Clin Chem Exam 3 Renal Physiology, Npn Compounds & Renal Disease Ii

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-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

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Characteristics of an ideal marker for renal clearance

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the amount filtered at the glomerulus...

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is equal to the amount excreted in urine

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-gold standard test for assessment of GFR
-an artificial carbohydrate that must be infused

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Inulin clearance

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Inulin is a ______________ not normally present in the body

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fructo-polysaccharide

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Inulin clearance is considered impractical b/c?

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the infusion must progress for an extended period of time to establish a constant plasma level

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Inulin clearance is the gold standard becuase

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what goes in, goes out

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the most commonly used solute to calculate GFR in the lab

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creatinine

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creatinine clearance is overestimated by

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10%

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97-137 ml/min/1.73 m^2

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creatinine clearance reference range for males

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88-128 ml/min/1.73m^2

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creatinine clearance reference range for females

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by the time you see low creatinine clearance...

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there is already a substantial amount of renal damage

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were more concerned about low clearance than high clearance b/c

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it is a sign of renal disease

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Decreses with:
- decreased RPF
-clogged basement membrance
-chronic renal disease
-age

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GFR or CrCl

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-does not require timed urine collection
-helpful in early detection of chronic kidney disease

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Esitmated GFR (eGFR)

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Used to monitor and assess renal function

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NPN compounds

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Arise from the breakdown of proteins and nucleic acids and include:
-urea
-creatinine
-creatine
-uric acid
-ammonia
-amino acids

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NPN compounds

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Is not a marker for renal disease, but can give an idea of how GFR is going. IS a marker for liver disease

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ammonia

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elevated level of NPN compounds in blood

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Azotemia

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-Major excretory product of urine metabolism
-Synthesized in liver from CO2 and ammonia arising from deamination of amino acids

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Urea

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-Freely filtered (MW=60D), 40-60% is reabsorbed and the rest is excreted by kidneys

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Urea

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Serum urea is reported as...

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BUN (blood urea-nitrogen)

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measurement of urea alone _____ a useful indicator of renal function

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urea

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-small amounts also secreted through GI tract and skin

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Urea

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the first thing to increase in dehydration

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Urea

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In analytical methods of urea the first step involves

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the hydrolysis of urea by urease and production of NH4

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the second steps in analytical methods of urea can involve

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quantitaion of ammonium ion by enzymatic method

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Interference in anlytical methods of urea include? (2)

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-citrate and flouride( inhibit urease)
-increased ammonium ion concentration

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6-20 mg/dL ; 10:1 to 20:1

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BUN reference range in Urea analytical methods

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What two tube tops do we not use in Urea analytical method?

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no blue top or grey top

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very high plasma urea concentration accompanied by renal failure

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uremia

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Decreased renal blood flow (CHF, dehydration)

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prerenal azotemia

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Intrinsic renal faliure (acute or chronic)-->decreased renal function

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renal azotemia

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obstruction in the urinary system(causes very high creatinine)

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post renal azotemia

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seen in:
-decreased protien intake
-liver disease
-severe diarrhea and vomitting
-pregnancy

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decreased urea concentration

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synthesized in liver from the breakdown of nucleic acids (DNA and RNA) and transported to the kidney

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uric acid

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Most is reabsorbed, rest is excreted by kidneys (most) and GI tract

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Uric acid

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present in plasma and monosodium urate

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Uric acid

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At >6.4 mg/dL, plasma is saturated with

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urate crystals and may also precipitate in the tissues

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3.5-7.2 mg/dLmale
2.6-6.0 mg/dLfemale

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Uric acid reference range

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-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

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Phosphotungstic method for uric acid

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uric acid is oxidized to allantoin by the enzyme uricase and differential absorbance is measured

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Uricase method for Uric acid

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In analytical methods for uric acid, samples must be

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either serum, plasma, or urine

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-caused by overproduction or underexcretion of uric acid
-increased catabolism of nucleic acid,purine rich diet=overproduction of uric acid
-renal disease= under excretion

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hyperuricemia

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Uncommon, secondary to other conditions

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hypouricemia

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occurs when uric acid is so elecated (>6 mg/dL) it precipitates our of solution in plasma

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Gout

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caused by overproduction of uric acid, purine rich diet, drugs or alcohol

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Gout

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occurs primarily between 30-50 years of age

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Gout

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-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

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Gouty arthritis

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-may be accompanied by uric acid stones in urinary tract
-to fix crsytals the pH of the body must be adjusted

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Gout

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Formed in the GI tract by the deamination of amino acids

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Ammonia

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-normally metabolized by the liver to produce urea
- At physiologic pH, exists in the blood as NH4

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ammonia

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Increase in plasma oH shifts the ammonia equilibrium to the right, resulting in

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increased NH3 concentration

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Increased blood ammonia levels

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hyperammonia

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Seen in:
-sever liver disease- not metabolized
-reye's syndrome
-renal disease
-inherited deficiency of the urea cycle enzymes

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Hyperammonemia

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Two analytical methods for ammonia

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-coupled enzymatic method
-ammonia ISE method

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-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)

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samples for analytic methods of ammonia

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sources of error in analytic methods of ammonia

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-hemolysis
-cigarette smoking by the patient
-ammonia in detergerents, reagents, water and glassware
-drugs

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low molecular weight cysteine protease inhibitor protein produced by all nucleated cells

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Cystatin C

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-freely filtered by glomerulus, reabsorbed and catabolized (rapidly) byt PCT
-produced and removed at a constant rate

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Cystatin C

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-Increased levels in serum indicates impaired renal function

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Cystatin C

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-rise can be measurable before increase in creatinine or decrease in GFR
-correlates with decreased GFR
-does not depend on age, muscle mass, etc.

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Increases serum Cystatin C

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Tests:
-creatinine
- BUN
-Creatinine Clearance
-Total protein
-uric acid
-cystatin C
-osmolality
-electrolytes

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Commonly used kidney function test

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-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.

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Acute Renal Failure

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-gradual decline in renal function over time
-occurs in five stages

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Chronic renal failure or kidney disease

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Stage:
-kidney damage with normal or not equal GFR
-GFR >90 mL/min/1.73m^2

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stage one of chronic kidney disease stages

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-kidney damage with normal or decreased GFR
-GFR= 60-89 mL/min./1.73m^2

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Stage two of chronic kidney disease stage

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-kidney damage with moderate decreased GFR
-GFR=30-59 mL/min/1.73m^2

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stage three of chronic kidney disease

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-kidney damage with severely decreased GFR
- GFR=15-29 mL/min/1.73m^2

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Stage four of chronic kidney disease

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-kidney failure
-GFR= <15mL/min/1.73m^2

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Stage final of chronic kidney disease

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-failure of kidneys to maintain its basic functions
-caused by a variety of intrinsic renal problems like hypertension, lupus or nephrotoxicity

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End stage renal disease

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Symptoms:
-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

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End stage renal disease

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-injury to glomerular tissue by immune complexes formed with bete hemolytic strep.
-Lab findings:
hematuria, proteinuria, reduced GFR, increased sodium, and hypertension

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Acute glomerulonephritis

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-loss of nephron mass over a prolonged period of time
-Lab findings: same as acute, except slight hematuria and proteinuria

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Chronic glomerulonephritis

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-Increased permeability of the glomerular basement membrane induced by disorders like diabetes mellitus, lupus,etc.

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Nephrotic syndrome

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Lab findings:
-hyperproteinemia, hypoproteinemia,(hypoalbuminemia), azotemia, hyperlipidemia, lipiduria
-Symptoms: edema

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Nephrotic syndrome

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-Acute and non- infectious pyelonephritis

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tubular disease

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-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)

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Tubular disease