What happens when the kidneys stop working

Question 1

List what happens when the kidneys stop working

Answer 1

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

Question 2

What is a consequence of a loss of excretory function

Answer 2

Accumulation of waste products

Question 3

What are the consequences of a loss of homeostatic function

Answer 3

Disturbance of electrolyte balance
Loss of acid-base control
Inability to control volume homeostasis

Question 4

Describe the consequences of a loss of endocrine function

Answer 4

Loss of erythropoeitin production

Failure to 1 alfa hydroxylase vitamin D

Question 5

Describe the consequences of an abnormality in glucose homeostasis

Answer 5

Decreased gluconeogenesis

Question 6

What are the severity of clinical features determined by

Answer 6

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

Question 7

What type of symptoms are common in chronic kidney disease

Answer 7

Flu-like symptoms

Question 8

Describe reflux nephropathy

Answer 8

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

Question 9

What is the normal range of plasma creatine

Answer 9

normal range = 50 to 110 micromol/L

Question 10

Summarise the clinical findings found in the patient

Answer 10

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

Question 11

Which symptoms could explain the anorexia and lethargy

Answer 11

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

Question 12

What can cause the salt and water imbalances

Answer 12

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

Question 13

What are the salt and water imbalances in patients who cannot excrete sodium

Answer 13

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

Question 14

Describe the implications of acidosis

Answer 14

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

Question 15

Describe the implications of hyperkalaemia

Answer 15

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

Question 16

Describe Kussmahl respiration

Answer 16

Breathing rapidly and deeply- air hunger- complication of acidosis- low pH has stimulated respiratory centre to get rid of CO2 to correct acidosis

Question 17

Why does hyperkalaemia have cardiac consequences

Answer 17

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.

Question 18

Describe the ECG in hyperkalaemia

Answer 18

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

Question 19

Describe the effects of hypokalaemia on ECG

Answer 19

risk of VF (sigmoid T-waves)

Question 20

Describe the metabolic consequences of kidney failure

Answer 20

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)

Question 21

What are the consequences of low 1-25 vit D

Answer 21

§ 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)

Question 22

What is the consequence of hypocalcaemia

Answer 22

Increased cardiovascular risk

Question 23

Describe the link between kidney failure and increased cardiovascular risk

Answer 23

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)

Question 24

How can we determine between acute and chronic loss of kidney function

Answer 24

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

Question 25

Describe the initial management plan for a patient with renal failure

Answer 25

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)

Question 26

Describe urea as a method for assessing GFR

Answer 26

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

Question 27

Describe creatinine as a method for GFR

Answer 27

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)

Question 28

Describe creatinine clearance as a method for GFR

Answer 28

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

Question 29

Describe inulin clearance as a method for GFR

Answer 29

Laborious - used for research purposes only- GOLD STANDARD

Involves endogenous injection and catheterisation.

Question 30

Describe radionuclide studies for GFR

Answer 30

EDTA clearance etc

Reliable but expensive

Question 31

Describe eGFR

Answer 31

estimated GFR - uses equations to calculate GFR from serum creatinine and patient factors such as age, ethnicity and sex; unreliable when GFR > 60ml/min

Question 32

What is eGFR

Answer 32

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

Question 33

Recall the MDRD equation

Answer 33

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

Question 34

Recall the CKD-EPI equation

Answer 34

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]

Question 35

describe the NICE guideline classification

Answer 35

Categorises patients based on GFR and their ACR (urine albumin: urine creatinine ratio) category.
links to risk of complications ( i.e CVD)

Question 36

Describe the long term management for kidney failure

Answer 36

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

Question 37

Describe renal replacement therapy

Answer 37

advanced CKD may necessitate haemo(dialysis) and/or transplant to replace the function of the kidneys

Question 38

Describe dialysis

Answer 38

usually started at GFR = 10ml/min or when indicated e.g. uraemia, severe hyperkalaemia, and uncontrolled acid-base disturbances

Question 39

Describe haemodialysis

Answer 39

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

Question 40

Describe peritoneal dialysis

Answer 40

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

Question 41

Describe transplantation

Answer 41

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

Question 42

Describe the dietary modifications in kidney failure

Answer 42

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