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Flashcards in L2 AKI CKD Deck (53):

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

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how to diagnose AKI

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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

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what causes different types of AKI

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differential diagnosis by pathophysiology of AKI

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clinical manifestation of AKI

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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

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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)

– improve perfusion, remove offending medications

– 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

– 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

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management of hyperkalemia

– Severe hyperkalaemia (K+ >6.5 mmol/L) is a medical emergency because of the risk of life threatening cardiac arrhythmias

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principle of management AKI

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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

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CKD risk factors

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CKD major cause

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algorithm for initial detection CKD

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drug that may worsen renal function

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uremic symptoms

cramps, restless legs, coma, hiccups


CVD in pt with CKD

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general management in pt with CKD

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what r some nutrition restrcition in CKD pt

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general fomula for manage CKD

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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

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preserving renal function in proteinuria or albuminia

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lipid and CKD, how to magage it?

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glucose control in CKD

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management complication in CKD - Na balance

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managing symptoms of CKD e.g. hyperkalaemia, acidosis, restless legs

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what is Pruritis and its management

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managing complication of CKD, VItD and phosphorous metabolism

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what r the bone disease associated with CKD

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managing complication - Vit D and phosphorous metabolism. draw flow chat of mechniasm

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what are the phosphate and Ca management in CKD pt

Phosphate management
– dietary restriction of protein often reduces PO4 intake

– PO4 binding agents

• Binds to dietary phosphate to prevent absorption
• Calcium containing preparations (e.g. CaCO3)
• Sevelamer & Lanthanum available for patients on dialysis

• Aluminium hydroxide (not first line due to accumulation and risk of encephalopathy)


–  If phosphate is controlled, calcium will typically remain in normal range

–  If level is low with normal phosphate consider vitamin D supplementation

–  Hypercalcaemia associated with increased risk of vascular calcification

Vitamin D therapy (calcitriol, paricalcitol)

–  suppresses PTH secretion and stimulates GI calcium absorption

–  care to avoid hypercalcaemia (less risk with paricalcitol) – monitor levels closely

–  If kidney function is still intact cholecalciferol can be used

–  Cholecalciferol may still be used for 25OH Vitamin D deficiency including in combination with calcitriol in advanced CKD

Calcimimetics (cinacalcet)

–  rapidly suppresses PTH secretion without increasing calcium absorption (risk of hypocalcaemia)

–  Cinacalcet can be used to treat hyperparathyroidism for individuals on dialysis

–  Monitor calcium levels every 1-2 weeks, do not initiate therapy if calcium is low

–  Caution in patients with seizures; Cincacalcet inhibits Cytochrome P450

–  EVOLVE trial did not demonstrate statistically significant difference in time to death or non-fatal CV event between cinacalcet and placebo


what to monitor for Vit D and phosphorous metabolism in CKD

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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)


–  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


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dialysis in CKD and types of dialysis

Progression of uraemic symptoms and/or hyperkalaemia will result in ESKD patients requiring dialysis or transplant

–  Two main modalities exist

– peritoneal dialysis (PD) – haemodialysis (HD)


indication for dialysis

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haemodialysis VS peritoneal dialysis

– blood (heparinised) pumped through dialyser (artificial kidney)

and returned to patient.
• Multiple times per week for hours


– catheter is inserted into abdominal cavity

– dialysate is run into abdomen and left for 30 minutes

– run into a collecting bag – Multiple times per day



advantages and disadvantages of haemodialysis

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peritoneal dialysis

Blood is cleaned inside the body.

PD cleans your blood and removes extra fluids using one of your body’s own membranes, the peritoneal membrane, as the filter.

The peritoneal membrane is the lining that surrounds the peritoneum or abdominal cavity, which contains your stomach, spleen, liver and intestines.

The peritoneal membrane filters waste and fluids from your blood into the solution. The solution containing the wastes is drained from your peritoneum after several hours and replaced with fresh solution.

Exchange takes approx 30 mins


what r the 2 tyoes of peritoneal dialysis

Two types of PD
– Continuous Ambulatory Peritoneal Dialysis (CAPD)

– Automated Peritoneal Dialysis (APD)

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advanatges and disadvantages of peritoneal dialysis

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prescribing during dialysis

- Dialysis drug clearance may significantly reduce drug efficacy if it is not accounted for.

– Drugs known to be significantly cleared by dialysis should be dosed after dialysis

e.g. NSAID, Antibiotics e.g. penicillin, vancomycin


–  Extends life and improves QOL (much more so than dialysis)

–  Specialist area;
– Combination immunosuppressive agents required to prevent rejection
– Many adverse effects and interactions to consider


advantages and disadvantage of renal transplantation 

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