What happens when the kidneys stop working Flashcards
List what happens when the kidneys stop working
Loss of excretory function
Loss of homeostatic function (BP, volume, K+, Na+, Acid-base)
Loss of endocrine function (erythropoietin production and VitD hydroxylation)
Abnormality of glucose homeostasis (makes glucose and metabolises insulin)
Think of what the kidney normally does
What is a consequence of a loss of excretory function
Accumulation of waste products
What are the consequences of a loss of homeostatic function
Disturbance of electrolyte balance
Loss of acid-base control
Inability to control volume homeostasis
Describe the consequences of a loss of endocrine function
Loss of erythropoeitin production
Failure to 1 alfa hydroxylase vitamin D
Describe the consequences of an abnormality in glucose homeostasis
Decreased gluconeogenesis
What are the severity of clinical features determined by
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.
In chronic kidney failure- you may not notice the drop in GFR
What type of symptoms are common in chronic kidney disease
Flu-like symptoms
Describe reflux nephropathy
Cystogram- inject dye into balder through catheter
Valve connecting bladder to ureter should be shut- and the stain should not show up in the ureters or kidneys- it can carry infection and scar the kidneys- but as you grow- the bladder gets bigger- shutting the valve
What is the normal range of plasma creatine
normal range = 50 to 110 micromol/L
Summarise the clinical findings found in the patient
Symptoms of extreme lethargy, weakness and anorexia
Clinically volume depleted resulting in severe hypotension
Elevated plasma urea and creatinine make diagnosis of renal failure.
This is complicated by
hyperkalaemia
hyponatraemia
metabolic acidosis
anaemia
ULTRASOUND - 2 small shrunken kidneys
Which symptoms could explain the anorexia and lethargy
FAILURE OF EXCRETIONN Accumulation of nitrogenous waste products, hormones, peptides and other ‘middle-sized’ molecules (Mol Wt 2-5000) FAILURE OF HOMEOSTASIS Acidosis Hyponatraemia Volume depletion (low blood pressure) FAILURE OF ENDOCRINE FUNCTION Anaemia (decreased erythropoietin) Chronic neurological damage- due to accumulation of waste products
What can cause the salt and water imbalances
It is more usual for patients with renal dysfunction to have difficulty in excreting salt and water. This leads to a tendency to retain sodium
Hypertension
Oedema
Pulmonary oedema
Salt and water loss can be found in patients with tubulointerstitial disorders in which the concentrating mechanisms have been damaged
What are the salt and water imbalances in patients who cannot excrete sodium
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. (concentrating abilities of tubules lost- hyper-osmolar IF not created)
This inappropriately high loss of salt and water results in volume depletion which causes the low blood pressure
DO NOT CONFUSE SERUM SODIUM LEVELS WITH TOTAL BODY SODIUM – CKD AND AKI ARE OFTEN ASSOCIATED WITH HYPONATRAEMIA
Describe the implications of acidosis
Caused by decreased excretion of H+ ions and by retention of acid bases
Buffered by H+ ions passing into cells in exchange for K+ ions – therefore aggravates tendency to hyperkalaemia
Another compensation mechanism is increasing CO2 loss through the lungs - Kussmahl respiration (air hunger)
Exacerbates anorexia and increases muscle catabolism (central and local mechanisms)- for the protein buffer mechanism
Describe the implications of hyperkalaemia
Caused by failure of distal tubule to secrete potassium
Exacerbated by acidosis - causes shift of potassium from intracellular to extracellular space
Can cause cardiac arrhythmias (usually initial loss of p waves and also bradycardia) and arrest
Can effect neural and muscular activity
Clinical features of hyperkalaemia are dependent on the chronicity of the hyperkalaemia
Describe Kussmahl respiration
Breathing rapidly and deeply- air hunger- complication of acidosis- low pH has stimulated respiratory centre to get rid of CO2 to correct acidosis
Why does hyperkalaemia have cardiac consequences
heart rate is in part controlled by the membrane potential of the cells which in turn is determined by the relative levels of K+ ion across the membrane. Increased plasma K+ will lead to membrane depolarisation. This depolarisation can be sufficiently large for a portion of Na channels to inactivate and therefore not be able to contribute towards the AP upstroke. This impairs conduction and excitability hence in severe hyperkalaemia there can be some heart block. The depolarisation may also be sufficient to reduce SA nodal cell upstroke therefore firing rate which will also cause bradycardia.
Describe the ECG in hyperkalaemia
Tall- tented T waves (greater in amplitude than QRS complex)
Broad QRS complex (bradycardia)
No P- wave
These signs with hyperkalaemia is a medical emergency- QRS will eventually flatten out- asystole- arrest
Describe the effects of hypokalaemia on ECG
risk of VF (sigmoid T-waves)
Describe the metabolic consequences of kidney failure
Decreased erythropoietin production in renal failure results in anaemia
Low 1-25 Vit D levels result in poor intestinal calcium absorption, hypocalcaemia (short term) and hyperparathyroidism (longer term)
What are the consequences of low 1-25 vit D
§ Low 1, 25-Dihydroxycholecalciferol (1,25-Vitamin D3) à poor intestinal calcium absorption:
o Hypocalcaemia – Short term.
o Hyperparathyroidism – Long term
Lower 1,25-(OH)2VitD3 and increased PTH because phosphate retention and low levels of calcitriol lead to hyperparathyroidism ( by causing hypocalcaemia)
What is the consequence of hypocalcaemia
Increased cardiovascular risk
Describe the link between kidney failure and increased cardiovascular risk
Unsure of mechanisms
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.
Risk of MI increased (CKD greater predictor than smoking)
How can we determine between acute and chronic loss of kidney function
Can’t distinguish with blood tests
§ Essentially, it’s 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.
CKD will also have chronic uremic symptoms
HOWEVER- CKD kidneys may be normal sized in diabetes, myeloma, amyloid and poly cystic kidney disease
Describe the initial management plan for a patient with renal failure
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)
Describe urea as a method for assessing GFR
Poor indicator
Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs (steroids), liver function etc
Will increase in urine output decreases
Go up in G.I bleeding
up on steroids
down in liver failure
Describe creatinine as a method for GFR
Affected by muscle mass, age, race, sex etc. Need to look at the patient when interpreting the result
§ 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)
Describe creatinine clearance as a method for GFR
Difficult for elderly patients to collect an accurate sample
Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)
o Overestimates GFR at low GFRs as a small amount of creatinine IS secreted into the urine
Describe inulin clearance as a method for GFR
Laborious - used for research purposes only- GOLD STANDARD
Involves endogenous injection and catheterisation.
Describe radionuclide studies for GFR
EDTA clearance etc
Reliable but expensive
Describe eGFR
estimated GFR - uses equations to calculate GFR from serum creatinine and patient factors such as age, ethnicity and sex; unreliable when GFR > 60ml/min
What is eGFR
Equation which automatically calculates an estimated GFR from serum creatinine
Result presented ml/min per 1.732 (normalised for BSA)
Easiest equation uses age and ethnicity
A variety of equations are used (CKD Epi and MDRD)
Generally unreliable once GFR >60ml/min
Generally unreliable in very obese or very thin patients
Alternative equations can include weight, albumin etc
Recall the MDRD equation
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
Recall the CKD-EPI equation
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]
describe the NICE guideline classification
Categorises patients based on GFR and their ACR (urine albumin: urine creatinine ratio) category.
links to risk of complications ( i.e CVD)
Describe the long term management for kidney failure
Glomerular Filtration Rate (GFR) as measured by 52 Cr EDTA clearance was 4.5 ml/min
Remained on regular haemodialysis for 4 hrs 3 times a week
Low potassium diet and fluid restriction
Erythropoietin injections to correct anaemia
1.25 Vitamin D supplements to prevent hyperparathyroid bone disease
Describe renal replacement therapy
advanced CKD may necessitate haemo(dialysis) and/or transplant to replace the function of the kidneys
Describe dialysis
usually started at GFR = 10ml/min or when indicated e.g. uraemia, severe hyperkalaemia, and uncontrolled acid-base disturbances
Describe haemodialysis
pumping blood via artificial kidneys where blood surrounded by electrolyte fluid to control solute, waste and water concentration of blood returned to body; can be done several times a week or daily, and at hospital or at home; risks of hypotension, infection and inflammation
Describe peritoneal dialysis
dialysate fluid pumped into peritoneal cavity, with peritoneal capillaries acting as blood source; ultrafiltration controlled by altering osmolality of the dialysate; allows a more independent life; risk of back pain, infection, catheter problems and peritonitis
Describe transplantation
provides best long term outcomes, and may come from living/cadaveric donors; new kidney placed extraperitoneally in the iliac fossa; requires immunosuppression so contraindicated in AIDS, infection and cancer
Describe the dietary modifications in kidney failure
Avoidance of high salt food as sodium will not be removed
Low potassium foods
Consideration of phosphate intake (not usually a problem in early CKD)
Do not restrict protein
Fluid restriction in advanced CKD
VitD supplementation
Iron tablets if anaemic
