What happens when the kidneys stop working? Flashcards
What happens when the kidneys stop working?
Loss of excretory function
- Accumulation of waste products
Loss of homeostatic function
- Disturbance of electrolyte balance
- Loss of acid-base control
- Inability to control volume homeostasis
Loss of endocrine function
- Loss of erythropoietin production
- Failure to 1 alpha-hydroxylase vitamin D
Abnormality of glucose homeostasis
- Decreased gluconeogenesis
How are clinical features of kidneys determined?
Clinical features are determined by the rate of deterioration
e.g. slow loss of kidney function may present asymptomatically whereas an acute loss of kidney function could be disastrous.
What is the clinical presentation of kidney failure?
- Symptoms of extreme lethargy, weakness and anorexia.
- Severe hypotension due to volume depletion.
- Elevated plasma urea and creatinine -> diagnostic of renal failure.
Complicated by; hyperkalaemia, hyponatremia, metabolic acidosis and anaemia.
What causes the symptoms of lethargy and anorexia?
Failure of excretion:
- Accumulation of nitrogenous waste products, hormones, peptides and other ‘middle-sized’ molecules (Mol Wt 2-5000)
Failure of homeostasis:
- Acidosis
- Hyponatremia
- Volume depletion (low blood pressure)
Failure of endocrine function:
- Anemia (decreased erythropoietin)
What causes salt and water imbalance?
- Normally, patients with renal dysfunction have difficulty excreting sodium (and thus retain water): hypertension and (pulmonary) oedema
- Sometimes, in patients with tubulointerstitial disorders (inner medulla - in which the concentrating mechanisms have been damaged), too much sodium is excreted (not reabsorbed) and thus water - this is a more specific renal failure
- Inability to decrease sodium excretion (i.e. increase sodium reabsorption) when sodium depleted.
- Osmotic diuresis - caused by high concentration small MW waste substances, e.g., urea.
- This inappropriately high loss of salt and water results in volume depletion which causes low blood pressure
Is the total body serum the same as serum sodium levels?
DO NOT CONFUSE SERUM SODIUM LEVELS WITH TOTAL BODY SODIUM - CKD AND AKI ARE OFTEN ASSOCIATED WITH HYPONATREMIA
What are the implications of acidosis?
- Caused by decreased excretion of H+ ions and retention of acid bases
- A buffering occurs as H+ passes into cells in exchange for K+ ions à aggravating hyperkalaemia.
- The Partially compensated metabolic acidosis tends to make patients tachypnoeic to increase CO2 loss through the lungs - known as Kussmahl respiration OR ‘air hunger’.
- The acidosis can exacerbate anorexia and increases muscle catabolism - for the protein buffer mechanism.
What are the implications of hyperkalemia?
Caused by the failure of the DCT to secrete potassium (and thus retains it).
- Exacerbated by acidosis - causes shift of potassium from intracellular to extracellular (to correct acidosis).
High blood potassium can cause cardiac arrhythmias (initial loss of p waves and bradycardia -> arrest).
- Can also cause neural and muscular activity.
- Clinical features of the effects of hyperkalemia are dependant on the chronicity (the state of being chronic)
How can progression of hyperkalemia be shown on an ECG?
- The ECG on the left shows the progression of the hyperkalaemia.
- T-wave peaks -> P-wave disappears -> bradycardia -> broadening of QRS complex -> ARREST
What are the results of decreased erythropoietin production and low 1-25 Vit D levels?
Decreased erythropoietin production: anaemia
Low 1-25 Vit D levels: poor intestinal calcium absorption, hypocalcaemia (short term) and hyperparathyroidism (longer term)
*Increased cardiovascular risk
Highlight the mechanism by which phosphate retention decreases calcium (ionised)
- Phosphate is retained in CRF and it tends to bind calcium
- This all results in an increased cardiovascular risk (as low EC calcium
How is cardiovascular disease linked to kidney disease?
A major outcome for a patient with chronic kidney disease is cardiovascular disease; you have the potential to get hypertension, secondary cardiac effects (arrhythmias), endothelial effects, lipid abnormalities etc.
What is acute vs. chronic kidney disease?
Essentially, it’s difficult to tell the difference clinically between the two (similar symptoms).
However, certain aspects can be teased out:
- CKD shows shrunken kidneys.
- AKD has a previously normal creatinine level whereas in CKD, creatinine has always been abnormally high
How can patient be managed?
- Intravenous normal saline to correct fluid depletion
- Intravenous sodium bicarbonate to correct acidosis
- Intravenous insulin and dextrose to lower plasma potassium (by driving K+ ions back into cells)
- Transfer to hospital for dialysis
How can GFR be assessed?
Urea
- poor indicator: confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc
Creatinine
- affected by muscle mass, age, race, sex etc hence need to look at the patient when interpreting the result
Creatinine clearance
- poor indicator: difficult for elderly patients to collect an accurate sample
- overestimates GFR at low GFRs (as a small amount of creatinine is also secreted into urine)
Inulin clearance (not used clinically anymore) - laborious - used for research purposes only
Radionuclide studies such as EDTA clearance
- reliable but expensive
