Renal Disease Flashcards
What is the incidence of AKI?
2/3 of all ICU patients
2x increased risk of death and raised >44micromol creatinine = 6.5x increased mortality
Why don’t we call this acute renal failure vs AKI? What approach should we use?
based on pre-renal (reversible) and acute tubular necrosis (structural histopathological)
ATN vs Pre-renal using plasma/urinary electrolytes/urea/creatinine
Problems
- abnormal biochem doesn’t predict rate of AKI resolution.
- cells seen in casts can be viable
- prerenal vs ATN doesn’t change treatment
Approach
- on a spectrum
- small increments are associated with increased mortality and increased risk of worsening function and increased length of stay
- ARF >30 definitions. Recognition of spectrum leading to AKI to standardise research definitions. RIFLE/AKIN criteria.
What are the criteria used to determine AKI? What are they useful?
RIFLE/AKIN
- value in prognostic power
- RIFLE (risk, injury, failure, loss, ESRD)
- AKIN (stage 1 2 and 3)
creatinine and urine output measurement.
High RIFLE - decreased renal recovery, longer ICU stay
What are Risk Factors for AKI?
General:
- age
- preop renal impairment
- IHD
- CCF
ICU
- sepsis
- shock
- nephrotoxins
Post surg:
- high risk surg
- emergency surg
Specific groups:
- high BMI, HTN, DM, COPD, preop ARB
- liver disease, anaemia and blood transfusion, general anaesthesia, thoracoscopic surgery
- cardiac bypass (time, excessive haemodilution)
Genetic factures - MHC class 2 genotype modulates risk
What are some nephrotoxins?
Nephrotoxic antibiotics
Gentamicin
- nil quality data, recent low quality paper
- historical case control study showed increase in ARF
- who shouldn’t? extrapolate from long term (w/h in DM/anaemia)
-
Contrast nephropathy
- common
- avoid using USS or other modalities
- avoid gadolinium due to risk of nephrogenic systemic sclerosis
- Tx: volume repletion (bicarb vs saline) only small trend favouring bicarb. NAC if used at high risk of contrast nephropathy use PO, high rate of anaphylaxis in IV
NSAIDS avoid
- low risk of AKI
- increase AKI in at risk population
ACE I and ARBs
- Cochrane review did not find protective properties
- post induction hypotension with vasoplegia post bypass with increased morbidity and mortality
- reduced trop and reduced AKI
- ACEI cause oliguria - ?Renal artery stenosis
What are some situations with AKI and how to treat them?
Rhabdomyolysis
- in trauma and ortho surgery
- nil high grade evidence, but high urine output and urine alkalinisation (pH >6.5)
- benefit in crush with high CK
- watch for K+, urate, phosphate
- avoid Ca2+ due to risk of calciphylaxis
Bypass
- reduce renal blood flow,
- re-perfusion injury and inflammation
- haemoglobinuria (pump associated)
- tx/prevention: long list of failed (dopamine, Map?70, fenoldopam, ACEi, frusemide). nil help from steroids.
- Nesiritide (synthetic BNP) helped though but used in decompensated HF increases mortality and reduced acute HF
- sodium nitroprusside during reperfusion helped
- heparin coated circuits helped.
Obstructive nephropathy rare
- reversible cause NTBM
- relieved within 1week most recovery (most within first 10 days)
What are some AKI biomarkers/prognosticators?
NGAL (neutrophil gelatinase associated lipocalin)
- elevated predicts AKI in paeds doesn’t translate to adult
- promise in cardiac, septic and liver transplant
other markers not accurate enough evidence (KIM-1, IL18, Cystatin C)
future lies in panels for sensitivity and specificity
Renal resistive index on doppler US
- distinguish from AKI from transient
What are some considerations for frusemide in AKI?
Consider: non overloaded with good BP, K+ okay but oliguric
Physiology:
- frusemide may convert to non oliguric renal failure.
- frusemide decreases oxygen demand in loop of henle, anti-apoptotic effects
- high dose have immunosuppressive effects
Avoid frusemide after metanalysis for:
- prophylaxis
- mortality
Adverse effects:
- tinnitus
- hearing loss
- vertigo
- agranulocytosis
Volume management
- avoid fluid overload, evidence of using early is weak.
Rhabdomyolysis
- alkaline diuresis (bicarb/mannitol) evidence
- frusemide induces aciduria increased urinary glycoprotein and nephrotoxicity
Practice points:
- circulates bound to plasma proteins - less diuresis in hypoproteinic patients. Conc albumin will increase response
- infusion produce more response
if oliguric
- intravascular hypovolemia - fluid boluses improve blood pressure.
- RCT for this is weak.
- fluid balance leaks to higher risk of death and adverse outcomes in sepsis.
What are some consideration with fluid administration?
Timing of fluid
- in first 6 hours beneficial
- type (voluven or saline, starches showing harm)
- albumin as safe as saline, improves mortality in SBP
- avoid chloride - Plasmalyte
Avoid excessive volume in vasodilation
- use pressors (norad vs dobutamine)
Euvolemic?
- CXR/exam not reliable
- consider fluid challenge/responsiveness
- CVP changes with fluid loading not reliable
Swan Ganz catheter
- wedge pressure correlates poorly with LV end diastolic volume (on decline in use)
Dynamic indices
- pulse pressure, ECHO indices
- pulse pressure variable ?12-15% variation (fluid responsive), <9% unresponsive
- Stroke volume variation - slightly better but nil mortality benefit
- oesophageal doppler (some benefit in bowel patients)
