Loss of Kidney Function Flashcards
(12 cards)
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 of 1 α-hydroxylase vitamin D.
▪ Abnormality of glucose homeostasis: Decreased gluconeogenesis (kidneys also produce glucose)
Clinical features are determined by the
rate of deterioration
I.E. A slow loss of kidney function may present
asymptomatically whereas an acute loss of
kidney function could be disastrous
Clinical symptoms
Complicated by?
▪ 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 waste products.
Failure of homeostasis
▪ Acidosis.
▪ Hyponatraemia.
▪ Volume depletion.
Failure of endocrine function
▪ Anaemia – decreased erythropoietin.
▪ Chronic neurological damage.
What causes the 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), too much sodium is
excreted (not reabsorbed) and thus water.
= This is a more specific renal failure.
Implications of Acidosis
Caused by?
▪ Caused by decreased excretion of H+
ions and retention of acid bases.
o A buffering occurs as H+ passes into cells in exchange for K+ ions → 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.
Implications of hyperkalaemia
Caused by? Exarcebated by?
▪ Caused by the failure of the DCT to secrete potassium (and thus retains it).
o 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).
o Can also cause neural and muscular activity.
o Clinical features of the effects of hyperkalaemia are
dependant on the chronicity (the state of being chronic).
▪ The ECG shows the progression of the hyperkalaemia.
o T-wave peaks → P-wave disappears → bradycardia →
broadening of QRS complex → ARREST.
Chronic Renal Failure to Hyperparathyroidism diagram (slide 19, lecture 8)
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Metabolic functions of kidney
Metabolic Functions of the Kidney
▪ Decreased erythropoietin production → anaemia.
▪ Low 1, 25-Dihydroxycholecalciferol (1,25-Vitamin D3) → poor intestinal calcium absorption:
o Hypocalcaemia – Short term.
o Hyperparathyroidism – Long term.
▪ Phosphate is retained in CRF and it tends to bind calcium.
▪ This all results in an increased CARDIOVASCULAR risk (as low EC calcium): you have the potential to get
hypertension, secondary cardiac effects (arrhythmias), endothelial effects, lipid abnormalities etc
Acute (AKD) vs Chronic Kidney Disease (CKD)
Difficult to tell the difference clinically between the two (similar symptoms).
▪ However, certain aspects can be teased out:
o CKD shows shrunken kidneys.
o AKD has a previously normal creatinine level whereas in CKD, creatinine has always been abnormally high.
Methods of assessing GFR: Traditional Methods
▪ Urea – General BAD measure of kidney function:
o Can be confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function, etc.
▪ Creatinine – Needs to be assessed in the CONTEXT of the patient:
o Creatinine levels VARY fro person to person NATURALLY as it’s affected by; muscle mass, age, race, sex, etc., I.E. A small Caucasian woman will have a much lower creatinine than a large African man. However, they would BOTH have the same healthy eGFR (~120ml/min).
▪ Creatinine clearance – A poor indicator:
o Difficult for the elderly to collect an accurate sample logistically.
o Overestimates GFR at low GFRs as a small amount of creatinine IS secreted into the urine.
▪ Inulin clearance – Not used anymore clinically:
o A very laborious method – involves endogenous injection and catheterisation.
▪ Radionuclide studies – Such as EDTA clearance.
o Reliable but expensive.
Methods of assessing GFR: Modern Methods
▪ MDRD Equation: o An equation that measures the serum creatinine while taking into account the CONTEXT of the patient. o Generally unreliable when: GFR > 60ml/min. In very obese or very thin patients.
▪ The NICE Guideline Classification:
o Categorises patients based on GFR and their ACR (urine albumin: urine creatinine ratio) category.
