KIDNEY FUNCTION

TESTS

Course teacher Speaker

Dr. M.L.Satyanarayana Nirmala R
MVHK 804
 Kidney functions
 Regulation of water and electrolyte balance
 Regulation of acid base balance.
 Regulation of arterial blood pressure.
 Excretion of metabolic waste products and foreign
chemicals.
 Hormonal Function : Secretion of erythropoietin,
renin,1,25 dihydroxycholecalciferol- conversion only in
kidney
 Metabolic Function : site for gluconeogenesis.
Why do kidneys fail?
 Most kidney diseases attack the nephrons, causing them
to lose their filtering capacity.
 Damage to the nephrons can happen quickly, often as the
result of injury or poisoning.
 But most kidney diseases destroy the nephrons slowly
and silently. Only after years or even decades will the
damage become apparent.
 Most kidney diseases attack both kidneys
simultaneously.
 The two most common causes of kidney disease are
diabetes and high blood pressure.
Diabetic Kidney Disease
 Diabetes is a disease that keeps the body from using glucose,
a form of sugar, as it should. If glucose stays in the blood
instead of breaking down, it can act like a poison.
 Damage to the nephrons from unused glucose in the blood is
called diabetic kidney disease
High Blood Pressure
 High blood pressure can damage the small blood vessels in
the kidneys. The damaged vessels cannot filter wastes from
the blood as they are supposed to.
Inherited and Congenital Kidney Diseases
 Some kidney diseases result from hereditary factors.
Polycystic kidney disease (PKD), for example, is a genetic
disorder in which many cysts grow in the kidneys. PKD cysts
can slowly replace much of the mass of the kidneys, reducing
kidney function and leading to kidney failure.
Glomerular Diseases
 Glomerular diseases attack the tiny blood vessels, or
glomeruli, within the kidney. The most common primary
glomerular diseases include membranous nephropathy, IgA
nephropathy, and focal segmental glomerulosclerosis. The first
sign of a glomerular disease is often proteinuria. Another
common sign is hematuria.
Other Causes of Kidney Disease

 Poisons and trauma, such as a direct and forceful blow to

the kidneys, can lead to kidney disease.
 Some over-the-counter medicines can be poisonous to
the kidneys if taken regularly over a long period of time.
 General considerations
 To determine the nature and extent of renal impairment
 Only in case of severe renal disease, It is possible to detect
abnormal function as kidney has tremendous reserve capacity
(50% of nephrons non-functional-detectable).
 Most renal function tests indicate functional competence the
kidney at the time of testing. They don't indicate
 specific cause,

 Acuteness/ chronicity of lesion,

 Degree of reversibility of the lesion.

 It is best to perform serial tests at appropriate intervals to
determine the extent of kidney damage, its reversibility to
establish prognosis and to determine the efficacy of
treatment.
 Precise measurement of renal functions requires
quantitative estimation of GFR, renal plasma flow and
maximal tubular excretory capacity.
 The result of renal function test must be evaluated in
combination with available clinical findings, radiography,
biopsy and other lab findings.
Kidney Function Tests

1. BUN
2. Creatinine
3. Urine protein/creatinine ratio
4. Water deprivation test
5. ADH test
6. Fractional electrolyte clearance
7. Sulfanilate clearance
8. Urinalysis
 1. Specific gravity
 It is measure of density of urine as compared to pure water.
(Sp 0-1).
 Sp. G reflects the diluting ability of the kidney. Sp. G of
urine is significantly altered by protein, glucose and other
abnormal solutes.
 If Sp, G of urine is 1.025 or more - collecting ducts & distal
tubes are responsible to ADR. Urine Sp. G varies inversely
with volume of urine excreted except in Diabetes mellitus
(large quantity of urine - high Sp. G).
 Methods of determination of Sp. G of urine:
 Using urinometer.
 Using refractometer
Normal values

Species Sp. G
Cattle 1.035
Horse 1.035 or more
Sheep and goat 1.030
Pig 1.015
Dog 1.025
Cat 1.030
Man 1.020
Decreased Specific gravity
 Administration of diuretics
 Parental fluids, corticosteroid therapy
 Following oestrous

Increased Specific Gravity

 Exogenous sources: High protein diet — increased BUN

concentration.
 Endogenous sources: Rapid catabolism of body tissues
(fever, infection) or gastro intestinal haemorrhages. —
Significant increase in BUN.
 Drugs: Increased protein catabolism (corticosteroids).
Decreased protein anabolism.
 Body fluid balance: Dehydration. Decreased renal
perfusion. Increased BUN. Decreased glomerular
filtration.
Rate of the excretion:
 Decreased GFR - increased BUN. Abnormal elevation of
BUN concentration as a result of renal impairment are not
detectable until 70 - 75% of nephrons of kidney become
non functional.
 Early stage of progressive renal disease: Mild increase in
BUN. As the disease progresses, destruction of small
number of nephrons, so there will be massive increased
BUN concentration.
 2. Blood Urea Nitrogen
 Test used to evaluate the ability of the kidneys to
remove nitrogenous waste from the blood.
 But this test is not sensitive as 75% of the kidneys
should be nonfunctional for BUN elevation
 Methods for estimation of BUN
1. Mercury cobining power
2. Nesslerization
3. Chromatographic technique – Urograph strips are used
 Procedure
 With long tip pipette place 0.2 ml serum, or plasma in a 1.0 x
75 mm test tube. Avoid wetting sides of the tube
 Place the urograph strip with taped end down. Be sure tip is not
bent and touches the tube only at the top and bottom. Don't
touch the indicator hand or the finger, measure the Height
(ram) of the colour change on the indicator band.
 Reading:
 No colour change - 10 mg/100 ml.
 For level above 10 mg, 0.5 mm = 2.5 mg / 100ml.
Interpretation of BUN:
Low values:
 Protein malnutrition.

 Extensive hepatocellular damage.

 Ability of hepatic cells to form urea is the last

function to fail
Increased BUN:
1. Prerenal cause:
 Reduced renal blood flow : Congestive heart failure,
Shock.
 Reduced net filtration pressure in the glomerulus.
– Hypotension, adreno cortical insufficiency, heart
failure, increased protein osmotic pressure and
dehydration
2. Renal causes; 70% of nephrons non functional
3. Post-renal uraemia:
 Perforation of urinary tract - urine escapes into
peritoneal cavity – absorption - Uraemia.
 Obstruction of urethra.
 3. Creatinine
 Creatinine is NPN substance formed during muscle
catabolism of creatinine and phosphocreatinine.
 Excretion is only by glomerular filtration, neither excreted
nor absorbed by the tubules, thus it can be used as rough
index for GFR.
 Factors influencing creatinine concentration are similar to
BUN. Except
1.Creatinine is not influenced by diet.
2.Daily production remains constant.
3.Not influenced by catabolic factors (urea formation).
Therefore, toxaemia, infection and drugs won't alter
creatinine levels.
As fewer non-renal influences creatinine level, it is
more specific for diagnosis and prognosis of
progressive renal diseases.
 Foin-wu method is used for estimation
Species Total NPN BUN Creatinine mg/
100ml
Bovine 20-40 6-27 1-2.07
Ovine 20-38 8-20 1.2-1.93
Caprine 30-44 13-28 0.9-1.82
Equine
20-40 10-20 1.2-1.9
Canine 17-38 10-20 1-1.7
Feline - 20-30 1-2
 Fractional electrolyte Clearance
 As concentration of of electrolytes in the urine reflects
glomerular filtration, tubular reabsorption and tubular
secretion, this test is used to evaluate tubular function.
 Normal values in dogs in % for fractional clearance of
sodium, chloride, potassium, and phosphate are <1,
<1, <20, and <40, respectively.
 Urine protein/urine creatinine ratio
 Divide urine protein concentration (mg/dl) by urine
creatinine concentration (mg/dl) to calculate ratio.
 Ratio less than 0.5 is normal
 Between 0.5-1 is doubtful but greater than 1.0 is
abnormal.
 In dogs suffering from gloerulonephritis, the values
range from 1-40 and even higher
 Dogs suffering from renal amyloidosis, the values are
usually higher than 10.0
 Water Deprivation test
 To differentiate low Sp. G due to increased water intake
and D. insipidus.
 After emptying the bladder using catheter, weigh the
animal.
 Withhold water .
 Give dry food if test continues more than 24 hrs.
 Measure urine specific gravity, osmolality and urine
/plasma osmolality ratio every 2-4 hrs.
 The test is continued until patient becomes dehydrated
or urine is concentrated. There is loss of 5% or more of
its body weight.
 In healthy dogs, the urine specific gravity
reaches 1.050 to 1.076 after water deprivation.
 Antidiuretic Harmone Test
 This test is perfomed when patients cannot concentrate
urine after water deprivation or in patients in which water
deprivation is risky.
 Inject intramuscularly 3-5U of vasopressin tannate oil.
 Provide water ad-libitum and empty bladder every 3-6 hrs
after injection.
 Measure specific gravity of urine at 0, 6, 12, 18, and 24
hrs.
 In healthy dogs, a maximum urine specific gravity of
1.024-1.060 at 8 hrs is expected.
 The maximal urine osmolality should be 1033-2001
 Maximal urine/plasma osmolality ratio should be 3.8 –
7.4
 Sulfanilate clearance test
 As sulfanilate is removed from the blood by glomerular filtration, its
clearance is used for evaluating glomerular function.
 Administer a 10% solution of sodium sulfanilate @ 20mg/Kg
BW by intravenous route
 Collect blood samples at 30, 60, and 90 min.
 Measure sulfanilate concentration
 Sulfanilate T1/2 for normal dogs can vary from 32-84 minutes.
 Dogs with significantly increased BUN ca have sulfanilate
T1/2values of 200 min or more.
 Thus renal diseases result in decreased sulfanilate clearance and
T1/2 time increase in renal diseases.
Renal biopsy
 Aim: To determine the precise cause of abnormality
in renal function.
 Indications:
 Persistent abnormal proteinurea.

 Renal failure

 To know prognosis.

 To aid in the treatment.

Methods of renal biopsy:

 Per cutaneous method
 Laprotomy
 Biopsy is the lost resort.
 Potential complication of renal biopsy is haemorrhage
 Before taking biopsy coagulation test, plate test,
activated clotting time should be known.
 Biopsy has to be taken from renal cortex.
 Before and after taking biopsy I/V fluids should be
administrated for several hours. Which is to aid in
diuresis which reduces clot formation in renal tubules
of renal pelvis which causes hydronephrosis.
 While taking biopsy, severe haemorrhage occurs
leading to acute anemia blood should be available for
transfusion.
Contraindications of renal biopsy

 Coagulopathies.
 Single functional kidney.
 Marked hydronephrosis.
 Marked contracted kidneys.
 Large cysts.
 Abscessation.
 Acute pyelonephritis.
 End stage of renal disease.