Renal Failure Symposium Flashcards
Treatment choices
Transplant
Peritoneal dialysis
Home haemodialysis
Physidia
Unit haemodialysis + satellite haemodialysis
Maximum conservative care - supportive care, symptom control
Erythropoeitin Stimulating Agent (ESA)
1) Darbepoetin alfa – Aranesp Weekly/fortnightly s/c injections or pen Self-administered/GP nurse/Community nurse 2) Epoetin beta - Neo-Recormon 2-3 times a week
Monitoring
Fortnightly/monthly BP and FBC
3monthly iron stores
Dialysis Access and Transplant Referral
Arteriovenous fistula formed >3 months before starting Hdx
Peritoneal dialysis catheter inserted 2 weeks before dialysis started
Referred to pre-transplant team when eGFR 15-20mL/min, aim for pre-emptive transplant
Start dialysis eGFR 5-10:
Symptomatic eg, nausea and generally unwell
Uncontrolled potassium
Fluid balance not responding to diuretics
Possible dietary interventions
Protein, potassium, phosphate, fluid/salt, fibre, vitamins and minerals
During kidney failure - what to eat
Avoid excess protein Optimise blood glucose Optimise blood pressure Weight management Increase fruit and veg Keeping active
Chronic Kidney Disease Related malnutrition
Potential dietary and fluid restrictions
Poor appetite secondary to uraemia and taste changes
Less time for food prep?
Managing conditions like these = higher incidence of depression/mood disorders
Protein energy wasting
Co-existing atherosclerosis, hypertension or diabetes
Micronutrient deficiencies due to losses during dialysis
Protein Recommendations UK
Targets: 0.8kg/kg ideal body weight
1-1.2g/kg ideal body weight in dialysis patients
Fluid balance
No kidney function 500-750mls per day
Impaired kidney function- generally encourage to drink
Transplant- Generally drink lots post transplant
Haemodialysis- 500mls plus 24 hour urine
Peritoneal dialysis- 750mls plus 24 hour urine
High potassium foods
Bananas, dried fruit, exotic fruits
Mushrooms, parsnips, sprouts, spinach, tomatoes
Chips, jacket potato
Coffee, hot chocolate, milk, fruit juice, cider, strong beer and stout
Chocolate, nuts
Lo salt, Marmite, Bovril
Phosphate
Targets: 1.1 – 1.7 mmol/L dialysis.
0.9 – 1.5 mmol/L low clearance
Ca and PO4 homeostasis required for bone health.
Pruritis (Itchiness)
Phosphate binders:
- Often required in addition to a low phosphate diet.
- Prescribed to take with meals.
- Difficult to remember for some patients.
- Lots of different types/ preparations.
High and low phosphate foods
high Dairy products,
Lower phosphate alternatives: oily fish with bones, shellfish, offal, nuts/chocolate, processed
Stop drinking dark fizzy drinks
Pathogenesis of the manifestations of CKD
Slow, progressive loss of functioning nephrons may not be noticeable.
This triggers maladaptive compensatory mechanisms
Either the loss of renal function or the adaptations to reduced renal function lead to the manifestations of kidney failure
The person with CKD may not feel different (silent disease).
CKD classification
CKD is classified by GFR - stages 1, 2, 3a, 3b, 4, and 5 depending of how high GFR is in ml/min/1.73
Benefits of good management of KD
Prevent or slow progression to renal failure
Reduce morbidities
Improve quality of life
Reduce costs
GFR and eGFR
GFR is equal to the sum of the filtration rates in all of the functioning nephrons. Actual GFR (eg by inulin clearance) is not routinely measured in clinical settings. Estimated GFR (eGFR) gives a rough measure of the number of functioning nephrons
Significance of Proteinuria
Indicative of glomerular disease (leaky glomerular basement membrane)
Proteinuria itself is nephrotoxic (causes downstream renal tubular cell damage)
Marker for increased risk of progression of renal disease
Major benefit from lower BP target, and ACE inhibitors
Measuring Proteinuria
Dipstick is inaccurate, and can miss significant proteinuria
Different ranges of ‘normal’ for people with or without diabetes
No need for 24 hr urine collection
Spot urine sample for protein:creatinine or albumin:creatinine ratio usually sufficient
All patients with CKD stage 3 or worse should have proteinuria measured at least once
Estimating 24 hour urine protein excretion from ACR and PCR
PCR/ACR (mg/mmol) x 10 ≈ 24 hour excretion (mg/24 hrs)
PCR = protein creatinine ratio
Proteinuria, BP targets and treatment
Measure PCR
Depending on value, BP/NICE targets are different, potential need for ACEIs
AKI - definition and epidemiology
AKI – a rapid (hours to days) decline in excretory kidney function
AKI – present in 1% of acute hospital admissions and 5% of hospitalised patients develop AKI
Only 0.5% of hospitalised patients require RRT for AKI (70 per million population/yr in the UK)
Despite advent of dialysis, AKI continues to have a significant mortality risk, mainly from infection and cardiovascular disease. Highest mortality is in MOF
What does AKI predict
Predicts mortality (and morbidity)
Predicts progression to CKD
Predicts progression to ESRD
Distant Organ effects of AKI
Brain: increased vascular permeability, increased microglia and GFAP, increased KC and G-CSF
Lung: increased vascular permeability/cytokines/chemokines/leukocyte trafficking; altered response to ventilator associated injury; dysregulated channels
Liver: increased leukocyte influx and oxidation products; decreased antioxidants and altered liver enzymes
GI tract: increased channel inducing factor/ potassium excretion
Bone Marrow: anaemia, coagulation disorders, immune function
Heart: Increased TNF alpha, IL1, neutrophil trafficking, apoptosis; decreased fractional shortening
Patients at increased risk of AKI
Pre-existing CKD
Age > 60
Comorbidity - diabetes, cardiac failure, liver disease
Pathological: sepsis, hypovolaemia, hypotension, contrast, post-op, drugs
Potentially reversible/actively treatable causes: obstruction, rapidly progressive glomerulonephritis, multiple myeloma
Targeted approach to physiological disturbances
Acidosis: treat with NaHCO3 (isotonic)
Hyperkalaemia: Correct acidosis; Insulin/Dextrose is only a temporary measure; Other electrolytes
Indications for urgent renal replacement therapy
Uncontrollable fluid overload
Uncontrollable, severe metabolic acidosis
Uncontrollable hyperkalaemia
Uraemic pericarditis / encephalopathy
