UROLOGY/CKD Flashcards
What is the most common composition of kidney stones?
Calcium oxalate
Investigation of renal calculi
- urine analysis
- renal function
- CT KUB and XR KUB should be performed on the same day
- approx ~50% of stones are radio-opaque
- US KUB can be used when avoidance of radiation is necessar (young patients, females) but CT is preferred imaging modality
-
Which renal stones can pass conservatively?
- majority of stones will pass within 6 weeks
- 60% of stones 5-7mm will pass spontaneously
- conservative mx: NSAIDs provide the most effective pain relief
- consider 400mcg dose tamsulosin
- dietary advice: low protein, low sodium may help reduce recurrence
Which subsets of patients need to be kidney stone free?-
Single kidney patients
Airline pilots
Definition of CKD
- GFR <60 which is present for > 3 momths with or without evidence of kidney damage
OR
- evidence of kidney damage with or without a decreased GFR present for > 3 months (evidenced by: albuminuria, haematurial, structural abnormalities, abnormal renal biopsy)
Risk factors: diabetes, HTN, established CVD, family history, obesity, smoker, > 60, ATSI, history of AKI
What are the 3 main points of screening for patients at risk of CKD?
- BP
- Urine ACR
- Blood test: creat/GFR
Algorithm for detection of CKD
- Screen at risk individuals, if urine ACR and eGFR are normal repeat in 1-2 years time (annually in pts with HTN or diabetes)
ABNORMAL GFR: if < 60 repeat in 7 days, if stable repeat GFR twice in 3 months
GFR > 20% REDUCTION: consider AKI, discuss with nephrologist
URINE ACR: if elevated repeat twice within next 3 months (preferably first morning void)
Describe the stages of renal function
Stage 1: GFR > 90
Stage 2: 60-90
Stage 3a: 45-60
Stage 3b: 30-45
Stage 4: 25-30
Stage 5: GFR <15 or on dialysis
Diet and nutrition goals in CKD
- varied diet richen in vegetables, fruits, multigrain cereals, lean meat, chicke, fish, eggs, buts, seeds and low fat dairy products
- limit salt to <6g/day
- limit intake of foods containing added sugars and saturated/trans fats
- avoid high calorie sweetened carbonated beverages
- dietary protein no lower then 0.75g/kg
- maintain albumin > 35
Obesity and CKD
Ideal BMI <25
WC <94cm in men and <80cm in women
Physical activity in CKD
Accumulate 150 to 300 minutes (2 ½ to 5 hours) of moderate intensity physical activity or 75 to 150 minutes (1 ¼ to 2 ½ hours) of vigorous intensity physical activity, or an equivalent combination of both moderate and vigorous activities, each week.
Do muscle strengthening activities on at least 2 days each week.
BP target in CKD
<130/80
Drug choice in management for cholesterol in patients >50 with CKD
Statin/ezetimibe combination
Immunisation in CKD
- influenza and pneumococcal disease is recommended for all with diabetes or ESKD
ACEI/ARBs and eGFR decline
- ACEI/ARBs cause reversible reduction in GFR
- provided reduction is <25% within 2 months of starting therapy you should continue ACEI/ARB therapy
- cease if reduction > 25%
What are the most common causes of ESRF in Australia?
DIABETES # 1
Glomerulonephritis # 2
Hypertension # 3
Polcystic kidneys # 4
Screening for CKD in ATSI population
- all patients >30 should have urine ACR, eGFR and BP done every 2 years
- or if 18-29 with one or more CKD risk factors
Once CKD is diagnosed through GFR/urine ACR what further diagnostic evaluation is required?
- renal USS
- repeat serum biochemistry
- FBC, CRP, ESR
- fasting glucose/lipids
- urine microscopy
What further investigation should be performed in patients with CKD and signs of systemic disease (rash, arthritis, features of connective tissue disease, pulmonary symptoms)?
Anti-glomerular basement membrane antibody
Anti-neutrophil cytoplasmic antibody
Anti-nuclear antibody
Extractable nuclear antigens
Complement studies
What further testing should be sought in patients > 40 with CKD and possible myeloma?
- serum and urine protein electrophoresis
YELLOW CLINICAL ACTION PLAN: CKD
GFR >60 + microalbuminuria or GFR 45-60 w/ normoalbuminuria
Goals: investigate cause, reduce progression, assess cardiovascular risk
Frequency of review: every 12 months
Clinical assessment: GP, weight, smoking
Labs: urine ACR, eGFR, biochemical profile, HbAqc, fasting lipids
ORANGE CLINICAL ACTION PLAN: CKD
- GFR 30-50 with microalbuminuria or GFR 35-40 norrmoalbuminuria
Goals: early detection and management of complications, adjustement of regular medications, referral when indicated
Frequency of review: every 3-6 months
Additional labs: FBC, calcium, phosphate, parathyroid homrone (6-12 monthly if GFR <45)
At what GFR should parathyroid hormone be checked and how frequently
GFR <45
- every 6 -12 months
RED CLINICAL ACTION PLAN: CKD
Goals: prepare for renal replacement if necessary
Frequency of review: 1-3 monthly
What are the 5 As?
Ask
Assess
Advise
Assist
Arrange
Which 2 groups of patients should have their CVD risk assessed?
Adults > 45
ATSI people > 35
CVD risk and CKD
- any patient with moderate to severe CKD is KNOWN to be at increased CVD risk
- > macroalbuminuria, eGFR <45
- > diabetes and age > 60
- > diabetes with microalbuminuria
- > familiar hypercholesterolaemia
- > SBP > 180, DBP >110
- > serum total cholesterol > 7.5
High risk = > 15% CVD risk
Diabetes targets in CKD
- BGL: 6-8 fasting or 8-10 post prandial
- HbA1c generally <7 (6.5-7.5)
Diabetic medications and CKD
Metformin: reduce dose GFR 30-60, contraindicated if GFR <30 (cease when unwell)
SGLT2 inhibitors: contraindicated in moderate renal impairment (GFR <45) (significant renal and CVD benefits in people with CKD and diabetes)
Gliptins (DPP4I): safe in CKD with dose adjustment
Sulphonyurea: dose reduction required GFR <30
GLP1 agonist: contraindicated GFR <30 (potential CVD benefits)
Which class of anti-hyperglycaemia may cause UTI?
SGLT2 inhibitors
- Increase urinary glucose excretion
HTN management in CKD
- ACEI/ARB (monitor GFR and K)
Consider adding
- CCB, diuretic or beta blocker
- refer to nephrologist if not consistently below target with atleast 3 anti-hypertensive agents
What rise in serum potassium is expected in CKD when ACEI are started?
>0.5mmol/L
Hence need to caution in patients with baseline potassium of >5.5
Diuretics in CKD
GFR >45 = non-loop diuretic (i.e. thiazides)
GFR <45 = loop diuretic (frusemide)
Frusemide can be safely used for management of fluid overload in all stages of CKD, including when GFR <30
-
Commonly prescribed drugs that adversely affect renal function in CKD
- aminoglycosides
- calcineurin inhibitors (cyclosporine, tacrolimus)
- gadolinium
- lithium
- NSAIDs, COX 2 inhibitors
- contrast
Prevention of AKI in CKD patients who are sick or dehydrated: medications to withhold
ACEI
ARB
NSAIDs
Diuretics
SGLT2 inhibitors
Increased risk of adverse effects due to reduce clearance: metformin, sulfonyluria, atenolol
SADMANS
Sulfonyluria, ACE, diuretics, metformin, ASRB, NSAIDs, SGLT2
Polycystic kidney disease
3 total cysts if < 40, 2 in each kidney if 50-60 or 4 in each kidney if > 60
- treatment: tolvaptan
Indications for referral to nephrologist in CKD
- GFR <30 (stage 4 and 5 of any cause)
- persistent albuminuria
- sustained GFR decrease of >25% within 12 months or sustained decrease of 15ml/min per year
- CKD with hypertension that is hard to control despite 3 anti-hypertensive agents
Not indicated if stable GFR > 30, urine ACR <30, controlled blood pressure
Signs and symptoms of acute nephritis
- oliguria
- haematuria
- acute HTN
- oedema
Acidosis in CKD
- GFR <30 = increased risk of metabolic acidosis
TreatmentL sodiBic: with aim to keep HCO3 > 22
Management of albuminuria in CKD
- degree of albuminuria relates to severity of disease
- target = 50% reduction in urine ACR
- management: ACEI/ARB, reduction of salt intake, spironolactone (with caution!)
Anaemia in CKD
- target Hb 100-115
- due to reduced EPOI, resistance to action of ESA, reduced iron absorption
- starts to develop when GFR <60
- aims of ESA therapy are ferritin 200-500 and TSAT 20-30%
- exclude other causes: b12/folate, IDA, GIT blood loss, TSH, hyperparathyroidism
Depression in CKD
- Common: 1/5 CKD and 1/3 on dialysis
- SSRIs safe in CKD
Microscopic haematuria in CKD
- r/o infection
- if there is associated reduction in GFR –> consider glomerulonephritis, urinary tract US, referral to nephrologist
- nil reduction of GFR –> consider urological malignancy, refer for cytolic and ultrasound + urological review
Management of hyperkalaemia
Target K < 6
- impaired urinary excretion of potassium
- may rise with ACEI/ARB
- K 6-6.5: low K diet, correct acidosis (HCO3 >22), thiazides, consider resonium, cease ACEI/ARB/spironolactone if K persistently > 6 and not responsigve
- K > 6.5 –> refer to ED due to risk of arrythmia
Target albumin in CKD
>35
CKD pruritis
- evening primrose oil
- skin emollients
- avoid soap and detergent
- topical capsaicin
- if pruritis and restless legs consider gabapentin
- can refer to dermatologist for UBV therapy
Management of restless legsin CKD
Check iron status and replace if deficient.
Home therapies such as massage, warm baths, warm/cool compresses, relaxation techniques, exercise.
Low dose dopaminergic agents or dopamine agonists.
Benzodiazepine
Stages of CKD and yellow/orange/red classification
CKD risk factors: who should be screened?
- smokers
- obesity, BMI > 30
- FHx
- Diabetes
- HTN
- ATSI > 30
- Established CVD
- History of AKI
Common presentations of glomerulonephritis
- nephritic syndrome:
- nephrotic syndrome
- GN and infection
- GN and drugs
- GN and purpuric skin rash
- GN and cancer
Causes of nephrotic syndrome
- minimal change disease
- membranous GN (HbsAg, CXR, mammogram)
- FSGS
- SLE (ANA, anti-ds SNA, C3, C4)
- Diabetes (FGL)
- Amyloid (urinary bence jones, serum and urine protein electrolphoresis)
Causes of nephritic syndrome
IgA nephropathy
Poststrep GN
SLE
Anti-GBM disease
ANCA vasculitis
Mesangiocapillary GN
Presentation of nephritic syndrome
- macroscopic haematuria (cola coloured urine)
- severe hypertension
- progressive oliguria and renal impairment
- unwell patient, often abrupt onset
Nephrotic syndrome triad
- oedema
- hypoalbuminaemia
- heavy proteinuria > 3.5g/day due to disruption of glomerula filtration barrier
What is the most common cause of GN?
IgA Nephropathy
Management of APSGN outbreaks
- occassionally outbreaks occur due to specific GAS strains
- management is to treat all children in community with any evidence of school sores with IM penicillin
Diagnostic criteria for PSGN
a) clinical
b) lab
CLINICALLY: at least of 2 of the following:
- facial oedema and/or peripheral oedema
- hypertension
- moderate haematuria on dipstick (2+ RBC)
LAB
- haematuria on microscopy
- evidence of recent strep infection: positive GAS culture or elevated ASO titre or anti-DNase B
- reduced C3 complement level
Management of PSGN
- IM benzathine penicillin regardless of whether skin sores or pharyngitis arte present at time of presentation
- admission!
Contact tracing with PSGN
- need names of family and household/close contacts of supsected case including adults and children who have been stating in the household 2 weeks prior to onset of symptoms
- need to examine skin for sores/scabies, BP to checked, urine to be checked and if sore present should be swabbed
- any child 12 months to 16 years are to be given LA bicillin whether skin sores a present or not
- if > 17 treat with Abx if infected skin sores present
- if scabies presenty treat with 5% permethrin or ivermectin if > 15kg for heavy or recurrent infections
Which class of CCB causes peripheral oedema?
Dihydropyridines (felodipine, amlodipine)
- causes peripheral oedema due to redistribution of extracellular fluid (rather than fluid retention)
- will not respond to diuretics
- may put patient at risk of volume depletion
When is urinary protein excretion highest?
In the afternoon!
Three initial investigations for men with LUTS
Urinalysis
Urinary tract ultrasound
Serum creatinine/estimated glomerular filtration rate
Common drugs whch may need to be reduced or ceased in CKD
- apixaban, dabigatran, rivaroxaban
- gabapentin, lithium, pregabalin
- opioids, benzos
- spironolactone, digoxin
- allopurinol, cochicine
- fenofibrate
- NSAIDs
Relative anatomy: haematospermia
- testes –> epididymis –> vas deference –> ejaculatory duct
- fluid from sminal vesciles, prostate and Cowper’s glands the mixes with the sperm to form ejaculate
Causes of haematospermia
- Infection: bacterial (STI, entococcus, TB), viral (HIV, CMV, HSV)
- Iatrogenic: post TRUS, radiation, post vasectomy
- Malignancy: prostate, bladder, testicular, urethral
- Trauma: coital trauma, pernieal trauma
- Prolonged abstinence
- Obstruction: duct obstruction, cysts or calculi
- Systemic disorders: HTN, CLD, lymphoma, leukaemia, amyloidosis, bleeding disorders
Red flags: haematospermia
Age > 40
Recurrent or persistent
Prostate cancer risk factors: family hx of African heritage
Constitutional symptoms (weight loss, anorexia, bone pain)
Approach to haematospermia
- screen for red flags (malignancy)
- common aetiologies: UTI/prostatitis/STI
- examination: BP, temperature, genital examination, DRE
- systems review: feature of CLD, lymphoma or leukaemia
- investigation: urine MCS, urine cytology, FBC, coags
- if STI suspected –> NAAT for chlamydia and gonorrhoea
- PSA in men > 40 or if abnormal DRE
Indications for urology referral: haematospermia
- Men > 40
- persistent or recurrent
- suspicious DRE fidning
- abnormal PSA
- suspicion of malignancy
- concurrent haematuria
