L2 AKI CKD Flashcards
what is AKI
Abrupt decline in renal function leading to an increase in serum concentrations of urea, creatinine & other substances (occurs over a period of days)
what r the major risk factor for AKI
PATIENT FACTORS: - old age (>75) - diabetes - atheroclerosis - chronic HT MEDICATIONS AND AGENTS RISK FACTOR - NSAIDS -ARB (angiotensin receptor blockers) - ACEIs (angiotensin converting enzyme inhibitors)
what r the current use biomarkers of AKI?
- increased serum creatinine
- increased urea nitrogen
how to diagnose AKI
Estimating Kidney Function in AKI
– Difficult because commonly used SCr based equation are not appropriate (assume stable SCr)
– Other equations such as Brater and Jeliffe may be more accurate than Cockcroft-Gault but less tested
what r the types of AKI and its pathophysiology
what causes different types of AKI
differential diagnosis by pathophysiology of AKI
clinical manifestation of AKI
AKI prevention
Identification of high-risk individuals
Optimisation of renal perfusion
– volume expansion and/or fluid therapy where appropriate
– vasopressors (e.g. adrenaline, dopamine) may be used once intravascular volume has been restored (patchy evidence however)
Avoidance of nephrotoxins wherever possible (and close monitoring when not)
– includes drugs, and combinations of drugs, e.g. triple whammy
Specific circumstances (examples)
– once daily dosing of aminoglycosides
– allopurinol and rasburicase to prevent tumour lysis syndrome
– Amphotericin whenever possible; limiting dose, rate of infusion.
Recognise that patients with pre-existing renal impairment are at higher risk of developing further renal insufficiency—treat and monitor accordingly
Temporarily withhold nephrotoxins (especially ACE-I, ARBs, NSAIDs) and diuretics (to prevent dehydration) when patients become unwell—either in the community or in hospital
Ensure that patients remain adequately hydrated, to maintain renal perfusion
AKI prevention (med perspective)
– Remember to monitor renal function after starting, or increasing the dose, of ACE-I or ARBs (check one to two weeks later)
– Where necessary, adjust drug doses in patients with renal impairment
– Monitor drug levels when using aminoglycoside (gentamicin) and/or glycopeptide (vancomycin) antibiotics - and adjust dose accordingly
– Hydrate the patient and consider using N-acetyl cysteine before procedures entailing radiological contrast media
how to manage pre-renal, intrinsic and post-renal AKI?
The most important step is to reverse the cause (which will depend on the type of AKI)
Pre-renal
– improve perfusion, remove offending medications
Intrinsic
– treatment of ATN primarily supportive
• no specific therapeutic intervention has been found to hasten recovery of kidney function
– use of diuretics to convert patients from oliguric to non-oliguric ATN not associated with improved outcomes
• may be helpful in volume management (need high doses e.g. >160mg frusemide), but cease if no response
– for AIN, avoid offending agent in future
Post-renal
– relieve obstruction
– All patients with significant AKI also require attentive management of volume, electrolyte (esp K+) and acid-base status, and nutrition
– Renal replacement therapy (RRT, dialysis) may be required in cases of severe AKI (hyperkalaemia, volume overload, severe acidosis, or overt uraemia)
what r the indication for renal replacement therapy
management of hyperkalemia
– Severe hyperkalaemia (K+ >6.5 mmol/L) is a medical emergency because of the risk of life threatening cardiac arrhythmias
principle of management AKI
drug dose consideration in AKI
– Optimising drug therapy for patients with AKI is challenging
– Factors that need considerations include; residual drug clearance, accumulation of fluids, and dialysis.
– For renally cleared drugs (>30% elimination unchanged in the urine), particularly for drugs with narrow therapeutic range, serum drug concentration and pharmacodynamic response is necessary.
what is CKD
– CKD is defined as kidney damage or GFR below 60ml/min/1.73m2 for 3 months or more irrespective of the cause.
– CKD is
– a long-term health condition (months/years),
preventable in many cases
– glomerular & tubular damage
– asymptomatic until much of the kidney function is lost
• compensatory and adaptive mechanisms maintain acceptable health until GFR is ~10 to 15 ml/min
evidence for CKD
– Evidence for CKD
– Proteinuria
– Reduced renal function
stages of CKD
CKD risk factors
CKD major cause
algorithm for initial detection CKD
drug that may worsen renal function
CVD in pt with CKD
general management in pt with CKD
what r some nutrition restrcition in CKD pt
general fomula for manage CKD
preserving renal function In HT pt with CKD
– both symptomatic of advanced CKD and pathogenic • lowering BP delays the rate of progression
– ACEIs/AT2RAs are generally the best agents (esp in diabetic nephropathy), CCB (dihydropyridine) are also preferred.
– most patients will require at least 2 drugs, probably more
– Simplify antihypertensive regimen wherever possible
– Once-daily agents should be used when possible
– Two agents (separate or fixed-dose combinations) can be considered as initial therapy for SBP >20 mm Hg above goal
– Fixed-dose combinations may be used for maintenance therapy after the antihypertensive regimen has been established
preserving renal function in proteinuria or albuminia
lipid and CKD, how to magage it?
glucose control in CKD
management complication in CKD - Na balance
managing symptoms of CKD e.g. hyperkalaemia, acidosis, restless legs
what is Pruritis and its management
managing complication of CKD, VItD and phosphorous metabolism
what r the bone disease associated with CKD
managing complication - Vit D and phosphorous metabolism. draw flow chat of mechniasm
what to monitor for Vit D and phosphorous metabolism in CKD
managing complications of CKD- anemia
Anaemia common in CKD
– Due to reduced EPO synthesis
– Reduced absorption of iron
– Resistance to the action of erythropoietin stimulating agents (ESA)
Targets:
– Hb 100-115g/L
– Prior to commencing erythropoietin stimulating agents (ESA), trial of iron supplementation is recommended maintaining transferrin saturation (TSAT) >20% and ferritin between >100 μg/L
– Once ESA commenced, maintain: Ferritin 200-500 μg/L; TSAT 20-30%
– Treatment can decrease morbidity/mortality, reduce LV hypertrophy, increase exercise tolerance, increase QOL
– May sometimes respond to Fe infusions, but commonly managed using ESA
– Use ESA cautiously- higher Hb levels associated with increased risk of cancer, death, cardiovascular events, and hospitalisation for CHF
– Hb should not exceed 130 g/L (increased risk of CV events)
– Note: AMH recommends not to exceed 120g/L
– TREAT (Trial to reduce cardiovascular events with Aranesp Therapy) failed to show a benefit in outcomes, but treatment with ESAs was associated with increased stroke (NEJM 2009;361)
– Most patients using ESA will also require Fe, and potentially folate and/or B12
– Ensure transferrin saturation 20%-30% and ferritin between 100 and 500μg/L
e.g. ESA Darbepoein alpha (Aranesp). – All appear to have similar efficacy, most differences related to duration of action, e.g. Eprex dosed twice weekly, Aranesp once weekly and Mircera once monthly
indication for dialysis
advantages and disadvantages of haemodialysis
what r the 2 tyoes of peritoneal dialysis
Two types of PD
– Continuous Ambulatory Peritoneal Dialysis (CAPD)
– Automated Peritoneal Dialysis (APD)
advanatges and disadvantages of peritoneal dialysis
advantages and disadvantage of renal transplantation
