Renal failure Flashcards
5 kidney functions
- Fluid/electrolyte balance
- Waste product excretion
- Acid/base balance
- EPO synthesis
- Vitamin D activation (calcitriol)
CKD: presentation
a) Usually diagnosed how?
b) Who should be screened?
c) Possible symptoms
d) Possible signs
a) Incidental U+E (eGFR), urine dip (proteinuria) or ACR
b) Anyone with history of:
- AKI, structural renal disease, recurrent stones, or BPH
- Diabetes, HTN, CVD, multisystem disease (eg, SLE)
- FHx of ESRF or familial renal disease
c) Usually only with severe CKD:
- Uraemic symptoms: anorexia, nausea, vomiting, muscle cramps, pruritus, headache, confusion
- Anaemic symptoms: lethargy, dyspnoea, pallor
- Overload: peripheral and pulmonary oedema
d) - Uraemia: excoriation,
- Anaemia: pallor
- Overload: oedema, effusions
CKD: investigations
a) Diagnostic tests
b) Bloods - tests plus possible findings
c) Other (eg. antibodies, imaging, special tests)
a) eGFR (blood) and ACR (urine)
b) - FBC: anaemia of chronic disease
- Glucose (DM) and cholesterol (dyslipidaemia)
- Electrolytes: Na+ (low), K+ (raised), bicarbonate (low)
- Bone profile: Ca2+ (low), Pi (high), Alk Phos (high), PTH (high), albumin (low)
c) - Antibodies: ANA, ANCA, anti-GBM, complement, Hep B/HIV serology
- Imaging: USS kidneys, CT KUB (stones)
- Special tests: myeloma screen, urine microscopy, renal biopsy
Chronic kidney disease (CKD).
a) Define
b) Staging
c) Define ‘renal failure’
d) Causes of CKD (3 big ones)
a) Albuminuria or eGFR < 60 for 3 months or more
b) Stages of CKD.
1: eGFR > 90 (with albuminuria)
2: 60 - 89 (with albuminuria)
3a: 45 - 59
3b: 30 - 44
4: 15 - 29
5: < 15 (ESRF)
(usually require dialysis at eGFR ~ 7)
c) Failure is one or more of:
- eGFR < 15
- Need for dialysis or transplantation
d) - Big ones: diabetes, HTN, old age
- Others: renovascular disease, GN, pyelonephritis, chronic NSAID use, myeloma, vasculitis, obstructive nephropathy, familial (eg. PKD)
Anaemia in CKD.
a) Causes
b) Management
a) - Iron deficiency (due to increased hepcidin levels, which inhibits iron absorption from the gut)
- Reduced EPO
b) IV iron (bypasses GI route), +/- EPO
CKD management.
a) Non-drug
b) Drugs
c) Monitoring
a) - Patient education
- Encourage exercise, weight loss, reduced alcohol and smoking cessation
- Dietary (if indicated): fluid and salt restrict, potassium and phosphate restrict, protein increase
- Control risk factors: DM, HTN, cholesterol, etc.
- Avoid nephrotoxic medication if possible (eg. NSAIDs, aminoglycosides, radiocontrast)
b) - Statin in all CKD for primary/secondary prevention
- ACE if: hypertensive, diabetic or proteinuric
- Immunisations - pneumococcal, annual influenza
- Bone protection: vitamin D, Ca2+, (+/- bisphosphonates)
- Phosphate binders
c) - Monitor eGFR, U+Es and proteinuria
- Monitor BP, glucose and other risk factors
Renal replacement therapy (RRT).
a) Types
b) eGFR threshold
a) Haemodialysis - 3x per week for 4h
Peritoneal dialysis
b) eGFR ~ 7
PD peritonitis.
a) Clinical fx
a) Cloudly PD effluent, pyrexia, abdominal pain
Peritoneal dialysis.
a) Advantages
b) Contraindications
c) Problems
a) Independence, fewer restrictions on diet and fluid intake
b) Need residual kidney function (20% in one kidney), stomas
c) Problems - PD peritonitis (aseptic technique vital), only lasts a few years due to peritoneal scarring (then need HD/transplant), weight gain
AV fistula.
a) Signs o/e
b) What is a fistula? What is an AV fistula?
c) Alternative to fistulae
a) Thrill (palpable) and bruit (auscultated)
b) - Connection between 2 endothelial surfaces
- Arterio-venous anastomosis
c) - AV graft
- Femoral line (lasts 7 days)
- CVC/ tunnelled line
- PD
Haemodialysis: problems and management
- Hypotension (headache, dizzy, nausea, reduced GCS) - managed with head down, feet up +/- fluids (don’t take BP meds on dialysis day)
- Cramps
- Strain on the heart
- Infection in the line
AKI: define
- ≥ 26.4 increase in serum creatinine over 48 hours, or
- ≥ 50% increase in serum creatinine over 7 days, or
- < 0.5 ml/kg/h urine output* for more than 6 hours
* urine output is more sensitive than creatinine
AKI: causes
a) Risk factors (renal, other, drugs)
b) Pre-renal (90%)
c) Renal
d) Post-renal
a) - General: elderly, diabetes, CVD, HTN,
- Renal: CKD, history of AKI, renal stones
- Drugs: NSAIDs, ACE/ARB, diuretics, aminoglycosides
b) - Hypotension/shock (sepsis, cardiogenic, etc.)
- Hypovolaemia (dehydration, vomiting, diarrhoea, burns, inappropriate diuresis)
- Overloaded states - CCF, cirrhosis, CKD
- Renovascular - RAS, CCF, NSAIDs, ACE/ARB
c) - Glomerulonephritis
- ATN: prolonged ischaemia, nephrotoxins (eg myoglobin, aminoglycosides, radiocontrast, myeloma protein)
- AIN: NSAIDs, infection, autoimmune (eg. SLE)
d) Obstructive: BPH/prostate Ca, stones, stricture, pelvic/ bladder Ca, neurogenic bladder, retroperitoneal fibrosis
AKI: assessment and investigations
a) Pertinent points in the history
b) Examination
c) Investigations
a) - HPC - vomiting, diarrhoea, fever, haematuria, obstructive symptoms, etc.
- PMHx - diabetes, HTN, CVD, kidney stones, BPH, etc.
b) - Signs of sepsis / shock
- Fluid status - overload (CCF), dehydrated (pre-renal)
- Abdomen - distended bladder (?post-renal - BPH)
c) - Bedside: urine dip (protein, blood, infection, casts)
- Bloods: FBC (infection, eosinophilia in AIN), CRP/ESR, U+E, clotting (DIC), CK (rhabdo),
- Imaging: USS (obstruction), AXR/CT (stones), CXR (pulmonary oedema)
- Special tests: antibodies (ANA, ANCA, etc.), myeloma protein electrophoresis, renal biopsy
AKI: management
a) Principles
b) Specific drugs to stop/avoid
c) Fluid balance
d) Electrolyte balance
e) Specific interventions that may help
f) Indications for dialysis
g) Best treatment is…?
a) - Treat the underlying cause
- Stop/reduce any precipitating factors (eg. NSAIDs)
- Optimise fluid and electrolyte status
b) - NSAIDs, aminoglycosides, contrast media
- ACE, ARB, diuretics (if hypovolaemic; if overloaded - may need to continue or increase diuresis)
- Swap other drugs (eg. morphine to oxycodone)
c) - If dehydrated - increase fluids (beware overload)
- If overloaded - restrict fluids and consider diuretics
- Monitor urine output and use fluid balance chart
d) - Potassium (K+) - may need restricting; consider insulin/dex, calcium resonium (Ca-Gluc if ECG changes)
- Phosphate, urea etc. may build up - monitor
- Bicarbonate, calcium, glucose - may deplete - monitor
e) - Sepsis - antibiotics
- GN/autoimmune - steroids, etc.
- Obstruction - catheterise, remove stone, nephrostomy, BPH management (medical, surgical)
f) AEIOU.
- Acidosis (metabolic acidosis, pH < 7.2, refractory to Rx)
- Electrolytes (K+ > 6.5 refractory to medical Rx)
- Intoxication
- Overload (pulmonary oedema, refractory to medical Rx)
- Uraemic pericarditis/encephalopathy
g) Prevention!
- identify at risk patients and manage risk factors
Patient has been admitted with AKI. For each of the following drugs, would you: Continue, Stop, Increase dose or Reduce dose?
a) Dalteparin 5000 units (prophylactic dose)
b) Dalteparin 50,000 units (PE treatment)
c) Furosemide 40 mg od
d) Amlodipine 5 mg od
e) Gentamicin 80 mg od
f) Diclofenac 50 mg tds
g) Phenytoin 300 mg bd
h) Morphine sulphate 20 mg bd
i) Aciclovir 800 mg 5x/day
j) Flucloxacillin 2g qds (treatment for endocarditis - hence big dose for tissue penetration)
k) Prednisolone 5 mg od (long term for PMR)
l) Ramipril 10 mg od
- Note: in hepatic/renal dysfunction, you can reduce the dose and still maintain the same therapeutic levels due to accumulation
a) eGFR < 20: half the dose of LMWH (or give an IV infusion of UFH); check APTT in 4 - 6 hours
b) As before
c) Depends on fluid status: if hypervolaemic may continue or increase; if hypovolaemic - stop
d) Depends on BP/extent of angina
e) Nephrotoxic: swap to something else treating gram-negative infection (eg. cephalosporins, tazocin, meropenem)
- note: metronidazole treats anaerobes only
f) Stop
g) Hepatic excretion (fat soluble - as for most drugs that cross the BBB; and HIV medications)
h) Switch to fentany 72h patchl/ oxycodone
i) Reduce
j) Reduce
k) Increase to 10 mg (around physiological dose)
l) Stop
ACE inhibitors.
a) CV indications
b) Indication in CKD
c) Effect on eGFR
a) HTN, HF, post-MI, post-stroke
b) Proteinuria (mostly diabetic)
c) Initial drop (hence bad in AKI); especially in renovascular disease (consider if they have: bruit, one small kidney on USS, resistant HTN, CVD/PAD)
- Then a slower eGFR decline relative to those not on ACE (hence good in CKD)
eGFR
- why is it more useful than creatinine in CKD?
- when can it not be used to assess renal function?
a) Accounts for age, gender and race; which corrects for muscle mass effects on creatinine levels
b) AKI
Protein collection.
a) Modern way to assess
c) Old way to assess
c) Why is urine dipstick flawed?
a) ACR: albumin-creatinine ratio
b) 24-hour collection
c) Tells you the concentration of protein, not the volume (affected by hydration levels/urine output)
Contrast nephropathy.
a) when does creatinine peak?
b) management
a) After 72 hours
b) - Avoid radiocontrast in at-risk patients if possible
- If required, optimal pre-hydration: IV volume expansion with isotonic sodium bicarbonate or 0.9% NaCl
PKD.
a) Genetics
b) Clinical features
c) Investigations
d) Management
a) - Mostly autosomal dominant (present in adulthood): PKD 1 (chromosome 16) and PKD 2 (chromosome 4)
- Autosomal recessive PKD usually presents in infancy
b) - Renal cysts - haematuria, loin pain, loin mass, HTN, recurrent UTI, chronic renal failure + need for dialysis/ transplant
- Cysts in the liver, pancreas, spleen and ovaries
- Berry aneurysms and SAH
- Mitral valve prolapse
c) - Diagnosed with renal USS
d) - Manage HTN
- Monitor UEs/creatinine (eGFR) and BP
- Regular follow-up in renal outpatients
- ESRF: require dialysis or transplantation
- Genetic counselling and testing offered
