Biochemical tests are commonly used in day-to-day practices for diagnosis of diseases. Liver function test and renal function tests are common tests done.

1. INTERPRETATION OF
COMMON BIOCHEMICAL
TESTS INCLUDING LFT &
RFT
Dr Chayanika Mishra
Pediatric Resident, Kolkata

2. COMMON BIOCHEMICAL TESTS:
 LFT
 URINE-RE/ME
 RFT
 TFT

3. CLASSIFICATION OF LFT:
 Tests for liver cell injury:
Alanine aminotransferase (ALT/SGPT)
Aspartate aminotransferase (AST/SGOT)
Lactic acid dehydrogenase
 Tests for cholestasis:
Alkaline phosphatase
Gammaglutamyl transferase
5-nucleotidase
Bilirubin (total & conjugated)
Urine urobilinogen
Serum and urine bile acids
 Tests for liver synthetic capacity:
Albumin and other proteins
Prothrombin time
Ammonia
 Specific serum tests:
Caeruloplasmin, Alpha-1 antitrypsin
AFP, Lipid profile

4. TESTS OF LIVER CELL INJURY:
AST ALT
Location Both mitochondrial and cytosolic
enzyme
Cytosolic enzyme
Hepatocytes, heart, skeletal muscle,
RBC, brain, pancrease, lung
Hepatocytes
False positive
Hemolysis-rough handling of blood,
difficult venipuncture
Myopathy, rhabdomyolysis
More specific and sensitive
for hepatocellular injury
Serum half life 18 hrs 48 hrs
In early acute hepatitis AST is higher, but by 48 hrs ALT is higher

5. Viral hepatitis:
 Elevation of transaminases precedes that of serum bilirubin by about 1 week.
 During recovery phase- steady fall in transaminases
 Secondary elevation / persistent elevation:
1. Recrudescence of hepatitis.
2. Development of chronic hepatitis.
 Sudden fall in a sick jaundiced patient- Acute fulminant hepatitis.
 Poor correlation between the extent of hepatocellular necrosis and the elevation
of transaminases.
Alcoholic hepatitis: De Riti’s ratio
 AST:ALT Ratio is always 2:1.
 Ratio is less than 1 in acute and chronic non-alcoholic hepatitis.
 Because:
1. Damage is primarily mitochondrial so more AST is realeased
2. ALT synthesis is more sensitive to pyridoxal 5- phosphate deficiency.

6. Very high transaminases: extensive hepatocellular necrosis
 Viral hepatitis
 Drug induced hepatitis- paracetamol
 Toxic hepatitis- Carbon tetrachloride & Amanita mushroom
 Ischaemic hepatitis- CCF Reduced perfusion/ hypoxia Leakage of enzymes
Non hepatobiliary cause of transaminitis:
 Primary muscle disease
 Celiac disease
 Addison’s disease
 Hyperthyroidism & hypothyroidism
 Anorexia nervosa
 Loss of fluid due to diarrhoea and vomiting- small transient elevation.
Very low transaminases:
 Patients with chronic hemodialysis, possibly due to dialysis or pyridoxine deficiency.

7. Asymptomatic transaminitis:
 Obesity
 Diabetes mellitus
 Alpha-1 antitrypsin deficiency
 Asymptomatic chronic hepatitis B and C
 Wilson’s disease
 NASH
These children need only follow up if:
 There is no clear risk factor for liver disease.
 Liver enzyme levels are less than 3 times normal.
 Liver function ( as gauged by S. bilirubin and albumin and prothrombin time )
is preserved.

8. Lactic Dehydrogenase:
 Acute viral hepatitis- ALT is very high. ALT:LDH ratio more than 1.5
 Ischemic hepatitis and paracetamol toxicity- LDH is very high. ALT:LDH less than 1.5

9. Alkaline phosphatase:
 Normal level up to 100 IU/L.
 Sources- Liver, bone, small intestine, leucocytes, kidney.
 Bone isoenzyme is high – Growing children, rickets, osteomalacia, osteogenic bone deposits.
Differentiated by 1. PAGE
2. Absence of rise of other liver specific enzymes- GGT, 5- nucleotidase.
 Elevated S. ALP:
1. Extra hepatic cholestasis- biliary atresia, sclerosing cholangitis, bile duct stricture/ cancer
2. Intra hepatic cholestasis- neonatal hepatitis, drugs.
 Dissociated Jaundice:
In incomplete biliary obstruction, bilirubin may be normal or slightly increased, while ALP is quite high.
Seen in SOL like metastasis.

10. Role of enzymes in differentiation of jaundice:
Type of jaundice Transaminases ALP
Hemolytic Normal Normal
Hepatocellular > 10 times ULN <3 times ULN
Cholestatic <3 times ULN >3 times ULN

11. Gamma glutamyl transpeptidase:
 Normal level up to 60 IU/L.
 Levels are higher in biliary tract disease and cholestasis than in hepatocellular
disease.
 Elevated GGT confirms that raised ALP is of hepatobiliary origin.
 GGT is a better test than ALT for monitoring of liver injury in valproate therapy.
 Isolated raised GGT is an early indicator alcohol consumption in otherwise healthy
adolescents.
5- Nucleotidase:
 Elevated in hepatobiliary disease not in bone disease.
 If elevated with ALP, it suggests ALP is of hepatic origin.

12. Serum Bilirubin:
Properties Unconjugated bilirubinemia Conjugated bilirubinemia
Mechanism Overproduction or impaired
uptake/conjugation of bilirubin
Decreased excretion or backward
leakage of the pigment.
Etiology Physiologic/breast milk jaundice
HDN, Haemolytic anaemia
Familial- GS, CNS
Hepatocellular jaundice
Cholestatic jaundice
Familial- DJS, RS
Water solubility Insoluble Soluble
Fat solubility Soluble Insoluble
Van den Bergh
reaction
Indirect (methanol) Direct (aqueous medium)
Albumin binding ++++ +

13. Specimen Test Pre-hepatic /
hemolytic jaundice
Hepatocellular
jaundice
Post-hepatic /
obstructive jaundice
Blood
Unconjugated bilirubin ++ ++ Normal
Conjugated bilirubin Normal Excretion is rate
limiting. It is the first
impairedactivity in
early phase, it is
increased
++
Alkaline phosphatase Normal 2-3 times increased 10-12 times
Urine
Bile salt Absent Absent Present
Conjugated bilirubin
(Fouchet)
Absent Present Present
Urobilinogens +++ Increased in early
cholestatic phase ;later
decreased as
production is low
Absent
Feces Urobilins ++ Normal or decreased Clay coloured

14. Albumin and other proteins:
 Hepatocyte synthesizes plasma proteins like albumin, prothrombin, transferrin,
fibrinogen, caeruloplasmin, alpha-1 antitrypsin, haptoglobin.
 Reduced levels of these reflect a decline in synthetic capacity of liver.
 But fibrinogen, caeruloplasmin, alpha-1 antitrypsin, haptoglobin are acute phase
reactants- may be raised in acute hepatitis.
 In liver disease fall in s. albumin is slow, as the half life of albumin is about 22 days.
Hence, low s. albumin is a sign of chronic liver disease rather than acute disease.
 Patients with compensated CLD may show a sudden drop in s. albumin during an acute
illness like sepsis. May be due to TNF & IL-1 produced in septicemia.
 Non hepatic causes of hypoalbuminemia:
1. Nephrotic syndrome.
2. PEM
3. Protein losing enteropathy

15. Serum Globulins:
 Produced by stimulated B lymphocytes, hence don’t directly test liver function.
 In CLD, the functions of reticuloendothelial cells of liver is impaired. Hence bacteria
can’t be destroyed and they reach the circulations, stimulating B lymphocytes to
produce immunoglobulins.
 4 types of S. globulins
1. Alpha-1 globulin- caeruloplasmin, alpha-1 antitrypsin and orosomucoid all are acute
phase reactants. Increased in any type inflammation.
2. Alpha-2 globulin- Haptoglobulin- acute phase reactant.
3. Beta globulin- Transferrin & beta lipoprotein.
4. Gamma globulin- IgG, IgM and IgA, synthesized in reticuloendothelial system by
plasma cells
 Gamma globulin level is increased in cirrhosis due to increased production.
Increased number of plasma cells may be the source.

16. Prothrombin Time:
 The PT is a measure of the time it takes for prothrombin (factor II) to be converted to
thrombin in the presence of tissue extract (thromboplastin), calcium ions and activated
factors V, VII and X.
 Normal values are 12-13 sec.
 Values >3 sec above normal indicate a risk of bleeding.
 PT prolongation due to reduced Vitamin K dependent factors seen in hepatocellular
jaundice (due to decreased production) and in cholestatic jaundice (due to reduced vitamin
k absorption).
 If PT normalises after vitamin K injection, that suggests cholestatic jaundice while in severe
hepatocellular jaundice PT remains prolonged.
 Factor VII has shortest half-life, so in a patient with early liver disease may present with an
isolated prolonged PT.
 In patient with liver disease, PT may be prolonged due to non hepatic causes like DIC.
Factor VIII is also synthesised from non-hepatic sources like the vascular endothelium.
Hence it’s level is usually normal in liver disease, unless it is being consumed as in DIC.
 Thus, factor VIII level may help to differentiate haemorrhage due to severe liver disease
alone ( in which Factor VIII activity is normal), from that due to accompanying DIC (in which
factor VIII level is depressed due to consumption).

17.  A prolonged PT is not specific for liver disease; may be seen in
1. Congenital deficiency of coagulation factors
2. DIC
3. Ingestion of drugs that affect the prothrombin complex.
 International Normalised Ratio (INR) system standardizes the PT for different
thromboplastin reagents.
 Liver biopsy contraindicated if INR is >1.3.
 INR helps monitor patients on warfarin therapy.
 Partial Thromboplastin Time (PTT):
 Measures generation of thrombin by the intrinsic pathway, which uses all the clotting
factors.
 Thrombin Time (TT):
 This test is sensitive to the levels of fibrinogen.
 The normal hepatocytes removes sialic acid residues from fibrinogen. Hence, in
hepatocellular damage, this function is decreased and fibrinogen molecules develop
excessive sialic acid content. This dysfunctional fibrinogen contributes to the haemorrhagic
diathesis of liver disease.

18. URINE-ROUTINE & MICROSCOPY
INDICATIONS FOR URINALYSIS:
 Suspected renal diseases like
glomerulonephritis, nephrotic
syndrome, pyelonephritis, and
renal failure.
 Detection of urinary tract
infection.
 Detection and management of
metabolic disorders like diabetes
mellitus.
 Differential diagnosis of jaundice.

19. URINE EXAMINATIONS:
 PHYSICAL EXAMINATION
 CHEMICAL EXAMINATION
 MICROSCOPIC EXAMINATION

20. PHYSICAL EXAMINATION:
COLOUR
 Normal urine color in a fresh state is pale yellow or amber and is due to the
presence of various pigments collectively called urochrome.
COLOUR CONDITIONS
Colourless Dilute urine ( Diabetes mellitus, Diabetes insipidus,
Overhydration)
Red Hematuria, Hemoglobinuria, Porphyria, Myoglobinuria
Dark brown or black Alkaptonuria, Melanoma
Yellow Concentrated urine
Yellow-green or green Biliverdin
Deep yellow with yellow foam Bilirubin
Orange or orange-brown Urobilinogen, Porphobilinogen
Milky white Chyluria
Red/orange fluorescence with uv light Porphyria

21. Odour
 Freshly voided urine has a typical aromatic odor due to volatile organic acids.
 After standing, urine develops ammoniacal odor due to formation of ammonia
occurs when urea is decomposed by bacteria).
 Some abnormal odours with associated conditions are:
 Fruity: Ketoacidosis, starvation.
 Mousy or musty: Phenylketonuria.
 Fishy: Urinary tract infection with Proteus, tyrosinaemia.
 Ammoniacal: Urinary tract infection with Escherichia coli, old standing urine.
 Foul: Urinary tract infection.
 Sulfurous: Cystinuria

22. Specific Gravity (SG) :
 Measure of concentrating ability of kidneys and is determined to get information about
this tubular function.
 It is basically a comparison of density of urine against the density of distilled water at a
particular temperature.
 Normal SG of urine is 1.016 to 1.022 in 24 hrs sample and also depends on the state of
hydration.
 SG of normal urine is mainly related to urea and sodium.
 Hypersthenuria - Causes of increase in SG of urine are diabetes mellitus, glycosuria,
albuminuria, fever and dehydration.
 Hyposthenuria - Causes of decrease in SG of urine are diabetes insipidus, pyelonephritis,
diuretics and alcohol.
 Isosthenuria - Low and fixed SG at 1.010 due to loss of concentrating ability of tubules
seen in end stage renal failure.

23. Reaction and pH
 Normal value ranges from 4.6-8.
 Urine pH depends on diet, acid base balance, water balance, and renal
tubular function.
Acidic urine Alkaline urine
Ketosis:
Diabetes mellitus, Starvation, Fever
Severe vomiting
Old ammoniacal urine sample
Chronic renal failure
UTI by Escherichia coli. UTI by bacteria that split urea to
ammonia - proteus or pseudomonas.
High protein diet. Vegetarian diet

24. Chemical examination of Urine.
 The chemical examination is carried out for the following substances :-
 Proteins
 Glucose
 Ketones
 Bilirubin
 Bile salts
 Urobilinogen
 Blood
 Haemoglobin
 Myoglobin
 Nitrite or leukocyte esterase

25. Proteins:
 Normally, kidneys excrete scant amount of protein in urine (up to 150 mg/24 hours)
 These proteins include:
 Proteins from plasma (albumin).
 Proteins derived from urinary tract:
1. Tamm-Horsfall protein- normal mucoprotein secreted by ascending limb of the loop of
Henle
2. Secretory IgA
3. Proteins from tubular epithelial cells, leucocytes and other desquamated cells.
 This amount of proteinuria cannot be detected by routine tests.
 Proteinuria refers to protein excretion in urine >150 mg/24 hours in adults.

26. Causes of proteinuria
 Glomerular proteinuria due to increased permeability of glomerular capillary
wall. e.g. nephrotic syndrome.
 Tubular proteinuria due to excretion of low molecular weight proteins which
are actively reabsorbed by proximal renal tubules in diseased conditions of
tubules. e.g. acute and chronic pyelonephritis, heavy metal poisoning,
tuberculosis of kidney, interstitial nephritis, cystinosis, Fanconi syndrome and
rejection of kidney transplant.
 Overflow proteinuria: When concentration of a low molecular weight protein
rises in plasma, it “overflows” from plasma into the urine. e.g
immunoglobulin light chains or Bence Jones proteins (plasma cell dyscrasias),
hemoglobin (intravascular hemolysis), myoglobin (skeletal muscle trauma) &
lysozyme (acute myeloid leukemia type M4 or M5).
 Hemodynamic proteinuria: Alteration of blood flow through the glomeruli
causes increased filtration of proteins. e.g high fever, hypertension, heavy
exercise, congestive cardiac failure, seizures,& exposure to cold.
 Post-renal proteinuria: This is caused by inflammatory or neoplastic
conditions in renal pelvis, ureter, bladder, prostate, or urethra.

27. Dipstick methods(e.g uristix):
 Dipstick methods(e.g uristix) : widely used test for Proteinuria, more convenient &
equally reliable.
 Colour changes from yellow to green.
 Light chain proteins & LMW tubular proteins are not detected by this method.
 Trace =5 to 20 mg/dl urinary prtn
+1 = 30- 100 mg/dl
+2 = 100- 300 mg/dl
+3 = 300 - 1000 mg/dl
+4 = > 1000 mg/dl
 Proteinuria in patients with Nephrotic Syndrome is massive (+3 or +4 by dipstick) &
selective, constituted predominantly of Albumin,without loss of proteins of higher
molecular wt.
 In the presence of tubular damage or physical injury to the glomerular barrier, the
proteinuria is non selective.

28. Microalbuminuria:
 Defined as urine albumin excreation between
30 to 300 mg within 24 hrs.
 Microalbuminuria is an indicator of
generalised endothelial dysfunction and is
regarded as a common pathway of injury to
both renal and systemic vascular beds.
 Associated with:
 Type 1 diabetes causing nephropathy.
 Childhood hypertension and obesity.

29. Glucose:
 Main indication for testing glucose in urine is detection of unsuspected diabetes
mellitus or follow-up of known diabetic patients.
 All of the glucose filtered by the glomeruli is reabsorbed by the proximal renal
tubules and returned to circulation.
 Normally a very small amount of glucose is excreted in urine that cannot be
detected by the routine tests. (< 500 mg/24 hours or < 15 mg/dl)
 Glycosuria results if the filtered glucose load exceeds the capacity of renal
tubular reabsorption.

30. Causes of Glycosuria:
 Glycosuria with hyperglycaemia:
 Endocrine diseases: diabetes mellitus, acromegaly, Cushing’s syndrome,
hyperthyroidism, pancreatic disease.
 Drugs: adrenocorticotrophic hormone, corticosteroids, thiazides.
 Alimentary glycosuria (Lag-storage glycosuria):After a meal, there is rapid intestinal
absorption of glucose leading to transient elevation of blood glucose above renal
threshold. This can occur in persons with gastrectomy or gastrojejunostomy and in
hyperthyroidism. Glucose tolerance test reveals a peak at 1 hour above renal
threshold (which causes glycosuria); the fasting and 2-hour glucose values are
normal.
 Glycosuria without hyperglycemia: Renal glycosuria
 This accounts for 5% of cases of glycosuria in general population.
 Renal threshold is the highest glucose level in blood at which glucose appears in
urine and which is detectable by routine laboratory tests. The normal renal threshold
for glucose is 180 mg/dl.
 The renal threshold is set below 180 mgs/dl but glucose tolerance is normal. The
disorder is transmitted as autosomal dominant.

31. Ketones:
 Excretion of ketone bodies (acetoacetic acid, βhydroxybutyric acid, and acetone) in
urine is called as ketonuria.
 Ketones are breakdown products of fatty acids and their presence in urine is indicative
of excessive fatty acid metabolism to provide energy.
 Normally ketone bodies are not detectable in the urine of healthy persons. If energy
requirements cannot be met by metabolism of glucose (due to defective carbohydrate
metabolism, low carbohydrate intake, or increased metabolic needs), then energy is
derived from breakdown of fats leading to formation of ketone bodies.
 Causes of Ketonuria:
 Decreased availability of carbohydrates in the diet:
1. Starvation.
2. Persistent vomiting in children
3. Weight reduction program (severe carbohydrate restriction with normal fat intake)
 Increased metabolic needs:
 Fever in children
 Severe thyrotoxicosis
 Protein calorie malnutrition

32. Bilirubin and bile salts:
 Unconjugated bilirubin is not water soluble, is bound to albumin, and cannot
pass through the glomeruli. Therefore, it does not appear in urine.
 Conjugated bilirubin is water soluble, is filtered by the glomeruli, and
therefore appears in urine.
 In acute viral hepatitis, bilirubin appears in urine even before jaundice is
clinically apparent.
 Bile salts enter the small intestine through the bile and act as detergents to
emulsify fat and reduce the surface tension on fat droplets so that enzymes
(lipases) can breakdown the fat.
 In the terminal ileum, bile salts are absorbed and enter in the blood stream
from where they are taken up by the liver and re-excreted in bile
(enterohepatic circulation).
 Bile salts along with bilirubin can be detected in urine in cases of obstructive
jaundice.
 Bile salts and conjugated bilirubin regurgitate into blood from biliary
canaliculi (due to increased intrabiliary pressure) and are excreted in urine.

33. Urobilinogen:
 Conjugated bilirubin excreted into the duodenum through bile is converted by
bacterial action to urobilinogen in the intestine.
 Major part is eliminated in the feces.
 A portion of urobilinogen is absorbed in blood, which undergoes recycling
(enterohepatic circulation).A small amount, which is not taken up by the liver, is
excreted in urine.
 Causes of Increased Urobilinogen in Urine:
 1. Hemolysis
 2. Hemorrhage in tissue.
 Causes of Reduced Urobilinogen in Urine:
 1. Obstructive jaundice.
 2. Reduction of intestinal bacterial flora: This prevents conversion of bilirubin to
urobilinogen in the intestine. It is observed in neonates and following antibiotic
treatment

34. Blood:
 The presence of abnormal number of intact red blood cells in urine is called as
hematuria.
 Causes of Hematuria:
 Diseases of urinary tract:
1. Glomerular diseases: Glomerulonephritis, Berger’sdisease, lupus nephritis, Henoch-
Schonlein purpura.
2. Non-glomerular diseases: Calculus, tumor, infection, tuberculosis, pyelonephritis,
hydronephrosis, polycystic kidney disease, trauma, after strenuous physical exercise.
 Hematological conditions:
Coagulation disorders, sickle cell disease.

35. Chemical Tests for Significant Bacteriuria:
 Nitrite test:
 Nitrites are not present in normal urine. Ingested nitrites are converted to
nitrate and excreted in urine.
 If gram-negative bacteria (e.g. E.coli, Salmonella, Proteus, Klebsiella, etc.)
are present in urine. Nitrites are then detected in urine by reagent strip
tests.
 Leucocyte esterase test:
 It detects esterase enzyme released in urine from granules of leucocytes.
Thus the test is positive in pyuria.
 If this test is positive, urine culture should be done. The test is not sensitive
to leucocytes < 5/HPF

36. Microscopic examination:
 Normal urine microscopy contains few epithelial cells, occasional RBC’s, few
crystals.
 Urine consists of various microscopic, insoluble, solid elements in suspension.
These elements are classified as organized or unorganized.
 Organized substances include red blood cells, white blood cells, epithelial cells,
casts, bacteria, and parasites.
 Unorganized substances are crystalline and amorphous material which are
suspended in urine and on standing they settle down and sediment at the bottom
of the container called as urinary deposits or urinary sediments.

37. Urinary findings in renal diseases:
Condition Albumin RBCs/HPF WBCs/HPF Casts/LPF Others
Normal 0- trace 0-2 0-2 Occasional -
Acute
Glomerulonephritis
1-2+ Numerous
dysmorphic
0-few Red cell,
granular
Smoky urine
or hematuria
Nephrotic
Syndrome
>4+ 0- few 0- few Fatty, hyaline,
waxy,
epithelial
Oval fat
bodies ,
lipiduria
Acute
pyelonephritis
0-1+ 0- few Numerous WBC, granular WBC clumps,
bacteria,
nitrite test

38. Renal Function Test:
1. To screen for kidney disease
Complete urine analysis
Plasma urea and creatinine
Plasma electrolytes
2. To assess renal function:
a- To assess glomerular function
Glomerular filtration rate
Clearance tests
Glomerular permeability
Proteinuria
b- To assess tubular function
Reabsortion studies
Secretion tests
Concentration and dilution tests
Renal acidifications

39. Serum creatinine:
 Creatinine is a breakdown product of creatine phosphate in muscle, and is
usually produced at a fairly constant rate by the body depending on muscle
mass.
 Normal range is 0.8-1.3 mg/dl in men and 0.6-1 mg/dl in women.
 Causes of increased serum creatinine:
 Impaired renal function
 Very high protein diet
 Anabolic steroid users
 Vary large muscle mass: body builders, giants, acromegaly patients
 Rhabdomyolysis/crush injury
 Athletes taking oral creatine.
 Drugs: • Probenecid • Cimetidine • Triamterene • Trimethoprim • Amiloride

40. Blood urea:
 Measurement of plasma creatinine provides a more accurate assessment than urea because
there are many non renal factors that affect urea level.
 Nonrenal factors can affect the urea level (normal adults is level 10-40mg/dl) like:
 Mild dehydration
 High protein diet
 Increased protein catabolism, muscle wasting as in starvation.
 Reabsorption of blood proteins after a GIT haemorrhage
 Causes of urea plasma elevations:
 Prerenal: renal hypoperfusion.
 Renal: acute tubular necrosis.
 Postrenal: obstruction of urinary flow.
 Blood urea is normally doubled when the GFR is halved.
 Parallel determination of urea and creatinine is performed to differentiate between pre-renal
and post-renal azotemia.
 Pre-renal azotemia leads to increased urea levels, while creatinine values remain within the
reference range.
 In post-renal azotemias both urea and creatinine levels rise, but creatinine in a smaller extent.

41. Clearance test:
 Clearance test is performed to assess the glomerular filtration rate (GFR).
 Clearance is defined as the volume of plasma (in ml) that could be completely
cleared off a substance per minute and is expressed as milliliter per minute.
 C = U × V /P
where, C: Renal clearance = GFR of a substance in ml/minute
U: Concentration of substance in urine (mg/100 ml)
V: Volume of urine in ml excreted per minute

42. Creatinine clearance test:
 Creatinine is an excretory product derived from creatin phosphate. The excretion of
creatinine is not influenced by metabolism or dietary factors.
 Creatinine is freely filtered at the glomerulus and is not reabsorbed by the tubules.
A small amount of creatinine is secreted by tubules. Because of these properties,
the creatinine clearance can be used to estimate the GFR.
 The creatinine clearance is determined by collecting urine over a 24 hour period
and a sample of blood is drawn during the urine collection period.
 Uv/p=GFR=creatinine clearance
where, U is urinary creatinine (mg/dl)
P is plasma creatinine (mg/dl)
V is volume of urine excreted (ml/minute)
 Decreased creatinine clearance:
 A very sensitive indicator of a decreased GFR.
 Reduced blood flow to the glomeruli may also produce a decreased creatinine
clearance.
 Acute or chronic glomerular damage can cause decreased glomerular filtration.

43. Thyroid function tests:
 Test that directly or indirectly measure the concentrations of T4 and T3:
1. Free T4
2. Total serum T4
3. Free T3
4. Total serum T3.
 The integrity of the hypothalamic-pituitary-thyroid axis is assessed by:
1. TSH
2. TRH
 Test that assesses intrinsic thyroid gland function includes:
1. Radioactive iodine uptake
 Test that detects antibodies to thyroid tissue includes:
1. Antithyroid antibodies

44. TFT Interpretation:

45. Evaluation of hyperthyroidism:

46. Thank you