RENAL FUNCTION TEST-MBBS PATHOLOGY PRACTICALppt

RENAL FUNCTION TESTS
Dr. Riti Yadav
Dr. Sugandhi varshney

Why test renal function?
 To asses the functional capacity of kidney
 Early detection of possible renal impairment.
 Severity and progression of the impairment.
 Monitor response to treatment
 Monitor the safe and effective use of drugs
which are excreted in the urine

When should we assess renal
function?
 Older age
 Family history of Chronic Kidney disease (CKD)
 Decreased renal mass
 Low birth weight
 Diabetes Mellitus (DM)
 Hypertension (HTN)
 Autoimmune disease
 Systemic infections
 Urinary tract infections (UTI)
 Nephrolithiasis
 Obstruction to the lower urinary tract
 Drug toxicity

What to examine???
Renal function tests are divided into
the following:
Urine analysis
Blood examination
Glomerular Function Test
Tubular Function Test

Blood examination
 Done to measure substance in blood that are
normally excreted by kidney.
 Their level in blood increases in kidney
dysfunction.
 As markers of renal function creatinine,
urea,uric acid and electrolytes are done for
routine analysis

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
 Creatinine is filtered but not reabsorbed in kidney.
 Normal range is 0.8-1.3 mg/dl in men and 0.6-1 mg/dl
in women.
 Not increased above normal until GFR<50 ml/min .
 The methods most widely used for serum creatinine
are based on the Jaffe reaction. This reaction occurs
between creatinine and the picrate ion formed in
alkaline medium (sodium picrate); a red-orange
solution develops which is read colorimetrically at 520
nm .

• 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

Blood urea
 Urea is major nitrogenous end product of protein and
amino acid catabolism, produced by liver and
distributed throughout intracellular and extracellular
fluid.
 Urea is filtered freely by the glomeruli .
 Many renal diseases with various glomerular, tubular,
interstitial or vascular damage can cause an increase in
plasma urea concentration.
 The reference interval for serum urea of healthy adults
is 10-40 mg/dl.
 Plasma concentrations also tend to be slightly higher in
males than females. High protein diet causes
significant increases in plasma urea concentrations and
urinary excretion.

 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,
 treatment with cortisol or its synthetic analogous
 States associated with elevated levels of urea in blood
are referred to as uremia or azotemia.
 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.
 Enzymatic Berthelot Method is used for blood urea
estimation:
 Principal:
 Urea + H2O Urease > Ammonia + CO2
 Ammonia + Phenolic Chromogen + Hypochlorite > Green Colored
Complex whoose absorbance is read at 570nm

Serum Uric Acid
 In human, uric acid is the major product of the
catabolism of the purine nucleosides, adenosine and
guanosine.
 Purines are derived from catabolism of dietary
nucleic acid and from degradation of endogenous
nucleic acids.
 Overproduction of uric acid may result from
increased synthesis of purine precursors.
 In humans, approximately 75% of uric acid excreted is
lost in the urine; most of the reminder is secreted
into the GIT

 Renal handling of uric acid is complex and
involves four sequential steps:
– Glomerular filtration of virtually all the uric acid in
capillary plasma entering the glomerulus.
– Reabsorption in the proximal convoluted tubule of
about 98 to 100% of filtered uric acid.
– Subsequent secretion of uric acid into the lumen of
the distal portion of the proximal tubule.
– Further reabsorption in the distal tubule.
 Hyperuricemia is defined by serum or plasma uric
acid concentrations higher than 7.0 mg/dl
(0.42mmol/L) in men or greater than 6.0 mg/dl
(0.36mmol/L) in women

Glomerular function tests
 The GFR is the best measure of glomerular function.
 Normal GFR is approximately 125 mL/min
 When GFR decreases to 30% of normal
moderate renal insufficiency. Patients remain
asymptomatic with only biochemical evidence of a
decline in GFR
 As the GFR decreases further severe renal
insufficiency characterized by profound clinical
manifestations of uremia and biochemical
abnormalities, such as acidemia; volume overload; and
neurologic, cardiac, and respiratory manifestations
 When GFR is 5% to 10% of normal ESRD

 Inulin clearance and creatinine clearance are used
to measure the GFR.
Creatinine Clearance:
 A simple, inexpensive bedside estimate of GFR.
 GFR= Ccr = {Ucr * Urinary flow rate(ml/min)} / Pcr
Normal Dec.Renal
reserve Mild
Renal imp
Moderate insuff.
Renal failure
ESRD
100-120ml/min
60-100ml/min
40-60ml/min
25-40ml/min
<25ml/min
<10ml/min

 Cockroft Gault Formula
Creatinine Clearance =(140-age)* weight in kg / S.creat.*72
(multiplied by 0.85 for females)
 MDRD Nomogram
GFR(ml/min)=170*S.creat.-0.999 *age-0.176 * BUN-0.170 *albumin0.318
(multiplied by 0.742 if female)

Tubular function tests
Urine Concentration Test
 The ability of the kidney to concentrate urine is a
test of tubular function that can be carried out
readily with only minor inconvenience to the patient.
 This test requires a water deprivation for 14 hrs in
healthy individuals.
 A specific gravity of > 1.02 indicates normal
concentrating power.
 Specific gravity of 1.008 to 1.010 is isotonic with
plasma and indicates no work done by kidneys.
 The test should not be performed on a dehydrated
patient.

Vasopressin Test
 More patient friendly than water deprivation test.
 The subject has nothing to drink after 6 p.m. At 8
p.m. five units of vasopressin tannate is injected
subcutaneously. All urine samples are collected
separately until 9 a.m. the next morning.
 Satisfactory concentration is shown by at least one
sample having a specific gravity above 1.020, or an
osmolality above 800 m osm/kg.
 The urine/plasma osmolality ratio should reach 3 and
values less than 2 are abnormal.

Urine Dilution (Water Load) Test
 After an overnight fast the subject empties his bladder
completely and is given 1000 ml of water to drink.
 Urine specimens are collected for the next 4 hours, the
patient emptying bladder completely on each
occasion.
 Normally the patient will excrete at least 700 ml of
urine in the 4 hours, and at least one specimen will
have a specific gravity less than 1.004.
 Kidneys which are severely damaged cannot excrete a
urine of lower specific gravity than 1.010 or a volume
above 400 ml in this time.
 The test should not be done if there is oedema or
renal failure; water intoxication may result.

Para Aminohippuric Acid Clearance
 Maximum secretory capacity of tubules for PAH is
nearly constantat about 80mg/min.
 A decrease in the TmPAH indicates tubular damage.
Micropuncturing
 Micropuncturing various part of tubule and
analysis of fluid for volume and composition.
Microcryoscopic study
 Studying slices of renal tissue at different depths.
Microelectrode study
 Measuring membrane potential of the tubular cells

Clinical significance of RFT in AKI
 The RIFLE criteria, proposed by the Acute Dialysis Quality
Initiative (ADQI) group, aid in the staging of patients with
AKI (previously ARF).

Addendum
Novel marker for non-invasive estimation of
Glomerular Filtration Rate and Early Renal
Impairment- Cystatin C
•Cystatin C is a nonglycosylated basic protein produced at a
constant rate by all investigated nucleated cells.
•It is freely filtered by the renal glomeruli and primarily
catabolized in the tubuli (not secreted or reabsorbed as an
intact molecule).
•As serum cystatin C concentration is independent of age, sex,
and muscle mass, it has been postulated to be an improved
marker of glomerular filtration rate (GFR) compared with serum
creatinine level. (Carlo D, Annalisa L. Serum Cystatin as a Marker of
Glomerular Filtration RateAmerican Journal of Kidney Diseases,
Volume 37, Issue 2, February 2009, Pages 448-450)

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