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77 Cards in this Set

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  • Back
-Stable concentration in plasma
-freely filtered at the glomerulus
-not reabsorbed, secreted, synthesized or metabolized by the kidney
-can be easily measured using calorimetric assays
Characteristics of an ideal marker for renal clearance
the amount filtered at the glomerulus...
is equal to the amount excreted in urine
-gold standard test for assessment of GFR
-an artificial carbohydrate that must be infused
Inulin clearance
Inulin is a ______________ not normally present in the body
Inulin clearance is considered impractical b/c?
the infusion must progress for an extended period of time to establish a constant plasma level
Inulin clearance is the gold standard becuase
what goes in, goes out
the most commonly used solute to calculate GFR in the lab
creatinine clearance is overestimated by
97-137 ml/min/1.73 m^2
creatinine clearance reference range for males
88-128 ml/min/1.73m^2
creatinine clearance reference range for females
by the time you see low creatinine clearance...
there is already a substantial amount of renal damage
were more concerned about low clearance than high clearance b/c
it is a sign of renal disease
Decreses with:
- decreased RPF
-clogged basement membrance
-chronic renal disease
GFR or CrCl
-does not require timed urine collection
-helpful in early detection of chronic kidney disease
Esitmated GFR (eGFR)
Used to monitor and assess renal function
NPN compounds
Arise from the breakdown of proteins and nucleic acids and include:
-uric acid
-amino acids
NPN compounds
Is not a marker for renal disease, but can give an idea of how GFR is going. IS a marker for liver disease
elevated level of NPN compounds in blood
-Major excretory product of urine metabolism
-Synthesized in liver from CO2 and ammonia arising from deamination of amino acids
-Freely filtered (MW=60D), 40-60% is reabsorbed and the rest is excreted by kidneys
Serum urea is reported as...
BUN (blood urea-nitrogen)
measurement of urea alone _____ a useful indicator of renal function
-small amounts also secreted through GI tract and skin
the first thing to increase in dehydration
In analytical methods of urea the first step involves
the hydrolysis of urea by urease and production of NH4
the second steps in analytical methods of urea can involve
quantitaion of ammonium ion by enzymatic method
Interference in anlytical methods of urea include? (2)
-citrate and flouride( inhibit urease)
-increased ammonium ion concentration
6-20 mg/dL ; 10:1 to 20:1
BUN reference range in Urea analytical methods
What two tube tops do we not use in Urea analytical method?
no blue top or grey top
very high plasma urea concentration accompanied by renal failure
Decreased renal blood flow (CHF, dehydration)
prerenal azotemia
Intrinsic renal faliure (acute or chronic)-->decreased renal function
renal azotemia
obstruction in the urinary system(causes very high creatinine)
post renal azotemia
seen in:
-decreased protien intake
-liver disease
-severe diarrhea and vomitting
decreased urea concentration
synthesized in liver from the breakdown of nucleic acids (DNA and RNA) and transported to the kidney
uric acid
Most is reabsorbed, rest is excreted by kidneys (most) and GI tract
Uric acid
present in plasma and monosodium urate
Uric acid
At >6.4 mg/dL, plasma is saturated with
urate crystals and may also precipitate in the tissues
3.5-7.2 mg/dLmale
2.6-6.0 mg/dLfemale
Uric acid reference range
-uric acid is oxidized to allantoin(water soluble product) and phosphotungstic acid is reduced to tungsten blue
-sodium carbonate provides the alkaline medium necessary for color development
Phosphotungstic method for uric acid
uric acid is oxidized to allantoin by the enzyme uricase and differential absorbance is measured
Uricase method for Uric acid
In analytical methods for uric acid, samples must be
either serum, plasma, or urine
-caused by overproduction or underexcretion of uric acid
-increased catabolism of nucleic acid,purine rich diet=overproduction of uric acid
-renal disease= under excretion
Uncommon, secondary to other conditions
occurs when uric acid is so elecated (>6 mg/dL) it precipitates our of solution in plasma
caused by overproduction of uric acid, purine rich diet, drugs or alcohol
occurs primarily between 30-50 years of age
-MSU crystals deposit in joints and soft tissue causing pain and inflammation.
-In sever cases, deposits of urates called tophi form in tissues surrounding the joints, causing deformities
Gouty arthritis
-may be accompanied by uric acid stones in urinary tract
-to fix crsytals the pH of the body must be adjusted
Formed in the GI tract by the deamination of amino acids
-normally metabolized by the liver to produce urea
- At physiologic pH, exists in the blood as NH4
Increase in plasma oH shifts the ammonia equilibrium to the right, resulting in
increased NH3 concentration
Increased blood ammonia levels
Seen in:
-sever liver disease- not metabolized
-reye's syndrome
-renal disease
-inherited deficiency of the urea cycle enzymes
Two analytical methods for ammonia
-coupled enzymatic method
-ammonia ISE method
-whole blood or plasma- immeadiately on ice and centrifuged in refrigerated centrifuge
-anticoagulants-EDTA or heparin
-centrifuge samples at refrigerated temperature and assay ASAP(w/in 20 mins)
samples for analytic methods of ammonia
sources of error in analytic methods of ammonia
-cigarette smoking by the patient
-ammonia in detergerents, reagents, water and glassware
low molecular weight cysteine protease inhibitor protein produced by all nucleated cells
Cystatin C
-freely filtered by glomerulus, reabsorbed and catabolized (rapidly) byt PCT
-produced and removed at a constant rate
Cystatin C
-Increased levels in serum indicates impaired renal function
Cystatin C
-rise can be measurable before increase in creatinine or decrease in GFR
-correlates with decreased GFR
-does not depend on age, muscle mass, etc.
Increases serum Cystatin C
-Creatinine Clearance
-Total protein
-uric acid
-cystatin C
Commonly used kidney function test
-sudden sharp decline in renal function as a result of acute toxic or hypoxic insult to the kidneys
-GFR is reduced to <10 ml/min.
Acute Renal Failure
-gradual decline in renal function over time
-occurs in five stages
Chronic renal failure or kidney disease
-kidney damage with normal or not equal GFR
-GFR >90 mL/min/1.73m^2
stage one of chronic kidney disease stages
-kidney damage with normal or decreased GFR
-GFR= 60-89 mL/min./1.73m^2
Stage two of chronic kidney disease stage
-kidney damage with moderate decreased GFR
-GFR=30-59 mL/min/1.73m^2
stage three of chronic kidney disease
-kidney damage with severely decreased GFR
- GFR=15-29 mL/min/1.73m^2
Stage four of chronic kidney disease
-kidney failure
-GFR= <15mL/min/1.73m^2
Stage final of chronic kidney disease
-failure of kidneys to maintain its basic functions
-caused by a variety of intrinsic renal problems like hypertension, lupus or nephrotoxicity
End stage renal disease
-weakness, tremors, loss of appetite, metabolic axidosis

Lab findings:
-Increased BUN and serum creatinine
-Decreased GFR(~5 mL/min)
-Increased serum phosphorus and potassium
-decreased serum calcium
-Increased BP
End stage renal disease
-injury to glomerular tissue by immune complexes formed with bete hemolytic strep.
-Lab findings:
hematuria, proteinuria, reduced GFR, increased sodium, and hypertension
Acute glomerulonephritis
-loss of nephron mass over a prolonged period of time
-Lab findings: same as acute, except slight hematuria and proteinuria
Chronic glomerulonephritis
-Increased permeability of the glomerular basement membrane induced by disorders like diabetes mellitus, lupus,etc.
Nephrotic syndrome
Lab findings:
-hyperproteinemia, hypoproteinemia,(hypoalbuminemia), azotemia, hyperlipidemia, lipiduria
-Symptoms: edema
Nephrotic syndrome
-Acute and non- infectious pyelonephritis
tubular disease
-decreased excretion/reabsorption of certain substances or reduced urinary concentrating ability (caused by drug toxicity, GNB, etc.)
-Lab findings: decreased GFR, acidosis (decreased H+ secretion)
Tubular disease