Kidney Disorders 1 Flashcards
Equations, Labs, AKI
Why do we check renal function?
monitoring and early recognition of CKD
-monitoring the effect of drugs on slowing progression
-predict the time to onset of ESRD
-evaluating risk of complications
adjust doses of medications excreted by the kidneys
monitoring nephrotoxic medications
What is creatinine?
by-product of muscle metabolism that is primarily eliminated by glomerular filtration
What is serum creatinine?
creatinine concentration in the blood
What happens to SCr when GFR is low?
SCr increases
What is the equation we use to calculate eGFR to stage CKD?
CKD-EPI
What is the equation we use to calculate CrCl for the purpose of drug dose adjustments?
Cockcroft-Gault
True or false: CKD-EPI can be used to estimate kidney function in a patient receiving dialysis
false
the machine is removing creatinine thus it is not a reflection of true kidney function
What are some sources of error in GFR estimating equations using creatinine?
non-steady state
-AKI
factors affecting creatinine generation
-race/ethnicity
-extremes of muscle mass and/or body size
-nutrition (high protein or supplements)
-muscle wasting diseases
-ingestion of meat
factors affecting tubular secretion of creatinine
-decrease by drug inhibition (TMP, cimetidine, fenofibrate)
factors affecting extra-renal elimination of creatinine
-dialysis
-inhibition of gut creatininase by antibiotics
-volume loss of extracellular fluids
higher GFR
interference with creatinine assay
-special or chemical interferences
Which equation do we use for most patients with stable renal function?
CKD-EPI and Cockcroft Gault
What is the main difference between the 2012 and 2021 version of CKD-EPI?
race has been removed from the equation
Differentiate between indexed/normalized eGFR and non-indexed/without normalization eGFR.
indexed/normalized
-standardized to a BSA of 1.73m2
-units: ml/min/1.73m2
-recommended for CKD staging/progression
non-indexed/without normalization
-adjusted according to patients BSA
-units: ml/min
-consider for drug dosing
When should you be cautious when using non-indexed/without normalization eGFR?
in the morbidly obese
-can lead to overdosing
What is urea?
aka blood urea nitrogen (BUN)
produced as a break down product of protein
What are the factors that can impact BUN levels?
dietary protein
GI bleeding
hydration status (high urea means low water)
Is BUN strictly regarded as a renal function test?
no
levels do rise in renal impairment
What are the effects of the kidney on BUN?
filtered by the kidney and also reabsorbed (therefore measurement underestimates GFR)
What is proteinuria?
general term for presence of increased amounts of protein in the urine
-nonspecific: albumin +/- other proteins
-persistent increase of protein in urine is a marker of kidney damage
How much protein is normally lost in the urine?
no/minimal amounts
Which type of protein is lost in the urine?
depends on type of kidney damage
-albumin excretion sensitive to damage from diabetes, HTN, glomerular disease
-LMW globulin excretion in tubulointerstitial kidney disease
How much albumin is normally found in the urine?
small amount
What is albuminuria?
albumin in the urine
increased levels are an early predictor of glomerular dysfunction
What is the screening test we use for albuminuria?
albumin : creatinine ratio (ACR)
What are the categories of albuminuria?
A1 (normoalbuminuria): < 3mg/mmol
A2 (microalbuminuria): 3-30mg/mmol
A3: (macroalbuminuria): > 30mg/mmol
using ACR
What are some potential causes of transient albuminuria?
recent major exercise
UTI
febrile illness
decompensated CHF
menstruation
acute severe elevation in glucose or BP
takeaway: need repeated tests to ensure its not transient
What is a urinalysis?
provides info about the physical and chemical composition of urine
What kind of information does a urinalysis provide regarding urine?
colour, turbidity
presence of cells, micro-organisms, casts, crystals
-granular casts, RBC casts, WBC casts
urinary eosinophils (interstitial nephritis)
pH analysis, specific gravity
glucose, ketones (diabetes/DKA)
leukocyte esterase and nitrite (UTI)
What is the use of urinary electrolytes?
differentiate causes of AKI
Describe when you are likely to see the following casts:
RBC casts
WBC casts
fatty casts
granular casts
RBC: proliferative glomerulonephritis
WBC: pyelonephritis or interstitial nephritis
fatty: diseases with proteinuria
granular: parenchymal diseases
What are casts?
cylindrical protein structures made in the tubules
issue: not always indicative of a problem
if theres cells in the cast (WBC or RBC)=pathological
What is an AKI?
a sudden decline in renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)
How can we classify AKI?
anuric
-less than 50 ml/day urine output
oliguric
-less than 500 ml/day urine output
non-oliguric
-greater than 500 ml/day urine output
What do all staging systems use for diagnostic criteria of AKI?
SCr and urine output
What are the typical timelines for the changes in SCr and urine output due to AKI?
SCr: may take up to 4 days before seeing an elevation
urine output: decrease is seen earlier but is non-specific
Why do we need to know a patients baseline SCr in the context of AKI?
all criteria based on detecting changes in SCr
What is the clinical presentation of AKI?
most patients are asymptomatic
-diagnosed based on lab criteria (increased SCr, BUN)
~50% are oliguric
may present with:
-signs and symptoms of dehydration (pre-renal)
-malaise, anorexia, N/V, pruritis (uremia)
-severe abdominal or flank pain (kidney stone?)
-decreased force of urine stream (obstruction)
-cola coloured urine (blood?)
-excessive foaming of urine (protein in urine)
-sudden weight gain, edema
What are the risk factors for AKI?
anything that decreases blood flow to the kidneys
pre-existing renal dysfunction
drugs account for ~20% of cases
How do we typically classify the cause of AKI?
based on the location of the problem
1. pre-renal (blood supply)
2. intra-renal or intrinsic (tubules, glomerulus, interstitium, vasculature)
3. post-renal (collecting tubule, ureter, bladder, urethra)
What is the most common cause of AKI?
pre-renal AKI
aka prerenal azotemia
Describe pre-renal AKI.
kidney not getting adequate blood supply to filter the blood
-hypoperfusion
kidneys themselves are healthy
What are some potential causes of decreased renal perfusion which could cause pre-renal AKI?
intravascular volume depletion
-hemorrhage, dehydration, burns, diuretics
decreased effective circulating volume
-HF, cirrhosis
hypotension
-vasodilators, septic shock
decreased glomerular filtration pressure
-ACEI/ARBs, NSAIDs
How does intrinsic AKI occur?
from direct damage to the kidneys
-due to ischemia, toxins, or disease
What are the four main types of intrinsic AKI?
- acute tubular necrosis
-endogenous (myoglobin) or exogenous (aminoglycosides), ischemia - acute interstitial nephritis
-idiopathic hypersensitivity immune reaction to drugs, infection - acute glomerulonephritis
-post strep antigen-antibody complexes - vascular kidney injury
-renal artery stenosis, HTN
Which type of AKI is the least common?
post-renal AKI
-<5% of cases
Describe post-renal AKI.
obstruction to urinary flow anywhere in the urinary tract
-urethral obstruction
-ureter obstruction
-bladder neck obstruction
What are the causes of post-renal AKI?
nephrolithiasis (kidney stones)
prostate enlargement
cervical cancer tumors
drugs that crystallize (sulfonamides, acyclovir, MTX)
What are the components in the diagnosis of AKI?
history
laboratory data
urinary sodium concentration (FEna)
urinalysis
others: renal ultrasound, biopsy
What are the expected lab values for a patient with an AKI?
increased SCr
increased BUN
acidosis
hyperkalemia
Why do changes in SCr lag behind the decrease in kidney function due to AKI?
slow accumulation, increased tubular secretion, and increased extra-renal clearance
What is FEna?
fractional excretion of sodium
-% sodium filtered by the kidneys that is excreted in urine
-not specific to kidney damage (affected by other factors)
When would you see FEna decrease? What about increase?
decrease: pre-renal AKI
increased: tubular damage
What are the goals of therapy for an AKI?
prevent further renal injury
minimize extra-renal complications
facilitate recovery of renal function back to baseline
What is the treatment of pre-renal AKI?
hydration with IV fluids if hypovolemic
-stop diuretics
BP support with vasopressors (dopamine, norepinephrine, vasopressin)
fluid removal in volume overload states with diuretics
stop/hold drugs that impair kidney function/urine flow
What is the treatment of intrinsic renal AKI?
discontinue offending agent
manage underlying autoimmune disease
What is the treatment of post-renal AKI?
catheter to restore urine flow
identify and remove obstruction
adequate hydration when giving drugs with potential to crystallize
What is the normal range for potassium?
3.5-5mmol/L
What is the primary route of potassium elimination?
kidney
-increased serum K+ seen with AKI and CKD
What is the potassium range for mild-moderate hyperkalemia?
5.1-7mmol/L
What is the potassium range for severe hyperkalemia?
> 7mmol/L
What is the treatment for mild hyperkalemia due to AKI?
may not require therapy or can use Kayexalate (sodium polystyrene sulfonate)
-delayed onset of effect (1hr)
-15 to 60g po BID-QID until K+ normalizes
furosemide IV to increase urinary excretion
What is the treatment for severe hyperkalemia due to AKI?
medical emergency
calcium gluconate to stabilize myocardium
to drive K+ into cells:
-rapid acting/regular insulin +/- glucose
-sodium bicarbonate IV infusion (if metabolic acidosis)
-salbutamol via nebulizer (if pulmonary congestion)
kayexalate
if refractory: dialysis
What is the management of fluid overload due to AKI?
diuretics
-furosemide +/- metolazone
What is the management of metabolic acidosis due to AKI?
sodium bicarbonate IV
When do we dialyze in AKI?
AEIOU
acidosis
electrolyte abnormalities (hyperkalemia)
toxic ingestions
fluid overload
uremia
