10 Flashcards
(36 cards)
1
Q
What is Acute Kidney injury?
A
- decline in the GFR that occurs during a short period of time
- decline in GFR is currently measured by an increase in serum creatinine ALTHOUGH creatinine is not an ideal marker
- an acute change in renal function in comparison to CKD
2
Q
What is the NICE guideline for detecting acute kidney injury?
A
- rise in serum creatinine of 26 or greater within 48 hours
- a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
- 25% or greater fall in eGFR in children and young people within the past 7 days
3
Q
What is anuria?
A
-usually indicates a blockage of urine flow or very severe damage to the kidneys, and is a less common form of AKI
4
Q
What is oliguria?
A
- diagnosed by examining the obligatory amount of cellular waste products that need to be excreted from an average sized individual
- approximates to 600mOsmol/day
5
Q
What is uraemia?
A
- defined as the clinical signs and symptoms of kidney failure
- results in a lack of secretory as well as excretory function in the kidneys
6
Q
How do you measure renal function?
A
- creatinine endogenous product in muscle cells at a constant rate
- creatinine excretion rate of excretion is relatively fixed
- MDRD formula used to give eGFR
- rise in creatinine rate means kidney function has dropped
- normal creatinine: 100-120 mmol/L
- eGFR >90ml/min
See session 10 AKI slide 12-15
7
Q
What is CKD?
A
- chronic kidney disease is a progressive loss of function over a period of months or years
- functioning renal tissue is replaced by ECM and gives rise to glomerulosclerosis and tubular interstitial fibrosis
- progressive loss of both excretory and hormone functions of kidney
- development of proteinuria and systemic hypertension
- symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing reduced appetite
See session 10 CKD slide 9-10
8
Q
List the stages of CKD
A
- CKD 1: eGFR > 90, with proteinuria/haematuria
- CKD 2: eGFR > 60, with proteinuria/haematuria
- CKD 3: eGFR 30-60 (P)
- CKD 4: eGFR 30-15
- CKD 5: eGFR <15
- end stage renal failure ESRF
See session 10 CKD slide 11
9
Q
What are the causes of CKD?
A
- diabetes nephropathy
- hypertension
- glomerulonephritis
- UTI
- polycystic kidney disease
- renal vascular disease
10
Q
What is the staging of AKI?
A
-stage 1: creatinine is 1.5-1.9 times the baseline
-stage 2: creatinine is 2.0-2.9 times the baseline
Stage 3: creatinine is 3.0 times the baseline
See session 10 AKI slide 19-24
11
Q
How does pre-renal disease cause AKI?
A
- most common cause of AKI
- defined as decreased renal perfusion
- if BP falls beneath a threshold level, the kidney is unable to maintain blood flow and the GFR declines
- kidneys themselves are not yet impaired, just unable to maintain blood flow and hence GFR
- pre-renal failure is reversible
- commonest cause: Acute Tubular Injury
- if not treated kidney cells are eventually starved of oxygen
- PCT are at most risk since they are less well perfused
- if pre-renal AKI is sustained for long enough intrinsic ATI can occur
12
Q
What are some causes of hypo-perfusion in regards to AKI?
A
- septic shock
- hypovolaemic shock
- cardiogenic shock
- medications
- AKI marker picks up pt’s with CVS disease
- AKI is not a marker of kidney disease
- cannot maintain perfusion to kidneys due to these types of shocks
See session 10 AKI slide 26-28
13
Q
What renal problems can cause AKI?
A
- drugs: antibiotics, NSAIDS, ACE inhibitors (best solution for kidney disease but may cause hypotension)
- sepsis
- rhabdomyolysis
- myeloma
- tubulointestitial diseases
- glomerulonephritis
See session 10 AKI slide 32-34
14
Q
How does post-renal disease cause AKI?
A
- indicates obstruction to urine flow after urine has left the tubules
- bladder outlet obstruction
- bilateral pelvic retreat obstruction
15
Q
How would you treat and manage AKI?
A
- dictated by the cause of the AKI
- pre-renal: restoration of renal perfusion by restoring volume or treating pump failure
- post-renal: if urinary tract obstruction then urological intervention is necessary to re-establish urine flow
- manage fluid balance
- recovery can take many weeks and treatment is supportive
- maintain good kidney perfusion, avoid nephrotoxic restricting various solutes and providing nutritional support
- dialysis is initiated if the kidneys can no longer excrete salt, water, potassium or other waste products or if acid-base balance is no longer maintained
- URINE DIPSTICK TEST IS VITAL
- prevention is better than cure
See session 10 AKI slide 35-43
16
Q
What is adult polycystic kidney disease (ACKD)?
A
- autosomal dominant
- mutation in either PKD 1 gene or PKD 2 gene
- cysts grow with age, generally presents in adulthood
- diagnosed with ultrasound (can’t exclude if < 30 years old)
- genetic testing (not widespread)
- prognosis depends on rate of increase in kidney size and age
See session 10 CKD slide 3-4
17
Q
What is the clinical disease in APCKD?
A
- cysts fluid filled an can cause secondary complications: pain, bleeding into cyst, infection, renal stones (stasis)
- hypertension very common (before renal function changes)
- rate of decline in function variable even between families
- increased incidence of intra-cranial aneurysms
- increased incidence of heart valve abnormalities
See session 10 CKD slide 5
18
Q
How can we manage APCKD?
A
- treat hypertension block RAAS
- diet: drink plenty of fluid (will slow progression of disease), low salt, normal but not excessive protein
- tolvaptan: is a vasopressin 2 receptor antagonist which stop you from reabsorbing water so you pee a lot
- others such as somatostatin analogues
See session 10 CKD slide 6
19
Q
What is the incidence of CKD?
A
-CKD is often asymptomatic so hard to measure
See session 10 CKD slide 12-15
20
Q
What is the aetiology of CKD?
A
- CKD is often associated with old age, diabetes, hypertension, obesity and CVD
- common causes:
- diabetes
- arteriopathic renal disease
- hypertension
- immunologic (ex. Glomerulonephritis)
- other systemic diseases (ex. Lupus)
- infection (ex. Pyelonephritis)
- obstructive and reflux nephropathies
- genetic family history of stage 5 CKD or hereditary kidney disease
See session 10 CKD slide 16-17
21
Q
What are the risk factors of CKD?
A
- any form of AKI
- proteinuria
- hyperlipidaemia
See session 10 CKD slide 26-27
22
Q
How do we investigate CKD?
A
- define degree of renal impairment
- define cause of renal impairment
- provide patient with diagnosis and prognosis
- identify complications of CKD
- plan long term treatment
- must ALWAYS MEASURE BP AND URINE DIPSTICK
- not helpful to just look at creatinine
- look at eGFR and blood tests
- USS, kidney biopsy, CT scan, MRI scan, MR angiogram
See session 10 CKD slide 18-20, 24
23
Q
What restrictions are there with using eGFR as investigation method for CKD?
A
- only accurate in adults, doesnt work in kids or pregnant women
- correction needed for black patients (not Asians)
- it defines chronic kidney disease and isn’t useful in acute kidney injury
- because it takes time for creatinine to change, so takes time for eGFR to change
See session 10 CKD slide 21
24
Q
What would you check for in a blood test investigating CKD?
A
- urea and electrolytes
- bone biochemistry
- LFT
- FBC
- CRP
- iron levels
- PTH
- check for auto-immune disease
See session 10 CKD slide 22-23
25
How is regulation of water and salt affected in CKD?
- 80-85% of CKD patients are hypertensive
- treatment: anti-hypertensives, diuretics, fluid restriction
- amount of urine produced depends on GFR
- CKD causes reduced GFR
- lose ability to maximally dilute and concentrate urine
- small GFR but same solute load causes osmostic diuresis
- nocturia common because they are insensitive to ADH secretion in order to get rid of the solute load
- low volume of filtrate reduces maximum ability to excrete urine therefore max urine volume much smaller
See session 10 CKD slide 28-30
26
How does hyperkalaemia occur in CKD?
- occurs once eGFR <20ml/min
- less likely when good urine output maintained
- may require: stopping ACE inhibitor, avoidance of other drugs that can increase K+, altering diet to avoid foods with high potassium
- can potentially lead to acidosis which would be treated with oral NaHCO3 tablets
See session 10 CKD slide 31-32
27
What are some causes of anaemia in CKD and how can we treat it?
Causes
- high hepcidin level: stops you from absorbing iron
- absolute iron deficiency
- blood loss
- decreased EPO production
Treatment
- important to treat because need to improve Hb and ultimately reduce mortality
- just giving EPO without any iron is ineffective
- so much replace iron first
- when iron supplies ok, re-check Hb and if Hb is still low then give EPO
See session 10 CKD slide 33-35
28
HOw does CKD cause mineral bone disease and how can it be treated?
- decrease in Klotho-FGF 23
- decreased vitamin D which leads to bone resorption
- increased osteoclastic activities
- stimulating Parathyroid glands leading to hyperplasia
- non bone calcification occurs in wrong places such as joints, vessels, skin
- can cause significant morbidity
- management: reduce phosphate intake, phosphate binders (to prevent malnutrition), 1-a-calcidol, vitamin D
See session 10 CKD slide 36-38
29
What are the main symptoms of CKD?
- tiredness
- breathlessness
- restless legs
- sleep reversal
- aches and pains
- nausea and vomiting
- itching
- chest pain
- seizure
30
What is end stage renal disease?
- CKD can progress to this
- reduced life expectancy
- reduced QoL
- transplant is best hope for survival
- when death is likely without renal replacement therapy
- eGFR <15ml/min
31
What is renal replacement therapy?
- required when native renal function declines to a level no longer adequate to support health
- usually when eGFR 8-10ml/min
See session 10 CKD slide 41-42
32
What symptoms occur with ESRD/dialysis?
- tiredness: overwhelming fatigue, physically and mentally incapacitated, feelings of guilt at needing rest
- difficulty sleeping
- difficulty concentrating
- CKD stage 5
- symptoms and signs of volume overload (oedema)
- nausea and vomiting/reduced appetite
- restless legs/cramps
- pruritis
- sexual dysfunction/reduced fertility
- increased infections
See session 10 CKD slide 43-44
33
What options do you have when kidneys fail?
- haemodialysis
- peritoneal dialysis
- conservative care (for older patients)
- transplants
34
What are the advantages/disadvantages of haemodialysis?
Advantages
- do not need to be responsible for own treatment
- can remain on haemodialysis for years
- 4 days free from treatment
Disadvantages
- fluid and diet restriction
- limited ability to travel
- CVS instability
- high capital cost
- hospital based
-nocturnal /home HD are better option as you need fewer meds, allows more dialysis hours, patients feel better
See session 10 CKD slide 46-50
35
What are the advantages and disadvantages of peritoneal dialysis?
Advantages
- low technology
- home technique
- easily learn
- allows mobility
- CVS stability better for elderly and diabetic
- little dietary restriction
Disadvantage
- frequent exchange
- unable to do long-term
- frequent treatment failure
- peritonitis
- limited dialysis dose rang
- high revenue cost
- body image problem
See session 10 CKD slide 51
36
What are the advantages/disadvantages of a kidney transplant?
Advantages
- freedom from dialysis
- restoration of near normal renal function
- improved quality and quantity of life
- cheap
Disadvantages
- requires immunosuppressive drugs
- operative mortality
- limited supply of organs
- not suitable for all
- still left with CKD
- new kidneys don’t last forever
-most transplants attach to iliac vessel so sit in pelvis
See session 10 CKD slide 52-57
