CKD & renal failure Flashcards
What are homeostatic functions of the kidney?
- Electrolyte balance,
- acid-base balance
- volume homestasis
- EPO production
- 1-alpha hydroxylase for vitamin D
- excretes nitrogenous waste, hormones, peptides, middle sizes molecules, salt & water.
- Glucose metabolism: gluconeogenesis (filter/reabsorb glucose) & insulin clearance
What does kidney failure lead to and why?
- Increased potassium & phosphate (not excreted),
- decreased bicarbonate so low pH (metabolic acidosis),
- salt & water imbalance
- low EPO so anaemia
- low calcium because low vitamin D, high PTH to compensate.
- Increased waste products: urea, creatinine.
- Insulin not cleared so insulin diabetics need less.
- Increased CV risk
How might chronic and acute kidney failure present?
- Chronic may present with abnormal blood results but feel ok because body adapted.
- Acute may present worse (skin rash, haemoptysis etc)
In case of kidney failure why metabolic acidosis? How will the body react to compensate for this?
- Less H+ ions excreted, less bicarbonate reabsorbed/produced so get metabolic acidosis.
- To compensate hyperventilation to get rid of CO2 (decrease)
What happens to urea, creatinine, sodium, potassium and haemoglobin in kidney failure?
- Urea, creatinine increase.
- Sodium can increase or decrease.
- Potassium increases.
- Heamoglobin decreases
Why anaemia in kidney failure?
less EPO production
What can cause acute kidney failure? How can this present?
Eating wild mushrooms.
- Can present with nausea/vomiting/reduced urinary output.
- Waste products increased, sodium/potassium/hb stay kind of in range (because acute).
- Acidosis so PCO2 decreases to compensate
What does kidney failure tend to do with salt and water?what does this elad to?
-Tend to get reduced secretion of salt & water (increased retention) leading to hypertension, oedema, pulmonary oedema.
When is salt and water loss seen?
In tubulointerstisial disorders (damage to concentrating mechanism)
Why do we get kidney failure acidosis and what can this cause?
- Reduced excretion of H+ ions, less bicarbonate so metabolic acidosis.
- Leads to anorexia & muscle catabolism.
Why do we get hyperkalaemia in kidney failure? What can cause this?
Decreased distal tube potassium secretion. acidosis
What are the symptoms associated with hyperkalaemia?
Cardiac arrhythmias, neural & muscular activity, vomiting to get rid of it
What are the ECG changes seen in hyperkalameia?
Broad P wave (reduced amplitude, disappears), peaked T wave, QRS widening, heart block, asystole, VT/VF (can lead to irregular heartbeat)
How does kidney failure cause hypocalcaemia? What is seen to compensate? What can this lead to?
Low vitamin D because of decreased 1-alpha hydroxylase activity, so leads to hypocalcaemia.
-to compensate hyperparathryoidism (inc PTH)
What does chronic renal failure do to phosphate?
Phosphate retention (hyperphosphataemia). Can cause itch
What do end-stage renal failure patients usually die from?
CV disease
What causes CV risk?
Hypertension, diabetes, lipid abnormalities, inflammation, oxidative stress, mineral/bone metabolism disorders
What is initial management for kidney failure? What do you do if they are hypovolaemic/hypervolaemic?
- If hypovolaemic - give fluids.
- If hypervolaemic - diuretics/dialysis trial
What do you do to fix the hyperkalaemia?
- To drive potassium into cell: sodium bicarbonate, insulin dextrose (caution).
- To drive out of body - diuretics/dialysis.
- To decrease gut absorption - potassium binders
What to do for long term management of kidney failure?
EPO injections for anaemia, diuretics for salt/fluid overload, phosphate binders, 1,25 Vit D supplements, symptom management.
- Home therapy: haemodialysis, peritoneal dialysis/assisted programmes.
- In centre therapy: haemodialysis 4 hours 3x a week for transplantation
What do you need to avoid in transplantable patients with kidney disease and why?
Transfusions.
Prevent sensitisation to prevent transplant failure
What kidney size in chronic kidney failure? What kidney size in acute kidney failure?
Chronic - small kidneys.
Acute - normal sized kidneys
What are traditional methods of assessing GFR and their disadvantages?
- urea: poor indicator confounded by diet, catabolic state, GI bleeding, drugs, liver function.
- creatinine: affected by muscle mass, age, race, sex.
- radionuclide studies - eg. EDTA clearance, reliable but expensive.
- creatinine clearance: hard for elderly to collect accurate sample, overestimates GFR at low GFR (small amount creatinine secreted into urine)
- insulin clearance: laborious, for research purposes only
When cant we see a trend for creatinine?
CKD-EPI . when EGFR above 90 cant see trend
What does NICE classification classify as kidney failure? What does it look at?
Looks at albumin creatinine ration ACR for proteinuria & GFR.
ACR <3 normal. 3-30 moderate increased. >30 very increased.
GFR >90 normal and high. <15 kidney failure