CKD Flashcards
What test is used to differentiate between IBS and IBD?
Faecal calprotectin - a marker for bowel inflammation
Criteria to diagnose AKI
- creatinine raise of 26 micromol/L or more within 48hours
- 50% of raise in creatinine occurred/presumed within 7 days
- decreased urine output to <0.5 ml/kg/hr
- in children: decrease of 25% in eGFR within 7 days
What’s ACR?
What is it used for?
ACR = albumin: creatinine ratio
used to classify CKD
What are the two biggest caused of CKD?
- hypertension
- diabetes
Diagnosis of CKD
- what and for how long
Reduction of eGFR measured 3 months apart
What’s ‘end stage’ CKD
eGFR <15 -> requiring dialysis, kidney transplant
Nephrotoxic drugs
(intrarenal cause of CKD)
- Lithium
- NSAIDs
- steroids
- methotrexate
- rifampicin
- Penicillin
- gentamycin
Two types of drugs that we need to check renal function after administration
- ACE inhibitors (influences glomerular hydrodynamics)
- anticholinergics (e.g. TCAs) -> as they may cause urinary retention
What is an alternative for NSAIDs in kidney disease
- Paracetamol
- co-codamol
Decreased eGFR - what do we need to consider (in terms of other drugs)?
drug review -> as some drugs’ doses need to be reduced
What effects do ACE inhibitors have on the kidney?
A. Renoprotective (especially if hypertension)
B. Potential for kidney failure if a person has bilateral renal stenosis - so need to monitor kidney function after introduction
What to do when we introduce ACE inhibitors?
- Do baseline eGFR and U&Es levels
- repeat in 7-10 days *
*if decreased renal function - potential underlying bi-lateral renal stenosis
What BP do we aim for in a diabetic person?
130/80 or less
* this is due to an already occurring disease that may contribute to CVS/renal and other organ damage
What vaccines should be offered and at what age for people with CKD?
Irrespective of age:
- flu jab -> once a year
- pneumococcal vaccine -> every 5 years
Do we need to refer a person with T2DM to an endocrinologist?
No - we can manage it at primary care
*unless difficult to manage
When do we refer a person with CKD to a nephrologist?
- progressive deterioration
- the decrease in eGFR 25% or more in 12 months
- sudden drop in short space of time
- eGFR <30
In what instances would we consider stopping ACE inhibitors (after their introduction)?
- drop in eGFR >25% from pre-Rx/baseline levels
- rise in creatinine >30%
- K+ levels > 6.0
*if parameters had decreased (but not enough to stop ACEinhibitors) -> repeat tests (U&Es and eGFR) in 2 weeks + compare with baseline
What medication we can use to replace ACE inhibitors with (in case they will cause renal #)?
- alpha blocker
or
- CCB
or
- beta blocker
Can we replace ACE inhibitor (in case of renal #) with Losartan?
No, as Losartan has the same mechanism as ACE inhibitors
When to refer to the nephrology team? (in CKD)
- Poorly controlled BP ( and patient on 4 drugs)
- CKD 4-5
- progressive decline >25% within 12 months
- persistant proteinuria
- bi-lateral renal stenosis
Introduction of what drug do we need to consider in pt with CKD in terms of the risks?
CVS risks -> give statins
What are the components of tests for CKD?
- creatinine
- eGFR
- albumin - creatinine ratio (ACR)
what is the principle behind albumin: creatinine ratio?
Normally, albumin is filtered back into the bloodstream (by the kidneys)
- if kidney are #, then more albumin will be present in the urine -> this is microalbuminuria test
- ACR -> comparing the creatinine to albumin in a sample -> allows to compensate for variations of urine concentration in ‘spot’ samples*
* i.e. we can say that there is microalbuminuria only when ACR is within certain ranges
When a female and a male patient is said to have microalbuminuria?
microalbuminuria is defined as
Female: ACR ≥3.5 mg/mmol
Male: ≥2.5 mg/mmol
Who should be offered tests for CKD?
- diabetes
- hypertension
- CVS disease (cerebrovascular disease, MI, peripheral vascular disease, ischaemic heart disease, chronic heart failure)
- structural renal tract disease: recurrent renal calculi or prostatic hypertrophy
- people with systemic diseases that may affect kidney (e.g. SLE)
- AKI
- opportunistic detection of haematuria
- people with relatives of end-stage CKD, genetic predisposition
What risks factors should not be taken into consideration if we consider testing for CKD?
- obesity alone (unless metabolic syndrome, diabetes or hypertension)
- gender, ethnicity, age
Monitoring eGFR in people on certain nephrotoxic drugs
- how often
- what drugs
- at least annually
- NSAIDs, Lithium, calcineurin inhibitors (cyclosporin or tacrolimus)*
- *calcineurin inhibitors* -> immunomodulating agents (to reduce inflammation) e.g. organ transplant, skin disorders, UC
How do we usually test for haematuria
Urine dipstick -> if 1+ or more positive -> evaluate further (e.g. microscopic urine analysis)
What results will differentiate persistent vs transient haematuria in the absence of proteinuria?
2 out of 3 positive strip tests would confirm persistent invisible haematuria
What diagnosis should we consider in persistent invisible haematuria (with or without proteinuria)?
urinary tract malignancy (in appropriate age group)
How should be a patient with persistent invisible haematuria (in absence of proteinuria) followed up?
Annual repeat testing:
- haematuria
- proteinuria
- albuminuria
- eGFR
- BP
*for as long as haematuria persist
What’ s the aim for (systolic and diastolic) BP in people with CKD?
Systolic: 140 mmHg
Diastolic: 90 mmHg
What’ s the aim for (systolic and diastolic) BP in people with CKD and diabetes?
systolic below 130 mmHg
diastolic below 80 mmHg
Low - cost renin-angiotensin (RAAS) system antagonist should be offered to people with CKD and…
- diabetes and ACR of 3mg/mmol or more
- hypertension and ACR of 30 mg/mmol or more
- ACR of 70 mg/mmol or more (irrespective of CVS disease or hypertension)
A. How to manage the risks of CVS in people with CKD?
B. when to increase the dose?
A. Offer _*Atorvastatin* 20mg_ -> primary and secondary prevention of CVS in CKD
B. Increase the dose if:
- >40% reduction in non-HDL has not been achieved
- eGFR is 30 ml/min/1.74m2 or more
*if eGFR is less than 30 ml/min/1.74m2 -> consult the use of higher dose with a renal specialist
CKD stages - table

Complications of CKD (other than CVS) + when an how to check for them
- anaemia - check haemoglobin level in people with GFR less than 45 ml/min/1.73m2
- bone conditions - if eGFR of 30ml/min/1.73m2 or more - do not routinely measure calcium, phosphate, PTH and vit D levels -> otherwise patients at lower categories should be under the care of a nephrologist and may need calcium/ vitamin D supplements, low phosphate diet and sodium bicarbonate (to prevent metabolic acidosis)
What may suggest that a person with CKD may be at higher risk of progression into end-stage kidney disease/ accelerated progression of CKD?
- 25% or more decrease in GFR category within 12 months
or
- decrease in eGFR of 15ml / min/ 1.73 m2 per year
How to identify the rate of CKD progression?
Obtain a minimum of 3 eGFR readings in a period of no more than 90 days
What further testing to do if there is a new finding of reduced eGFR in a person with established CKD?
repeat eGFR within 2 weeks -> to exclude causes of acute deterioration of GFR
For how long do we monitor a person after AKI?
2-3 years after AKI
*even if serum creatinine has returned to baseline-> this is because patients with AKI are at increased risk of developing CKD
Why NSAIDs may increase risk of kidney #?
NSAIDs will inhibit prostaglandins -> afferent arteriole constriction -> kidney underperfusion
Can we combine ACE inhibitors and NSAIDs?
Not - as both of them would cause acute AKI
(ACE inhibitors -> renal artery stenosis; NSAIDs -> afferent arteriole constriction)
Which drugs and why may cause kidney # in case of biochemical;/ electrolyte changes?
- Increased Potassium-> K+ supplements, K+ diuretics, Ispaghula husk
- High sodium content -> antiacids
- Excessive vitamin D replacement -> alphacalcidol
What drugs may cause crystalluria (crystals found in the urine) and therefore obstruction?
- sulphonamides
- acetazolamide
- methotrexate
What drugs have the potential to cause glomerular damage?
- penicillamine
- gold
- aptopril
- phenytoin
- penicillins
- sulphonamides
- rifampicin
What drugs have the potential to cause interstitial nephritis?
- penicillins
- cephalosporins
- sulphonamides
- thiazide diuretics
- furosemide
- NSAIDs
- rifampicin
What drugs have the potential to cause Acute Tubular Necrosis?
Drugs that cause direct toxicity to the renal tubules:
- aminoglycosides
- amphotericin*
- ciclosporin
*amphotericin - anti-fungal med
What drugs may cause analgesic nephropathy?
paracetamol and/or aspirin combinations
It is reversible
What drug can cause nephrogenic diabetes insipidus?
Lithium
In general (classes), what drugs to be careful about in CKD?
- antibiotics
- H2 receptor antagonists
- Digoxin
- anti-convulsants
- NSAIDs
General principles in prescribing in renal impairment
- avoid nephrotoxic drugs (when possible)
- dose adjustment for CKD - depending on the stage
* dialysis can remove some drugs
* dose adjustment done either by:
a) size of an individual dose is reduced
b) increased interval between doses
RAAS - pathway (physiology)

Vitamin D pathway (physiology)

EPO production in the kidney (negative feedback mechanism- physiology)

What does ACR detect?
Proteinuria
*it is more sensitive than urinalysis
Normal eGFR and increased ACR - is patient at risk of CVS?
Yes

True or false
1. CKD can be diagnosed on 2 eGFR results taken one month apart
2. Abnormal levels of proteinuria for ≥3 months, with or without a decrease in GFR, is diagnostic of chronic kidney disease
- False -> at least 3 months apart needed for Dx of CKD
- True (look at categories in terms of ACR as well)
True or false
1. Urine dipstick testing can be reliably used to detect microalbuminuria
2. After Acute Kidney Injury (AKI) people are at 4-fold greater risk of developing CKD, even if their renal function completely normalizes.
1. False -> various urine dipstick may be more or less sensitive (most may not detect microalbuminuria)
2. True - should monitor kidney function for 2-3 years
True or false
If a CKD patient’s K rises from 4.5 to 5.5 after starting Ramipril you should always stop the drug.
False - Stop ACE if rises to ≥6 (Don’t start ACE if initial K is>5)
True or false
If a CKD patient’s eGFR drops from 60 to 44 after starting Ramipril you should always stop the drug.
True – Stop if eGFR falls by more than 25% of pre-treatment level
In that case, there is a fall of 16=26% of 60
True or false
A patient with normal eGFR and severe proteinuria may be at higher risk of progression than a patient with reduced eGFR but no proteinuria
True – Significant proteinuria is a high risk for progression
True or false
All patients with CKD4 should be referred to Nephrology
True - patients with CKD4 should be referred (according to NICE guidelines)
What to do if a patient is <40 years old, has URTIs symptoms and cola-coloured urine?
Refer to nephrologist (likely to have acute glomerulonephritis)
- some patients <40 yrs with cola-coloured urine and an inter-current (usually upper respiratory tract) infection will have an acute glomerulonephritis
Urological referral for further investigations should be considered in
Urological referral for further investigations:
- all patients with macroscopic haematuria (any age)
- all patients with symptomatic non-visible haematuria
- all patients with asymptomatic non-visible haematuria at age of 40 or >40
When is a nephrological referral needed?
Nephrological referral for the patients:
- who have had a urological cause excluded
- have not met the referral criteria for a urological assessment
*need for a nephrology referral in this situation depends on factors other than simply the presence of haematuria
- nephrology referral is recommended if there is concurrent factor (mentioned on another flashcard)
A concurrent factors (apart from haematuria) that will prompt nephrology referral
- proteinuria (ACR ≥30mg/mmol)
- isolated haematuria (in the absence of significant proteinuria) + hypertension (in those aged <40)
- visible haematuria that happens with an infection (e.g. URTI)
2 weeks bladder cancer pathway referral criteria
An appointment within 2 weeks for bladder cancer:
- aged 45 and over and have:
- unexplained visible haematuria without urinary tract infection or
- visible haematuria that persists or recurs after successful treatment of urinary tract infection, or
- aged 60 and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test