Acute Kidney Injury Flashcards
What can the causes of AKI be classified into?
pre-renal
renal
post renal
give examples of pre renal causes of AKI?
dehydration circulatory collapse hypovolemia blood loss RAS dehydration heart failure medications liver failure (albumin low, low oncotic pressure) CLD HYPOPERFUSION OF KIDNEYS! [fluid overload; oedema, ascites, increased RR, decrease oncotic pressure so fluid moves out and less fluid intravascularly so decreased BP and RAS to compensate and maintain perfusion.]
give examples of renal causes of AKI?
acute tubular necrosis acute glomerulonephritis acute cortical necrosis renal vascular damage necrotising papillitis
give examples of post renal causes of AKI?
intratubular
uretal
urethral
stones, tumours, prostatitis, pelvic tumours, retroperitoneal pelvic tumour , strictures,
what is the most common cause of acquired AKI?
‘surgical triad’
- post operative volume depletion
- infection
- nephrotoxic drugs
describe the presentation of renal syndromes?
acutely, insidious slow progression, symptoms relating to aetiology (proteinuria), signs (nephrotic-rash), haematuria, hypertension
what groups are at risk of AKI?
elderly diabetics vasculopaths known chronic renal impairment significant cardiac dysfunction chronic liver disease drugs (ACE inhibitors (efferent vasodilation), NSAIDS (afferent vasodilation, aminoglycosides, contrast mediums)
what are the ways of screening for AKI?
urinalysis for proteinuria and non visible haematuria
blood pressure
prostate examination
what investigations are of use in patients with suspected AKI?
haematology (FBC, coagulation profile)
biochemistry (profile, CRP, glucose)
microbiology/virology (hepatits, blood cultures)
radiology (ultrasound, CXR)
immunology (ANA, ANCA, C3, C4) others (myeloma screen-presents as hypercalcaemia, anaemia and kidney failure), ECG
describe the relationship between creatinine and actual GFR?
As GFR falls, creatinine rises
Normal serum creatinine is not synonymous with normal GFR
Creatinine level not a good indicator of kidney function (don’t rely on it)
describe the patient pathway for a patient with AKI?
GP -> nephrologist and MDT (low clearance clinic for advice about dialysis) -> dialysis (haemodyalisis, peritoneal dialysis) -> transplant (sometimes patients go straight from clinic to transplantation avoiding dialysis)
what are the life threatening complications of AKI?
Hyperkalaemia Pulmonary oedema Intravascular volume depletion Uraemic encephalopathy Pericardial fluid
what are the functions of the kidneys?
Excretory-elimination of waste products of metabolism (water soluble drugs)
Regulatory (electrolyte homeostasis, acid base balance, fluid balance, blood pressure control
Metabolic-metabolism of vitamin D
Endocrine-erythrpoetin, vitamin D RAAS
what is the classification of AKI?
stage 1 RISK
stage 2 INJURY
stage 3 FAILURE
describe stage 1 AKI?
actual/rise in serum creatinine >25
% rise from baseline >150%
urine output <0.5ml/kg/h for 6 hours
describe stage 2 AKI?
% rise from baseline >200% / urine output <0.5ml/kg/h for 12 hours
describe stage 3 AKI?
actual/rise in serum creatinine >354
% rise from baseline >300%
urine output <0.3ml/kg/h for 24 hours or anuria for 12 hours
define oliguria?
Volume of urine below which at maximum urinary concentrations the body cannot excrete the products of metabolism
why might a sick patient be acidotic?
Failure to remove acid by renal system
Overload of buffering system
Production of other acids eg lactic acid from tissue hypoxia
what would an ECG show in patients with hyperkalaemia?
Tenting of T waves
Widening QRS complex
Disappearnce of p waves
Sine wave pattern
what clinical methods are used to assess intravascular volume?
Body weight Skin turgor Postural blood pressure Mucous membrane JVP-elevated=overload Lung bases, peripheries
what methods are used in patients with AKI in ICU for monitoring progress?
Observation CVP line BP and pulse Arterial line for blood gas Blood test Urine output and fluid balance chart
what are the main complications in chronic renal failure?
Anaemia -EPO Renal bone disease-Vit D Acidosis –acid base balance Malnutrition Uraemia
what is chronic renal dysfunction?
Permanent usually progressive reduction in renal function
until proven otherwise what should absolute anuria be assumed to be?
urinary tract obstruction
what is the most common way of measuring kidney function?
GFR
what is GFR?
equivalent to kidney function, above 90-120ml/min/1.73m2 (volume, time and body surface area). difference In male and females.
mGFR
eGFR
what is mGFR?
(measured)(inulin)-not used often in clinical practice. Inulin used for research and numerous samples are needed. Nuclear scans eg DTPA, MPG3.
what is eGFR?
what are the different methods to calculate eGFR?
estimated) (used in clinical practice), urea and creatinine and cystatin C (new). Ideal marker need to be substance kidney freely filters doesn’t excrete or absorb.
- Mainly creatinine (from muscles, everyone has different muscle mass (60-110 normal) low muscle mass /pregnancy is the only cause of low creatinine,
- urea no longer used as small molecule so passes across membrane, produced by liver so urea levels affected by liver disease)
- Cystatin C production over 24 hours and is similar across everyone
define AKI?
Reversible loss of kidney function (GFR) within hours to days. If deranged kidney function for more than 6 weeks-chronic
Sepsis with AKI has a much larger mortality rate than sepsis on its own
what classification systems can be used for AKI and what measurements do they use?
RIFLE
AKIN
creatinine and urine output
how many stages are in the AKIN classification system?
stages 1-3
what are the stages in the RIFLE classification system of AKI?
risk injury failure loss ERSD (end stage renal disease)
what is the urine output;
- normally
- anurea
- oliguria
- polyuria
- 1-1.5L (0.5/weight in Kg x24)
- <200mL over 24 hours
- 200-1L over 24 hours
- > 2L
what information can be gained from 24 hour urine collection?
Proteinuria Hormones Hypertension follow up Adrenal tumours Electrolytes Creatinine clearance
what is the gold standard for getting a protein urine sample?
24 hour urine collection
how can a patient with AKI be identified?
- Blood test-creatinine
- Can be asymptomatic depending on degree of renal failure
- History (BP symptoms-headaches, visual disturbances, Volume-hypervolaemia, hypovolaema, thirst, nausea, vomiting, oedema, Drugs)
if the afferent and efferent arterioles are even what is the GFR?
normal
if the afferent arteriole and efferent arteriole are both constricted what is the effect on GFR?
reduced GFR
if the afferent arteriole is normal and the efferent is constricted what is the GFR?
increased GFR
if the afferent arteriole is constricted and the efferent is normal what is the affect on GFR?
decreased GFR
- what is the main cause of inpatient AKI?
in which of these scenarios is AKI likely/unlikely to develop
- missing one kidney
- blockages of both ureters
- blockage of urethra
- kidney stones in one ureter
- volume related
- unlikely
- likely
- likely
- unlikely
how is a diagnosis of AKI confirmed?
- Blood tests (U&E, creatinine, electrolytes, FBC, Hb, HCT, WCC, CRP)
- Urine dip (protein, blood. Nit, leu
- Ultrasound imaging- structure, size (usually 9-12cm enlarged in diabetes, smaller in scarring, fibrosis, hypperfusion), stones, obstruction (enlarged), number of kidneys
- ABG – potassium, metabolic acidosis
- Immune screen- ANCA, anti GBM, ANA, anti-dsDNA, protein electrophoresis, complement
- what is glomerulonephritis?
2. what are the 3 cell types of the glomerulus?
- inflammation of the glomerulus
2. endothelial, epithelial, mesangial
describe the histology of a normal glomerulus?
capilliary loop
bowmans space (urine collects)
mesangium (holds capillary loop in place)
podocytes with foot like processes
what are the different histological patterns in glomerulonephritis?
minimal change membranous GN mesangial proliferative focal segmental GN, focal segmental glomeruloclerosis, diffuse endothelial proliferative, mesangiocapillary, crescentic
what makes up the filtration barrier of the glomerulus?
endothelial cells fenestrated, glomerular basement membrane trilaminar, podocyte with foot like processes
- what is primary glomerulonephritis?
2. what is secondary glomerulonephritis?
- disease originates or only affects the kidney
2. kidney damage is result of another disease such as type 1 diabetes
what are the consequences to the loss of function of the glomerular basement membrane?
blood loss
protein loss
describe blood loss in patients with GMB loss of function?
Non visible/visible
Nephritic syndrome
Due to IgA nephropathy
-Visible haematuria, 1-2 days following URTI in younger patients
-Worse prognosis if; proteinuria, hypertension, scarring on biopsy, male, abnormal renal function
-36% progress to ESFR
describe protein loss in patients with GMB loss of function?
Asymptomatic
Nephrotic syndrome: peripheral oedema, proteinuria, hypoalbuminaemia, hypercholesterolaemia (increased infection and thromboembolic risk). >3.5 grams/day.
-Get oedema due to capillary hydrostatic pressure forcing fluid out of capillaries and interstitial hydrostatic pressure causing fluid to move into capillaries, capillary oncotic pressure (albumin) and maintain fluid in capillary, interstitial oncotic pressure-keep fluid in interstitial space. In nephrotic syndrome due to albumin being low there is balance so fluid into interstital space and secondary hyperaldosteonism and salt and water retention
what is minimal change glomerulonephritis?
Nephrotic syndrome but normal microscopy
describe steroid responsive nephrotic syndrome?
Most children with nephrotic syndrome will have minimal change disease and most will respond to steroids so treat without biopsy=steroid responsive nephrotic syndrome
Some relapse on steroid withdrawal (relapsing nephrotic syndrome)
describe steroid dependent nephrotic syndrome?
Some never respond to steroid (steroid resistant nephrotic syndrome-need biopsy showing either inherited abnormality of podocyte proteins or other cause such as FSGS.
what is FSGS (focal segmental glomerular sclerosis)?
some of glomerulus normal and some is sclerosed
describe membranous glomerulonephritis?
- thickening of capillary loops
- Proteinuris with or without renal impairment
- 1/3 spontaneous recovery, 1/3 persistant proteinuria, 1/3 ESFR
- Mainly autoimmune
- Associations with adenocarcinoma of lung and GI, hepatitis B, SLE, drugs
- Treatment-immunosuppression if progressive disease
