmaul respiration (deep rapid breathing)
What changes will there be in concs of urea, creatinine, sodium, potassium and haemoglobin in end stage renal failure
- Urea higher
- Creatinine higher
- Sodium can go up or down (in her it’s down a bit though because of her poor appetite)
- Potassium higher
- Haemoglobin lower
What changes will there be in pH, pCO2, pO2, HCO3- and base excess in end stage renal failure
- pH will be lower
- pCO2 will be lower as she’s hyperventilating so she’s expelling CO2
- pO2 will be up a bit as she’s hyperventilating so she’s bringing in O2
- HCO3- will be lower
- Base excess will be lower or norma
They have increased H+ because less is excreted because of the kidney failure so the patient has metabolic acidosis which is compensated by resp rate increasing to decrease CO2 to shift equation left
Summary if end stage renal failure
- Symptoms of extreme lethargy, weakness and anorexia (end stage renal failure patients present this way with itching because of hyperphosphatemia)
- Clinically volume depleted → severe hypotension
- Elevated plasma urea and creatinine meaning she has renal failure
- This complicated by:
- Hyperkalaemia (main one to focus on)
- Hyponatraemia
- Metabolic acidosis
- Anaemia
- US showed 2 small shrunken kidneys
Acute renal failure conc of urea, creatinine, sodium, potassium, haemoglobin?
- Urea higher
- Creatinine higher
- Sodium could be either
- Potassium higher
- Haemoglobin normal (because it’s acute renal failure so there’s still some EPO around)
What changes will there be in pH, pCO2, pO2 and HCO3- for acute renal failure
- pH lower
- pCO2 lower
- pO2 higher
- HCO3- lower
Mild metabolic acidosis with respiratory compensation
How does kidney failure affect salt and water balance?
- Kidney failure tends to reduce secretion of salt and water leading to:
- Hypertension
- Oedema
- Pulmonary oedema
In what kind of circumstances can salt and water loss be seen though? (3)
- In tubulointerstitial disorders- damage to concentrating mechanism of urine
- Seen right after kidney transplant- there’s a bit of damage to tubules and they pee out a lot of water
- Seen also after kidney obstruction is relieved, kidney can’t concentrate urine and you get kidney failure
What may be a cause of AKI?
Hypovolemia
What does hyponatremia mean and what does it not mean?
- It does not mean reduced total body sodium
- It’s to do with how much free water you have- you’ll have more in hyponatremia
This means that for treatment you may not want to give them salt but instead want to remove excess free water
Describe how acidosis happens in renal failure
- Reduced excretion of H+ ions which means you become acidotic
- Cells take up this H+
What does acidosis do to potassium ions
The cells taking up the H+ also forces K+ out of the cells leading to hyperkalaemia
What are the 2 causes, then, of hyperkalaemia?
- Acidosis
- Reduced distal tubule potassium secretion
What are the symptoms of hyperkalaemia? (3)
- Cardiac arrhythmias
- Neural and muscular activity
- Vomiting
What does symptom presentation of hyperkalemia depend on
Chronicity of the disease- if it’s acute hyperkalaemia then these symptoms show but if its chronic then body adapts and they don’t show
What ECG changes come up in hyperkalaemia? (6)
- Peaked T waves
- P waves broaden, have reduced amplitude and disappear
- QRS widening
- Heart block
- Asystole
- VT/VF (ventricular tachycardia/ventricular fibrillation)
What health consequences does this have? (2) hyperkalaemia
- Anorexia
- Muscle catabolism
What effects does reduced EPO and reduced 1-25 Vit D levels have?
- Reduced EPO → anaemia
- Reduced 1-25 Vit D levels:
- Reduced intestinal calcium absorption
- Hypocalcaemia
- Hyperparathyroidism
Chronic renal failure causes phosphate retention and low levels of 1-25 vitD thus hypocalccaemia thus hyperparathyroidism
How does chronic renal failure affect vit d levels
- There’s also phosphate retention in chronic renal failure (phosphate usually excreted by kidneys)
- This contributes to low levels of 1-25 vit D and hypocalcaemia and therefore hyperparathyroidism
What risk does this all increase overall?
Cardiovascular risk
A pt with ckd more likely to die from cardio disease than end stage renal failure
What is the major predictor of end stage renal failure?
Ckd
What is the major outcome for a patient with CKD?
Cardiovascular disease
patient with CKD is more likely to die from cardiovascular disease than end stage renal failure
What standard cardiovascular risk is there for kidney failure patients? (3)
- Hypertension
- Diabetes
- Lipid abnormalities
Additionally can cause inflammation,oxidative stress,mineral bone metabolism disorder
What are the 2 main things we want to treat in initial management?
Fluid balance
Hyperkalaemia
Fluid balance- how do we manage hypovolaemia vs hypervolaemia?
- Hypovolaemia- give fluids
- Hypervolaemia- trial of diuretics/dialysis
Hyperkalaemia- what are the 3 ways we manage it?
- Drive it into cells- how? (2)
- sodium bicarbonate- how does this work?
- Binds to H+ to push equation to the right
- H+ come out of cell into blood to equalise this and K+ goes back into cell
- insulin dextrose- why do we need to be careful with this one?
- There are fatalities associated with it due to hypoglycaemia
- We only use it when potassium >6.5 or there are ECG changes
- sodium bicarbonate- how does this work?
- Drive it out of the body- how?diuretics/dialysis
- Reduce gut absorption- how?Potassium binders
What different long term management options are there? (4)
- Conservative treatment- what does this include? (5)
- EPO injections to correct anaemia
- 1,25 vit D supplements for hypocalcaemia
- Diuretics to correct salt water overload
- Phosphate binders- for hyperphosphataemia so reduces itching
- Symptom managements e.g. nausea
- Home therapy- what does this include? (2)
- Haemodialysis
- Peritoneal dialysis/assisted programmes
- In centre therapy- what does this include?Haemodialysis, 4 hours 3 times a week
- Transplantation
Can see needles going into a fistula (connecting artery to vein in anterior cubital fossa) which makes a big cephalic vein- 1 to take blood out and 1 to bring it back in
What is important to keep in mind for managing patients in hospital with kidney disease in terms of taking blood from them?
Take it from the back of the hand and not anterior cubital fossa or cephalic vein at wrist level because we need it for the fistula and it can scar up (stenosis) and we can’t do the fistula
A fistula is a connection between an artery and a vein to allow vein to thicken for repeated dialysis
If a patient is fit for transplantation, why do we need to avoid transfusions?
Transfusions sensitise patients to the antigens in the blood of the donor and then if they then get a kidney donation from someone else who shares similar antigens to the blood donor there’s increased risk of transplant failure
How do we assess kidney function
Urea
Creatinine
Radionuclide studies
Creatinine clearance
Inulin
Egfr
- Urea- is this a good indicator and why?
- No it’s a poor indicator
- Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc
Creatinine- is this a good indicator?
- It’s affected by muscle mass, age, race, sex etc
- We need to therefore look at the patient when interpreting the result (if they’re small/big, M/F etc)
- We look at the trend of creatinine (if we know what normal creatinine is) which is useful
Radionuclide studies- are these good indicators?
- EDTA clearance etc
- Very reliable but expensive
- Used for donors
Creatinine clearance- is this useful?
- Difficult for elderly patients to collect an accurate 24 hour urine sample
- Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)
Inulin clearance- is this useful?
Laborious so used for research purposes only
We mainly calculate estimated GFR (eGFR)- what is the main factor in this
Serum creatinine
As kidneys get better and actual GFR goes up, the eGFR becomes less accurate
- What do we do with people with normal/high eGFR in kidney disease patients then?
We look at creatinine trend e.g. someone could have increase in creatinine 30 → 60 but still have eGFR >90 so it won’t be picked up
What do we use to classify CKD? (3)
- Proteinuria
- ACR (albumin:creatinine ratio)
- GFR
More protein means more risk of end stage renal failure
Kidney failure risk equation
Validated risk prediction tool for kidney replacement in next 2-5 years for adults with stable CKD stages 3A to 5. Don’t use in pt with rapidly changing eGFR
Calculate fro, age sex CKD-EPI urine albumin creatinine ratio
Use:
Patient understanding of CKD diagnosis jn the context of multi comobidity, identification of high risk ckd patients:
-targeted patient engagement or education
-aggressive risk factor management
-refer to secondary care
When do we see small or normal sized kidneys
Small in ckd
Normal size in aki
