Renal Failure Flashcards
What are the 4 main roles of the kidneys?
Homeostatic
Endocrine
Excretory
Glucose metabolism
What are the excretory functions of the kidney?
Nitrogenous waste Hormones Peptides Middle sized molecules (Mr of 2-5000) Salt and water
What are the endocrine functions of the kidney?
Erythropoietin
1 alpha hydroxylase
What are the homeostatic functions of the kidneys?
Electrolyte balance
Acid-base balance
Volume homeostasis
What are the glucose metabolism functions of the kidney?
Gluconeogenesis
Insulin clearance
What can go wrong during kidney failure?
Each of the 4 functions can be affected
What happens when homeostatic function of the kidneys is affected?
The electrolyte balance is disturbed due to lack of excretion of potassium
Increasde potassium Decreased bicarb Decreased pH Increased phosphate Salt and water imbalance
What happens when endocrine function of the kidneys is affected?
Loss of ability to process vitamin D
Leads to decreased Ca2+ levels, anaemia
Increased PTH to try and compensate for low serum Ca2+
What happens when excretory function of the kidneys is affected?
Lack of excretion of urea, creatinine and insulin
Increased urea
Increased creatinine
Decreased insulin requirement
What happens when glucose metabolism function of the kidneys is affected?
Impaired glucose metabolism
What risk is increased with kidney failure?
CVD risk
What can affect clinical presentation of kidney failure? i.e. why might kidney failure symptoms display differently in clinic
Rate of deterioration
Cause of kidney failure
75F - Mrs EH Presents to A&E 3 week history of feeling of 'having the flu' Increasingly weak No appetite Drinking only 2 cups of tea/ day 24hr history of being too weak to move
PMH = kidney issues after birth of 2nd child, reflux, MI 2 years ago, high plasma creatinine (163 umol.L) at time of MI, and eGFR of 138 mol/min
Examination = Very unwell, pale, cold hands Capillary refill decreased Lungs clear on auscultation HR = 50/min; low BP of 67/35 mmHg; O2 sats 100% JVP not visible, tachypnoeic
What will be the patient’s blood volume status?
Hypovolemic - due to low BP, cannot see jugular venous pressure at the clavicle, cool hands (vasoconstriction) and reduced capillary refill
Why is Mrs EH tachypnoeic with normal O2 sats and clear lungs on auscultation?
Respiratory compensation for metabolic acidosis
What will be the effect on the concentration of: Urea Creatinine Sodium Potassium Haemoglobin
in the blood tests?
Urea = increased Creatinine = increased Sodium = anywhere Potassium = increased Haemoglobin = decreased
Blood results due to lack of excretion
What will be the effect on the concentration of: pH pCO2 pO2 Bicarbonate ions Base excess
pH - decreased (acidotic) pCO2 - decreased pO2 - increased (good O2 sats) Bicarbonate ions - decreased Base excess - decreased
Due to metabolic acidosis with respiratory compensation
Why is pCO2 decreased and O2 normal in Mrs EH’s blood gas results?
Hyperventilation to compensate for metabolic acidosis = breathes off CO2 = low pCO2
Ventilation = good = normal pO2
CO2 + H2O H2CO3 HCO3- + H
Summary of Mr EH’s clinical findings =
Symptoms of extreme lethargy, weakness and anorexia
Clinical volume depletion = severe hypotension
Elevated plasma urea and creatinine make diagnosis of renal failure
What would be the next investigation?
Ultrasound (USS) - shows 2 small shrunken kidneys
What does it mean clinically to find 2 small shrunked kidneys?
CKD
Acute presentation of a chronic kidney disease
54 -
Previously fit and well
Admitted with 2 day history of nausea, vomiting
1 day history of reduced urinary output after eating wild mushrooms
Examination: Alert and orientated Temp = 36.4 degrees HR = 79; RR = 16; BP = 143/81 mmHg Normal skin turgor
What will be the patient’s blood volume status?
Euvolemic
What will be the effect on the concentration of: Urea Creatinine Sodium Potassium Haemoglobin
in the blood tests?
Urea - increased Creatinine - increased Sodium - anywhere Potassium - normal / increased Haemoglobin - normal / decreased (not too much)
What will be the effect on the concentration of:
pH pCO2 pO2 Bicarbonate ions Base excess
pH = decreased
pCO2 = decreased
pO2 = normal / high
Bicarbonate ions = decreased
Mild metabolic acidosis with respiratory compensation
Why might Hb not be low in this patient?
Acute kidney failure - not enough time for erythropoetin levels to go down and show up in the blood work
What would be the next investigation?
USS - normal sized kidneys with no obstruction
What is interesting about salt and water balance?
Can cause kidney failure
OR
Can be a symptom of kidney failure
What happens to the salt water balance in kidney failure?
When may water loss be seen?
Kidney failure tends to reduce secretion of salt and water - leads to hypertension, oedema, pulmonary oedema
BUT - salt and water loss may be seen in tubulointerstitial disorders – damage to concentrating mechanism in the kidneys
Leads to hypovolemia, which may be the cause of AKI (acute kidney injury)
Why does hyponatremia not always lead to reduced total body sodium?
Fluid balance is affected (i.e. hypo/hypernatremia), total amount may still remain within range
What occurs in kidney failure acidosis?
CO2 + H2O H2CO3 HCO3- + H+
So if acid (H+) increased, there is retention of bases as H+ combines with HCO3- to decrease acidosis
Acidosis causes symptoms of anorexia and muscle catabolism
Why might hyperkalaemia occur in kidney failure?
How might this present clinically? What do the symptoms depend on?
Less postassium secretion in the distal tubule
Acidosis
Symptoms = cardiac arrhythmias, neural and muscular activity, vomiting
Symptoms depend on chronicity
How may arrhythmias caused by hyperkalaemia show up on an ECG ?
Peaked T waves
P wave = broadened, reduced amplitude, amy disappear completely
QRS widening
Heart block
Asystole
VT (ventricular tachycardia) / VF (ventricular fibrillation)
What do you give to treat hyperkalaemia?
Bicarbonate
To reduce H+
So potassium can return to cell
How can metabolism in the kidneys be affected during kidney failure?
Reduced erythropoietin = anaemia
Reduced 1-25 Vit D levels = reduced intestinal calcium absorption, hypocalcaemia, and hyperparathyroidism
Why may patients with kidney failure present with hyperparathyroidism?
There is low 1-25 vit D and phosphate retention in chronic renal failure
Calcium binds with phosphate so it is pooped out rather than absorbed by the body
Therefore increased PTH release to compensate for low serum Ca2+
What is a predictor of end stage renal failure?
CV (cardiovascular) risk -
Higher CV risk = higher CKD risk
Why is CV risk more important than the CKD risk calculated from CV risk?
In the elderly, more likely to die from increased CV risk (so CVDs e.g. stroke, MI etc.) rather than end stage renal failure
What are the standard factors that can affect CVD risk?
What are the additional CV risks in renal failure?
Hypertension
Diabetes
Lipid abnormalities
Inflammation
Oxidative stress
Mineral/bone metabolism disorder
What is the initial management for kidney failure?
Restore fluid balance -
Hypovolemic = give fluids
Hypervolemic = trial of dieuretics / dialysis
Treat hyperkalaemia =
Drive K+ into cells via sodium bicarbonate and insulin dextrose
Drive K+ out of the body using diuretics (if there is sustained fluid output)/ dialysis, laxatives would buy time if dialysis machines were busy (potassium pooped out instead of being absorbed)
Gut absorption - potassium binders
How do gut absorption potassium binders work?
Bind to potassium in the gut that comes from food etc.
Stops potassium from being absorbed into the body via the gut
What are the long-term management options for kidney failure?
Conservative
Home therapy
In centre therapy
Transplantation
What are the long term conservative management strategies for kidney failure?
Erythropoietin injections to correct anaemia
Diuretics to correct salt water overload
Phosphate binders
1.25 vit d supplements
Symptom management
What are the home and in centre therapies for long term management for kidney failure?
Home therapy = haemodialysis; peritoneal dialysis / assisted programmes
In centre therapy = haemodialysis, 4hrs 3x / week
What is the ultimate aim in renal failure?
Transplantation if fit enough
Why may dialysis not be appropriate?
The side effects are awful - nausea, fatigue
Must come in 3x a weak
Some patients will live just as long with conservative management as they would with dialysis
How does haemodialysis work?
Haemodialysis = blood removed from patient, filtered, put back into patient
Blood travels through tubes to dialysis machine
Blood is pumped in a counter current direction on one side of a semi-permeable membrane, whilst the other side contains a carefully balanced fluid
High osmotic drag pulls in fluid from the blood
Waste and extra fluid is drained out of the patient
What is a fistula? How is it created?
Created by connecting artery to vein - vein swells up and becomes ‘juicy’
Allows for easier insertion of needle
Useful for dialysis machine where blood is being taken out of the body to be filtered
Why should transfusions be avoided in patients that are eligibile for kidney transplants?
Blood transfusions = sensistisation against blood = transplant failure (body more likely to reject the donor)
As a renal patient, what should be avoided clinically?
Avoid taking blood or IV lines into the veins in the ante-cubital fossa
Due to need for fistula in the future
What are the traditional methods of assessing GFR (glomerular filtration rate)?
Urea = poor indicator, confounded by many factors e,g. diet, catabolic state, GI bleeding (bacterial breakdown of blood in the gut), drugs, liver function etc.
Creatinine = affected by muscle mass, age, race. Need to look at the patient when interpreting the result and use trends
Creatinine clearance = labourious and overestimates GFR at low GFR rates as it takes into account the secreted creatinine, Also difficult for elderly to collect an accurate sample
Insulin clearance = laborious and so only used for research purposes
Radionuclide studies = EDTA clearance etc. It is reliable but expensive, so only used for donated kidneys to check function prior to transplantation
So how is eGFR calculated clinically nowadays (for MDRD)?
Modification of diet in renal disease
Using serum creatinine conc.
GFR (mL/min/1.73m2) = 175 x (SCr)-1.154 x (Age)-0.203 x (0.742 if female) x (1.212 if Afr American)
How is eGFR calculated for CKD epidemiology collaboration?
CDP - EPI = epidemiolgy collab
GFR = 141 x min (SCr/K,1)-α x max (SCr/K,1)-1.209 x 0.993Age x 1.018 [if female] x 1.159 [if black]
How can patients with renal issues be classified?
Using eGFR AND proteinurea
Increased proteinuria = reaching end stage renal failure
