Chronic Kidney Disease and Renal failure Flashcards
LO:
- 2-BRS-URO-1: Urogential homeostatic mechanism: summarise the mechanisms regulating ion/water balance and acid-base homeostasis under normal and pathological conditions.
- 1-BRS-URO-3: Genitourinary disorders: Summarise the pathology and pathophysiology of genitourinary disorders.
- 1-BRS-URO-4: Genitourinary disorders: Describe the clinical features and treatment options of genitourinary disorders.
Session Plan
Kidneys in health
GHEE
When kidney is working normally it has 4 main roles
- Homeostatic function-electrolyte balance, acid-base base, volume homeostasis
- Endocrine function
- Glucose metabolism
- Excretory function-what the kidney gets rid of
Kidney failure
Homeostatic function
Homeostatic function goes so the kidneys are no longer getting rid of potassium, so potassium will go up. The kidney is involved in acid-base balance, it produces bicarbonate, so if kidney is failing, it stops producing bicarbonate so bicarbonate levels drop and that means pH decreases, also because it is unable to get rid of hydrogen ions so hydrogen ions increase, so you become acidotic. Phosphate found in lots of our food especially dairy, bones of fish and chocolate etc so if eating phosphate and can’t get rid of this phosphate levels will go up, and then you get salt and water imbalance.
Kidney failure
Endocrine function
If endocrine function goes, you lose the ability to activate vitamin D, because 1-alpha hydroxylase is in the kidney. So you get a reduction in activated vitamin D and so your calcium levels go low (as vitamin D is needed for calcium absorption) and because your calcium levels are low, your body automatically tries to push them up, and so PTH goes up and it increases osteoclasts activity and gets it from bones.
If erythropoietin is not produced by kidney, then you get anaemia.
Kidney failure
Excretory function
If you lose excretory function, everything that comes out of the kidney can’t get out so it goes up, so your urea and creatinine goes up. Your insulin requirements go down because you kidneys get rid of insulin so because they are not getting rid of it, their endogenous insulin will go up, so may no longer need to be on diabetic drugs.
Kidney failure
Glucose metabolism
All of these when kidneys start to fail increase cardiovascular risk.
Kidney failure clinical presentation
Variable presentation, not all the same!
Rate of deterioration affects what the presentation is and also what you find when you start to do tests. And also the cause of the renal failure can affect presentation eg if someone presesnts with acute kidney injury because of sepsis, the main presentation will be due to sepsis, rather than the kidney failure.
Kidney failure Case 1
Read X-ray
This is her X-ray from when she was younger. With X-rays, always look for asymmetry, so have the line down the middle. There is white stuff on right which looks abnormal but not on left. There is a tube coming into bladder injecting contrast, and then this contrast is travelling up the right ureter and into the kidney, but it isn’t travelling up the left ureter. So the patients right kidney is the bad kidney, because it allows contrast to reflux back up ureter to kidney.
Reflux is one of the main causes of kidney disease, because if you don’t have a competent valve system between your ureter and bladder, then you get infections going up into the kidney, and you get pyelonephritis and scarring, usually happens as a child
What will be the patient’s blood volume status?
Why tachypneic (ie high RR) with normal oxygen sats and clear lungs on auscultation?
1) =hypovolemic
When see someone with kidney failure-assess their volume. She has a low blood pressure and can’t see their JVP (at 45 degrees you should be able to see jugular vein at clavicle, if we laid her done we might be able to see it?). Cold as trying to preserve blood supply to core and capillary refill is slow.
2) =Respiratory compensation and metabolic acidosis
When looking at blood gas, write down this equation. They are acidotic so increased H+ so pushes equation to left so trying to get rid of extra CO2 so hyperventilating to breathe off CO2 and as breathing more with normal lungs O2 levels will go up.
What will be the effect on the concentration of urea, creatinine, sodium, potassium, haemoglobin?
Excretion has gone, so kidney isn’t getting rid of things, so Urea, creatinine and potassium will go up. The sodium could be anywhere depending on case so can’t guess. Hb will be low.
What will be the effect on the pH,pCo2, pO2, bicarbonate and base excess?
pH down because she’s acidotic, base excess and bicarbonate will be down, pCO2 will go down, pO2 will be slightly up as they’re tachypnoeic with good oxygen sats.
Her CO2 goes down as she is trying to compensate by hyperventilating.
Kidney failure Case 1 – Summary of clinical findings
Urea and creatinine are up which gives diagnosis, just by looking at patient can’t guess, need blood tests for diagnosis.
First test is to look at kidney via ultrasound, to check you are not missing something that is treatable. She has 2 small shrunken kidneys, so this is chronic kidney disease, these kidneys are scarred and you’re not going to get these kidneys back.
Salt water balance has been disrupted, she’s hyponatraemic, she has low volume, acidosis, she’s anaemic etc.
This is a chronic kidney disease
Kidney failure Case 2
This is a more acute kidney failure.
RR-on higher side but normal.
Most results are normal. Skin turgor is how taught the skin is
What will be the patient’s blood volume status?-such a key question in kidney failure. Always start with this.
=euvolemic
What do you think her blood results will show?
Urea and creatinine and potassium are up, Hb down a bit but not too low, sodium-can’t tell, could be anywhere
As acute, toxin has just wiped out kidney so hasn’t had time for effect bone marrow to show so Hb normal
What does her blood gas show?
(get blood gas before blood test results)
pCO2-slightly low, pH down, bicarbonate down, pO2 is normal to high
Ultrasound scan of kidneys, ureters and bladder
Always exclude obstruction
Kidney failure – salt and water balance
Salt and water balance can be a cause of renal failure, so if you’re hypovolemic you’ll get acute kidney injury but it is also a symptom so when assessing fluid balance need to find which one it is and think what is it doing, is it due to kidney failure or is it causing it. This guides you on treatment.
Kidney failure tends to REDUCE secretion of salt and water leading to:
- Hypertension
- Oedema
- Pulmonary oedema
BUT Salt and water loss may be seen in tubulointerstitial disorders – damage to concentrating mechanism & also remember hypovolemia may be the cause of AKI.
Eg in early transplant patients, who can’t concentrate urine, or people who have had an acute kidney injury, when the kidneys start to recover, they often are very polyuric.
Kidney failure – salt and water balance
Kidney is controlling fluid and salt levels. So the fluid level goes up, you can have normal levels of salt or you can have higher levels of salt but you will be hyponatraemic. So it is the fluid balance you have to look at, especially in hypernatraemia, you’ve got to understand is this hypervolemia, euvolemic or hypovolemia hypernatraemia.
Kidney failure – acidosis
If H+ go up due to renal failure you get acidosis and so you have higher levels of protons and that goes into the cells and when hydrogen moves into the cells, potassium moves out. So the acidosis contributes to the hyperkalaemia. To treat hyperkalemia, we often give sodium bicarbonate, so when given sodium bicarbonate in the acute setting, it is not just to treat the acidosis, but it is more to treat the hyperkalaemia. If you treat the acidosis, the hydrogen ions go down so the potassium can go back into the cells.
This acidosis is what casues a lot of the symptoms eg anorexia and muscle catabolism.
Kidney failure – hyperkalaemia (medical emergency)
Causes and symptoms:
Lack of secretion of potassium, not a filtration problem
Symptoms based on chronicity: If not used to having high potassium you’ll get cardiac arrhythmias, and disrupted neural and muscular activity since potassium plays an important role in depolarisation, but can also be fairly non specific and may just be vomiting etc eg in dialysis patients who have this a lot of the time.
Kidney failure – hyperkalaemia
ECG changes:
- Peaked T waves-first sign
- P wave - broadens
- reduced amplitude -
- then it disappears
- QRS widening
- Heart block
- Asystole
- VT/VF (ventricular tachycardia and fibrillation-lifethreatening)
Kidney failure – metabolism
Anaemia as less stimulus on bone marrow by erythropoeitin. (Note: will only see decreased Hb in CKD as takes a while to effect bone marrow)
Vitamin D leads to calcium being absorbed by gut, so if reduce vitamin D you get reduced calcium absorption and hypocalcaemia. Body tries to correct this by increasing PTH which is trying to mobilise the calcium from the bones, so you get renal bone disease.
All these effect on metabolism cause increase cardiovascular risk.
Kidney failure – metabolism
The phosphate builds up in your body and binds to calcium. This causes your calcium levels to decrease, which may weaken your bones.
Calcium phosphate is in bones so if get high phosphate levels, that contributes to the hypocalcaemia and contributes to the hyperparathyroidism, which affect bones, so give patients phosphate binders eg calcium tablets which bind with phosphate so they poo out the phosphate rather than absorbing it and low phosphate diets.
Kidney failure – cardiovascular risk
Focus is cardiovascular risk for patients with CKD.
Kidney failure – Cardiovascular risk illustation
As go through stages of CKD, cardiovascular death risk goes up increasingly.
Kidney failure – standard Cardiovascular risk and additional risks
Standard cardiovascular risk (basic risks that could have even caused CKD)
- Hypertension
- Diabetes
- Lipid abnormalities
Additional risks
- Inflammation
- Oxidative stress
- Mineral/bone metabolism disorder-renal bone disease, you get calcification of the aortic valves and vessels, so in CT vessels light up from calcium deposition
Kidney failure – Initial management
First look at fluid balance! and also ask if they are peeing
If no urine output but hypervolemic don’t give diuretics as won’t be able to offload fluid so they need to go on dialysis.
Sodium bicarbonate drives potassium into the cells. Insulin dextrose also does this but risk of hypoglycaemia can happen so always follow hospital guidelines.
Other way is getting potassium out of body is giving diuretics eg furosemide. But if they are hypovolemic no use trying to drive urine output of someone who doesn’t have enough fluid so get their fluid levels up first or dialysis if they haven’t got urine output as giving sodium bicarbonate or insulin dextrose a few hours later it will just bounce back again, so got to get it out of body somehow.
Also stop gut absorption of potassium so can give them lactulose to give them diarrhoea, but now we use potassium binders so poo out potassium instead of absorbing it.
Kidney failure – Initial management Case 1
Hypovolemic and hyperkalemic
Kidney failure – Long-term management
-Very much driven by patient
In all fit patients transplantation is our aim, but in some elderly and frail, this isn’t appropriate so can give conservative and dialysis. In some patients they don’t live longer on dialysis that conservative and also dialysis is needed 3 times a week and is not tolerated well in elderly.
When phosphates go high it can cause itching so teach them about a low phosphate diet. Treat nausea and other symptoms. Give alfacalcidol to treat vitamin d deficiency
If patients want dialysis can choose home haemodialysis (blood out into machine and then back in) or in hospital-peritoneal dialysis (have tube through abdominal wall which sits in peritoneum, fluid poured into peritoneum and lining of peritoneum is semi-permeable membrane and fluid has glucose at concentration for their need, and this pulls fluid into the peritoneum and also can get drag and diffusion of urea, creatinine, potassium, and then patient drains out fluid and have machine that pumps fluid in and out of patient overnight.) Other option is haemodialysis where blood comes out of patient and into machine and then back into patient-haemodialysis is mostly done in hospital.
Kidney failure – Long-term management
Top left is next stage dialysis machine in his house. He has fistula in arm and he injects it into here himself
Top right-home peritoneal dialysis. Tube goes into peritoneum and she goes to bed and machine pumps fluid in and is drained over night. Machine warms fluid that goes in.
Bottom-needles going into fistula created by joining artery into vein and vein swells so can get needles into it easily. The blood is pumped out and have fluid going the opposite direction creating a countercurrent, and have a semipermeable membrane for diffusion.
If you see someone with kidney disease, this is where they are heading.
They need their veins, as some people on dialysis for 40+ years, so veins are their life line
Preferred treatment is transplant.
If give anaemic patient with CKD a transfusion, then you sensitise them. The donor for that blood has foreign antigens, so it makes antibodies. So then if they’re offered a kidney and that kidney donor has the same foreign antigens as that blood donor, the patient already has antibodies against that kidney. So by transfusing kidney patients uneccessarily, you can sensitise them, and then you reduce the success of transplantation later in their life
So renal anaemia is treated by erythropoeitin and IV iron, don’t give transfusion unless emergency.
TRADITIONAL METHODS OF ASSESSING GFR
Urea-not that great as very variable, in vegetarian it will be low, in meat eater it will be high
Creatinine-trend is useful overtime, but between patients it isn’t useful, specific to patient
Collect urine sample for 24 hours-laborious and time consuming, overestimates GFR as can’t account for the fact that creatinine is also secreted as well as filtered.
Inulin clearance is quite laborious, so don’t usually use in clinical practice
Radionucleotide use is in kidney donation, to make sure donor has good enough renal function to donate. Plasma clearance of 51Cr-EDTA can be used to estimate GFR with high accuracy, and it is one of the best available indices of renal function, even for patients with a GFR as low as 15 ml/min.
So what do we use? =EGFR
Estimated GFR <= serum [creatinine]
Note: not perfect as still uses creatinine as main factor
Equation takes account of age and sex but not race as Race won’t be written on form so have to do end calculation yourself.
CKD-EPI is prefered as High eGFR is more accurate. The problem with the MDRD is that you can have good renal function, but it might underestimate your function by quite a bit so people get referred when they don’t need to be referred. Different hospitals use different things.
NICE guidance classification
Classify patients not only due to eGFR but also albuminuria ie whether they are leaking protein. Risk is worse if leaking protein.
So if you’ve got reduced EGFR but no proteinuria, your risk is much less than if you have high levels of albuminuria/proteinuria
Kidney failure – the patient
Session review
