Kidney Function Testing

FUNCTIONS OF THE KIDNEYS1

1) Excretory function:
Serves to rid the body of most of the undesirable end products of metabolism as well as any
excess of inorganic substances ingested in the diet. e.g.
o Non protein nitrogenous compounds
o Organic acids
o Electrolytes e.g. Na, K, Cl
2) Regulatory function:
The mechanisms of differential reabsorption and secretion, located in the tubules of a
nephron, are the effectors of regulation
85% of filtered bicarbonate
60-70% of filtered Na, K and H2O
Reabsorption 75% of filtered Ca
Most amino acids
PCT
All glucose
Uric acid
Secretion Phenosulfonphthaline (PSP)
Creatinine
20-25% of filtered Na, K without H2O
Loop of Henle Reabsorption
Active transport of Cl- followed by Na

Reabsorption 10% Na+ coupled by H + and K+

DCT
Secretion H+ to generate NH4

Reabsorption H2O (ADH)

Collecting tubules

3) Water homeostasis:
Approximately:
70% of H2O of tubular fluid is
reabsorbed in PCT
5% in loop of Henle
10% in DCT
Remainder in the collecting
ducts

Countercurrent multiplier system:

The mechanism through which a large
osmolal gradient is established in the
interstitial tissue between the
corticomedullary junction and the tips of
renal papilli.
The system is lost in renal failure.

‫ منال‬.‫د‬.‫ محاضرة أ‬1

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 Kidney Function Testing

4) Acid-Base homeostasis: Kidney normally works to retain bicarbonate and loose H through:
Phosphate buffer (monohydrogen  dihydrogen)
Ammonia
Loss of undissociated acid
CO2+H2O

CA
- +
HCO3 H + HCO3 H
Na Na Na2 HPO4

Glutamine NaH2 PO4 NB:

NH4 NH3 + - HA
H A - Na-H exchange is energy
(undissociated)
Glutamate dependent process

NH4 A + +
NH4 NH3 - K competes H in Na-H exchange
α ketoglutarate in case of high intracellular K
Plasma & Glomerular Filtrate
Tubular Cell
interstitial Fluid
5) Endocrine function:
1ry production of erythropoietin, renin and prostaglandin
2ry activation of vit D by 1, 25 dihydroxycholecalciferol

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 Kidney Function Testing

Renal Monitoring
1) Clearance of various compounds: to estimate GFR and ERPF
2) Assessment of glomerular permeability: by determining the type of protein in urine.
3) Measurement of non-protein nitrogenous compounds.
4) Measurement of the concentrating ability of tubules.
5) Testing for acid-base disorders.
6) Other tests of renal significance.
1) Renal clearance:
Definition: Clearance of a substance is the theoretical amount of blood that is cleared from this
substance by the kidney.
- Specification: completely filtered by glomeruli, not reabsorbed or excreted by tubules.
- Reference substance is inulin
- Radioisotopic measurement: using Tc DTTA (Diethylene triamine penta-acetic acid). Value in
split renal function test.
- Effective renal plasma flow (ERPF): is a measurement of tubular secretory function combined
with GFR estimated by 131I-labeled hippuran.
- Non-radio labeled measurement:
GFR → by creatinine clearance
ERPF → by para amino hippuric acid.
???? use of urea, β2 microglobulin, RBP, α1 microglobulin in???
Creatinine Clearance:
Procedure:
- Hydrate the patient at least 600ml H 2O
- Withhold tea, coffee, drugs on the day of the test.
- Proper collection, ensure urine flow rate 1-2 ml/min: Begin with empty bladder at
specific hour and collect bladder urine at that hour next day.
- In lab, measure the precise volume, time
- Calculation UxV 1.73
X
P A
Sources of error:
- Error in recording the time, loos of portion of urine e.g. urine retention.
- Vigorous exercise.
- Low hydration.
Reference interval:
♀ 88-128 mL/min
♂ 97-137 mL/min
Estimation of creatinine clearance from plasma creatinine level:
- Applying Siersbæk – Nielsen nomogram: Interplotation between s. creatinine, age and
weight and then extrapolate to get the clearance.
Limitations:
 Potential obesity error
 Random error in plasma creatinine measurement.
- Applying Cockcroft and Gault algorithms: ‫للحفظ‬
140- age (yrs.) X 2.12 X weight (kg) X K(0.85)
s. creatinine X BSA (m2)
- Recently, cystatin C proved to be a better estimate of GFR.

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 Kidney Function Testing

NB: To calculate the reference interval of creatinine clearance for every individual depend on
weight (Kg), urinary and plasma creatinine.
Urine creat. (mg/Kg/day) X wt. (Kg) X 100
s. creat. (mg/dL) X 1440

2) Glomerular permeability:
Glomerular membrane is designated to restrict passage of protein molecules over 15000 D
Normal protein excretion in urine is less than 150mg/d.
Source of protein in urine:
- Tam Horsfall protein from epithelial cells of DT.
- Urokinase from tubular cells.
- Secretory protein A from epithelial cells of T cell basemen membrane protein.
Types of proteinuria:
I. Intermittent proteinuria:
- Benign transient: in young children → disappears.
- Functional: excess proteinuria without renal disease e.g. febrile illness, exercise, …
- Postural or orthostatic: glomerular in origin.
II. Persistent proteinuria:
Pre-renal (overload) e.g. hemoglobinuria, light chain proteinuria.
Renal:
Glomerular →
Tubular →
Post renal: caused by inflammatory or degenerative lesions of renal pelvis, ureter, bladder, …
Glomerular proteinuria:
Measurement of total protein in urine
Urine protein electrophoresis
Measure of selectivity:
IgG clearance
(N: <0.16)
Albumin clearance

IgG clearance
(N: <0.2)
Transferrin clearance

U.T. protein (N: <0.2)

U. creatinine (>3.5 suggestive of nephrotic syndrome)

Urinary albumin
(N: <0.01) (In random sample)
U. creatinine

Albumin Clearance
Permeability index = (N: <0.001)(0.005 in nephrotic)
Creatinine Clearance
Microalbuminuria:
Definition: Albumin concentration above normal but still below the detection of
conventional dipstick test when albumin excretion rate between 20-200 μg/min (30-
300mg/24h urine).
Nil Microalbuminuria  Macroalbuminuria
30 mg/day 300 mg/day

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 Kidney Function Testing

Importance: Early prediction of renal impairment occurs in 30-40% of type I DM.

Results are expressed as:
- as mg/day (N<15mg/day)
- as albumin excretion rate μg/min (N<10μg/min).
- albumin / creatinine ratio (N <0.01).
Reference interval of urinary albumin excretion:
μg/min mg/d Ratio
Normal <10 <15 <0.01
IDDM 20-200 30-300 0.02-0.2
Diabetic nephropathy >200 >300 >0.2
Tubular Proteinuria:
Includes all urinary proteins < 40KD.
Markers of tubular proteinuria:
1. β2 microglobulin (11.8KD) 2. α1 microglobulin (25-33KD)
Production all nucleated cells. Liver
Role of kidney 95% freely filtered by the glomeruli, Freely filtered by the glomeruli,
reabsorbed and catabolized by PCT reabsorbed and catabolized by PCT.
Forms 2 forms:
a. Bound to albumin and IgA (95%)
b. Free (5%).
Causes of 1. Malignancies e.g. MM, lymphoma, Old age,
increase CLL, Hepatoma
2. Autoimmune diseases e.g. SLE, liver
diseases,
3. Chronic inflammations,
↓ in severe liver impairment.
Stability Unstable in acidic urine  Needs Advantage: Stable in urine.
alkalinization
3. Lysozyme (MW 15KD)
- Lysozymuria is an indicator of PCT dysfunction.
- Considered as an early predictor of tubular dysfunction.
Llysozyme clearance
- Fractional excretion of lysozyme=
Creatinine clearance
4. Retinol Binding Protein (MW 21KD)
- Synthesized by liver.
- Considered as an indicator of PCT dysfunction.
- ↑ in normal pregnancy
- ↓ in:
 Chronic liver disease
 Malnutrition
 Zinc deficiency.
- Considered as a reliable marker due to slow degradation and more stable.
5. NB: N-acetyl β-D-Glucosaminidase (NAG):
Is considered as marker of tubular function although its mol. Wt. =140KD.
Present in two forms:
A (acidic) B (basic)
As → in serum , CSF. I → intermediate isoenzyme in livo?? Ser??
At → tissue e.g. kidney, liver, urine P → pregnant serum

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 Kidney Function Testing

- Urinary NAG is of tubular origin

Urine A: B ratio 10:1
Increased in:
- Diabetic patients with complications
- Glomerulonephritis, urinary tract infection (B form).
Questions
Which RFT to use for diabetic nephropathy?
The disease attacks the glomeruli  Microalbuminuria
However, diabetes was found to affect also the tubules.
Which RFT to use for SLE?
Tests for glomeruli
Which RFT to use for lead poisoning?
Tests for tubules

Enzymuria
Sources of urinary enzymes:
 Synthesis by the tubules.
 Altered membrane permeability
 Exfoliation of tubular cells.
 Impaired tubular reabsorption.
- Important enzymes in urine:
Lysozomal NAG β glucoronidase galactosidase
Brush border ALP GTT ALT
Cytosolic ALT LDH
Mitochondrial AST
- Expression:
Enz. Activity IU/L
 Random sample
u. creat mg/L

 Timed sample Enz. Activity IU/L

GFR
Usefulness in renal diseases:
1. Acute renal injury Brush border enzymes Intestinal fraction of ALP
2. Chronic renal injury Lysozomal enzyme (NAG)
3. UTI LD5 β-NAG
4. Mitochondrial AST
5. Renal transplant Successful transplant enzymuria 3-5 days
monitoring Rejection a. Acute  NAG
A/B ratio
I, cI2 form
 Int. ALP (S3 of PCT)
b. Functionless ↑ lysozomal enz.
transplant or ↑ LDH
ATN ↓ brush border enz.

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 Kidney Function Testing

3) Measurement of non-protein nitrogenous compounds2

- Catabolism of protein and nucleic acids results in formation of NPN
- Urinary nitrogenous metabolites include:
A. Urea 55-90%
B. Creatinine 2-3%
C. Uric acid 1-1.5%
D. Amino acids <1%
E. Ammonia 10-20%
Urea
- Synthesized in liver
- >90% excreted through the kidney, neither reabsorbed nor secreted by tubules but freely
filtered by glomeruli
- About 40-70% urea moves back into the blood = highly diffusible. Hence low estimation of
GFR.
- Moreover, the influence of non-renal variables as diet and hepatic synthesis (?? Usefulness
in GFR).
- The main value in BUN/creatinine ratio (N12-16)
↑ ratio
With N creat With ↑ creat
- Prerenal azotemia e.g. - Postrenal azotemia e.g.
Heart failure Nephrolithiasis
Massive hge Prostatism
Plasma loss in burns Tumors of genitourinary tract
Loss of ECF in cardiac surg. - Prerenal azotemia superimposed
Pyloric stenosis on renal dis.
Acute pancreatitis NB: ↑ in both urea and creatinine
Intestinal obstruction but more rise of urea due to
- ↑ protein in diet obstruction ….. more back diffusion
- ↑ protein metabolism
- GIT Hge…. Reab. Of bl. Proteins

↓ ratio
With ↓ BUN With ↑ creat
- ↓ protein intake - Acute tubular necrosis
- Severe liver disease - Chronic interstitial nephritis
- Starvation - Dialysis (urea is more diffusible
than creat and thus corrected by
dialysis faster)
Uric acid
- Major product of purine nucleosides catabolism.
- Renal handling:
 glomerular filtration
 reabsorption in PCT 98-100%
 secretion into distal portion of PCT

2
Note: Uric acid, creatinine or urea usually come in written exams

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 Kidney Function Testing

 Further reabsorption in DCT.

 Net urinary excretion 6-12% of the filtered amount.
Hyperuricemia Hypouricemia
1. Essential hyperuricemia (1ry) 1. Severe liver diseases
 Overproduction 2. ↓ tubular reabsorption:
 Under excretion  Congenital: Fanconi syndrome.
Secondary causes:  Acquired:
2. Renal retention: Over ttt with uricosuric drugs.
 Renal failure Chemotherapy e.g. 6 mercaptopurine
 Drugs e.g. diuretics, salicylates. which inhibit purine synthesis
 Organic aciduria: acetoacetate, 3. Bronchogenic carcinoma
lactate due to interference with urate 4. NHL
tubular secretion
 Poisons: Lead, alcohol.
 Endocrinopathies:
hyperparathyroidism
3. Increased turnover of nucleic acids:
 Myeloproliferative syndromes.
 Chemotherapy of malignant tumors
4. Specific enzyme defects:
Deficiency of HGPRT enzyme
(Hypoxanthine-guanine phosphoribosyl-
transferase): Complete or partial.
Diagnosis of hyperuricemia:
Hyperuricemia >7mg/dL ♂
>6mg/dL ♀
Urinary uric acid <600 mg/dL Uricosuric drugs (probenicid)
>600 mg/dL Inhibitors of Purine synth (allopurinol).
uric acid / creatinine Ratio in urine >1

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 Kidney Function Testing

4) Assessment of the concentrating ability of the tubules

A. Specific gravity:
Definition: It is the ratio of the weight of a substance to the weight of equal volume of water
(relative density).
Measurement:
 By refractometer, urinometer
 Correction:
 by Glucose (glucose 1g  SpG by 4), protein (protein 1g  SpG by 4)
 by temperature (3oC SpG by 1)
Reference Range:
 N in 24 hr urine = 1015 -1025
 Morning sample > 1023
Abnormal level:
 Low fixed sp.G = 1010 in CRF
B. Osmolality:
 Better than Sp.G.
Urine Range: 50-1200 mosm/Kg
Random sample: 300-900 mosm/Kg
After 12 H2O restriction: 850-1200 mosm/Kg
Serum Osmotic limits: 230-490 mosm/Kg
Ref. range: 278-298 mosm/Kg

Urine osmolality N in random sample → 1-3

 Ratio of
Serum osmolality After 12h restriction  3-4.??
↓ in tubular defect, diabetes insipidus (0.2-0.7)
Serum Na
 Ratio of N→ 0.43-0.5
Serum osmolality
↓ in acute toxicity of drugs (e.g. salicylates) due to increased s. osmolality with normal
Na → according to extent of this lowering dialysis is needed.
Normal ratio in dehydration due to ↑↑ in both analytes.
 Osmolal clearance: Means the volume of urine that is required for isoosmolal clearance
of solute load
U osm X V (ml/min)
Osmolal clearance
P osm
Measurement: by osmometer: measures the depression of freezing point  the more the
solutes, the more the depression in freezing point relative to control.
C. Free water clearance
Means hypothetical rate at which water is excreted during production of hypotonic urine in
excess of that required for excretion of solute load in isoosmolal urine
CH2O = V - Cosm
- Negative free water clearance means rate at which water is reabsorbed from tubular
fluid during the production of hypertonic urine
TCH2O = Cosm - V

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 Kidney Function Testing

D. Fractional excretion of Na:

Urinary Na/ serum Na
Fr ex Na (%) = X100 (N 1-1.5%)
Urinary Creat / serum creat
- Renal failure index:
Urinary Na
RFI (N 1-3 mmol/L)
Urinary creat / serum creat
Application: DD of acute tubular necrosis (ATN) and prerenal azotemia:
ATN (Acute tubular necrosis) PRA (Prerenal azotemia)
Caused by ischemia, nephrotoxicity to decreased kidney perfusion.
tubules Intact tubules which can absorb Na
Main defect ↓reabsorption of Na → ↑ urinary problem is just to give fluid, if no fluid
Na given  renal azotemia
urine output ↑→ defect in conc. ability → U ↓
osmolal. 300-350 mosm/Kg
BUN/creat ratio ↓ <10 ↑ >20
U/P urea ↓ <3 ↑ >8
U/P creatinine ↓ <20 ↑ >40
U/P osmolality ↓ <1 ↑ >3
U osmolality ↓ <350 mosm/Kg ↑ >500 mosm/Kg
Urine Na ↑ >40 mEq/L ↓ <20 mEq/L
Fr ex Na ↑ >1.5 ↓ <1
RFI ↑ >3 mmol/L ↓ <1 mmol/L
Tc H2O ↓ ↑
Diseases associated with disturbances in the renal concentrating mechanism → polyuria
Marked polyuria Moderate polyuria
hypotonic urine after water deprivation inability to produce hypertonic urine
- Diabetes insipidus - Hypercalcemia
- Hereditary nephrogenic diabetes insipidus - Hypokalemia
- Chronic lithium toxicity - Chronic pyelonephritis
- Sickle cell nephropathy - End-stage renal disease
- Amyloidosis
- Interstitial nephritis

DI Neph. DI Hysterical
Plasma osmolal. >290 mosm/Kg >290 <275
Urine osmolal. <600 mosm/Kg <600 <600
Sp.G <1018 <1018 <1018
H2O deprivation leads to:
- Urine osmolal. <200 mosm/Kg <200 >800
- Sp. G. Low fixed 1010 1010 >1020
- Urine output Persistence of polyuria Polyuria Oliguria
Vasopressin test leads to:
- Urine osmolal. ↑ No effect ↑
- Sp. G. ↑ No effect ↑
- Urine output Oliguria No effect Oliguria
- Thirst Stopped No effect Continues

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 Kidney Function Testing

E. Testing of acid – base disturbances

- Urine :
 pH
 Renal excretion of NH4+
Urinary HCO3-/ Plasma HCO3-
 Fractional excretion of bicarb (%) = X100 (N 3-5)
Urinary Creat / plasma creat
 Measurement of dissolved CO2 after alkaline load (bicarbonate)
 Measurement of pH after acid load (NH 4Cl)
 Measurement of K level after Na sulfate intake.
- Plasma:
 Cl-
 Ca
 Na
 P(i)
 K
NB: Action of NaSO4 is to increase Na-H exchange. So, no K-H exchange
↑ K & H in urine (normal response).
Application: Diagnosis of RENAL TUBULAR ACIDOSIS.
Characterised by:
- Hyperchloremia due to ↑ reabsorption as a result of concentration of extracellular
volume.
- Acidosis with inappropriate loss of HCO3- and ????
- Normal anion gap = (Na+ + K+) – (Cl- + HCO3-)
- Impairment of Na-H exchange → Na wasting.
Types: Proximal RTA (Type II) Distal RTA (Type I)
Distal is still workingbetter than distal type
U pH >5.5 but <5.5 during acidosis >5.5
+ Low at pH>5.5 but normal at pH<5.5 Low
U NH4 Excr.
- Severely impaired Slightly reduced
Reabsorption of HCO3
- >15% >5
(Fr. Exc HCO3 )
Plasma K Low or normal Low
Plasma Cl High High
Plasma Ca Low Low
Plasma P(i) Low Low
CO2 after alk. Load No increase
pH after acid load No change
K after Na2SO4 ↓ H loss, ↑ K loss in urine
Quantity limited variety of RTA
Type III Combined proximal and distal RTA
Type IV Selective aldosterone deficiency:
Plasma K → high (‫)أهم حاجة‬
Urine pH >5.5
Reabsorption Of bicarb → slightly reduced
Plasma Cl- → high
Urine CO2 after alk. Load → increased
NH4 exc. → low
Fr. Ex. HCO3- → low

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 Kidney Function Testing

Dialysis
Definition: A technique used to remove toxic substances in the blood when the kidneys can’t
satisfactorily remove from the circulation.
Types: Either hemodialysis or peritoneal dialysis
Complications:
- Cardiovascular disease
- Hypertension
- β2 microglobulin amyloidosis
- malnutrition
- underdialysis
- dialysis encephalopathy and dialysis dementia
- renal osteodystrophy and hyperparathyroidism.
Assessment of adequacy of renal dialysis:
UKM (= Urea kinetic modeling)
 Urea is uniformly distributed in total body water
 Continually added to the pool of protein metabo??
 Removed continuously by residual renal function intermittently by dialysis following a
first order ???
Application:
Predialysis urea - Postdialysis urea
Urea reduction ratio (URR) = X100
Predialysis urea

>60% if dialysis is adequate

Kt / V = total urea clearance / distribution volume
Ct = C0 X e- Kt/V t= time of dialysis
Where :
K = urea clearance
V= volume of urea distribution
Ct= post dialysis urea
C0= predialysis urea
Calculation of Kt/V is calculated using a computer program provided by the
manufacturer of the dialysis system.

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 Kidney Function Testing

Renal disease and the role of the laboratory

End stage renal disease (ESRD):
→ stages of chronic progressive renal disease
Remaining renal S. Creat (mg/dL) S. urea
function %
Decreased renal reserve 50-75 1-2.5 15-30
Renal insufficiency 25-50 2.5-6 25-60
Renal failure 10-25 5.5-11 55-110
Uremic syndrome (ESRD) 0-10 >8.0 >80
Biochemical characteristics of the uremic syndrome (= CRF) ‫هام جدا‬
1. Retained metabolites
Urea, creatinine and uric acid
2. Fluid, acid-base and electrolyte disturbances
Fixed urine osmolality: lost concentrating ability of tubules.
Hypo or hypernatremia
Hyperchloremia: retention
Hyperphosphatemia
Metabolic acidosis: due to defective excretion of organic acid.
Hypo or hyperkalemia: high due to retention.
Hypocalcemia ( activation of vit D)
Hypermagnesemia: retention
3. CHO intolerance
Insulin resistance → delayed response to glucose loading
4. Lipid metabolic abnormality:
Hypertriglyceridemia ↓ HDL-C
5. Altered endocrinal function:
2ry hyperparathyroidism: prolonged stimulation due to hypocalcemia may lead to tertiary
hyperparathyroidism.
Hypoaldosteronism (hyponatremia + hyperkalemia, which may be changed to hypoK+
hypoNa due to water retention  dilutional)
Altered thyroxin metabolism
Gonadal dysfunction (↑ prolactin, ↑ LH, ↓ testosterone)
Osteomalacia
↓ erythropoietin production

Acute renal failure:

Means abrupt reduction of renal function and subsequent retention of nitrogenous wastes
(azotemia: DD pre renal azotemia vs acute tubular necrosis)
By oliguria reduced GFR in days to weeks
Raised creat. Daily
s.↑ urea, creatinine, K, PO4-, Mg2+
S.↓ Na, Ca, pH
Urine epithelial cells and casts

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 Kidney Function Testing

Glomerular diseases
 Acute Nephritis:
c.c.c. rapid onset of hematuria, proteinuria < 3 g/d, Na & H 2O retention →
hypertension and oedema.
Oliguria
Hematuria and red cells casts.
s.creatinine, urea, K
Na - ASO - antihyalorunidase
C3 (consumptive)→ membranoproliferative GN, SLE
 Rapidly progressive glomerulonephritis (RPGN)
c.c.c. by fulminant clinical course → renal failure in weeks to ???
Types:
Idiopathic:
Type I with Ab against glomerular basement membrane
Type II with immune complex and complement deposition
Type III with (80%) anti-neutrophil cytoplasmic antibodies (ANCA)
2ry  to strept. Infection, endocarditis, SLE, vascular ???
 Chronic glomerulonephritis:
c.c.c. by prolonged downhill course → end in ESRD.
 Nephrotic syndrome:
c.c.c. by heavy proteinuria > 3.5 g/d
hypoalbuminemia <3g/dL
generalized oedema and hyperlipidemia
s:  triglycerides, cholesterol, α2 globulin
↓ IgG
U: Oval fat bodies & lipid casts
↓C3 if underlying GN
Tubular diseases:
 Acute tubular necrosis
 Renal tubular acidosis
 Tubulointerstitial nephritis
c.c.c. by acute stage → leukocytic infiltration of interstitium and tubules with various
mixtures of lymphocytes. Interstitial oedema and scattered foci of tubular necrosis.
Chronic stage → mononuclear cell infiltration with tubular atrophy
Caused by Bacterial or viral infections
Hypersensitivity to drugs e.g. methicillin, ana???
Diagnosed by ↓ GFR, tubular dysfunction with ↓ conc. ability and metabolic acidosis.
 APN & CPN (acute & chronic pyelonephritis)
APN c.c.c. bacteriuria, pyuria, leucocyte casts
+ve urine nitrate - need C & sensitivity test
Blood: Leucocytosis
CPN c.c.c. radiological findings → cortical scarring, retracted p???
Urinary tract obstruction
Sequels: predispose to urinary tract infection
Raise tubular pressure → destroy nephrons → CRF
Diagnosis: Radiological

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 Kidney Function Testing

Lab: Earliest is loss of conc. ability of tubules

↓ acid excretion
↓GFR - ↑ Urea & N. creatinine

F. Other tests of renal significance:‫غير مهم‬

Diagnosis of pseudohypoparathyroidism (parathyroid H. resistance) (Ellsworth Howard test)
Injection of PTH pre & post analysis of u.Ph, creat, cAMP & pl Ph, ???
Renal threshold phosphate conc (TMP/GFR) 1 - phosph. Clearance
N: ↓???
= Creatinine clearance

u.cAMP X plasma creat

cAMP excretion = (N:↑10-12 fold)
u. Creatinine

Analytical methods: ‫من كتاب د عال‬

Important points:
Reference and current method studied, others just names
Urea Urease method
Potentiometry
Creatinine:
Picric
Pseudocreatinine
Uric acid
Uricase
Na molybdate
HPLC reference

mohammad_emam@hotmail.com

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