RENAL FUNCTION TESTS

• Excretion of waste products

• Regulation of acid-base balance
• Regulation of salt-water
• Formation of renin and erythropoietin
 Assessment of renal functions
• Urine analysis
• Concentration and dilution tests
• Blood chemistry
• Renal clearance tests
• renal biopsy
URINE ANALYSIS
 PHYSICAL EXAMINATION
 Volume in 24 hours – Adults: 600-2000ml
 Color: Pale yellow to colorless
 Appearance: Clear
 Odour: Aromatic
 Specific Gravity: 1.003-1.030
 Osmolality: 300-900 mOsm/kg of water
 pH: 4.6-8.0 [average: 6.0]
 CHEMICAL EXAMINATION
 PROTEIN: Qualitative test: Negative
Quantitative test: <150 mg/24 hours
 GLUCOSE: Qualitative test: negative
Quantitative test: <500mg/24 hours [<15 mg/dl]
 Ketones: Qualitative test: Negative
 Bilirubin: Negative
 Bile Salts: Negative
 Occult blood: Negative
 HEMOGLOBIN: negative
 MICROSCOPY
• 1-2 red cells/HPF
• pus cells or epithelial cells/HPF
• Occasional hyaline casts/LPF
• Phosphate, oxalate or urate crystals depending on
urine pH
 BACTERIOLOGIC EXAMINATION
• In suspected case of any infection (UTI)
• It is done by proper and aseptic collection of
midstream specimen of urine.
CONCENTRATION AND DILUTION
TESTS
• These tests are designed to evaluate functional
capacity of the renal tubules.
• The ability of the nephron to concentrate or dilute
urine is dependent upon both functional activity of
the tubular cells in the renal medulla and the
presence of anti diuretic hormone (ADH).
• Failure to achieve adequate urinary concentration
can be due to either defects within the renal medulla
(nephrogenic diabetes insipidus), or due to the lack
of ADH (central diabetes insipidus).
• In concentration test, an artificial fluid deprivation is
induced in the patient for more than 20 hours. If the
nephron is normal, water is selectively reabsorbed
resulting in excretion of urine of high solute
concentration (specifc gravity of 1.030 or more).

• In dilution test, an excess of fluid is given to the

patient. Normally, renal compensation should result
in excretion of urine with high water content and
lower solute concentration (specific gravity of 1.003
or less).
BLOOD CHEMISTRY
Impairment of renal function results in elevation of
end-products of protein metabolism.

• urea (normal range 20-40 mg/dl)

• blood urea nitrogen (BUN) (normal range 10-20
mg/dl)
• creatinine (normal range 0.6-1.2 mg/dl)
RENAL CLEARANCE TESTS
• A clearance test is employed to assess the rate of glomerular filtration
and the renal blood flow.
• The rate of this filtration can be measured by determining the excretion
rate of a substance which is filtered through the glomerulus but
subsequently is neither reabsorbed nor secreted by the tubules.
• The glomerular filtration rate (normal 120 ml/minute in an average
adult):
C =UxV
P
where
C is the clearance of the substance in ml/ minute;
U is the concentration of the substance in the urine;
V is the volume of urine passed per minute; and
P is the concentration of the substance in the plasma.

The substances which are used for clearance tests include

inulin, mannitol, creatinine and urea.
• inulin clearance tests: Inulin, a mixture of fructose
polymers, is considered the ideal substance for the
clearance test since it is filtered from the glomerulus
and is excreted unchanged in the urine.

• creatinine clearance test: The clearance of creatinine

is determined by collecting urine over 24-hour period
and a blood sample is withdrawn during the day. The
‘endogenous’ creatinine clearance test is easy and
routinely employed method of estimating GFR.
• urea clearance test: the sensitivity is much less than the
creatinine or inulin clearance because plasma
concentration of urea is affected by a number of factors
(e.g. dietary protein, fluid intake, infection, trauma,
surgery, and corticosteroids) and is partly reabsorbed by
the tubules.

• Para-aminohippuric acid (PAH) clearance test is

employed to measure renal blood flow (unlike the
preceding tests which measure GFR). PAH when infused
intravenously is both filtered at the glomerulus as well as
secreted by the tubules and its clearance is measured by
determining its concentration in arterial blood and urine.
ACUTE RENAL FAILURE
 Acute renal failure (ARF) is a syndrome characterised by
• Rapid onset of renal dysfunction
• chiefly oliguria (<400ml/day) or anuria (<150 ml/day)
• sudden increase in metabolic waste-products
– Urea: >50 mg/dl
– Creatinine: >1.5mg/dl
• consequent development of uraemia
 ETIOLOGY
• Pre-renal
– Hypovolemia
– Shock
– Dehydration
– Renal artery thombosis
– Renal ischemia
– Burns
– Reduced cardiac output
• Renal
– Intra-vascular disease of the renal vessel
– Glomerulonephritis
– PCKD
– ATN
– Toxins
– Acute tubulointerstitial nephritis
– pyelonephritis
• Post renal/obstructive: compression anywhere along
the lower urinary tract – ureter, bladder neck,
urethra

Intra-luminal Intra-mural external

Calculus Neoplastic growth Renal neoplasm
Thrombus Stenosis Bladder neoplasm
Foreign body Prostate neoplasm
Aberrant vessels
Phimosis
Urethral neoplasm/
Rupture
 CLINICAL FEATURES

 Syndrome of acute nephritis:

• Renal dysfunction results from extensive proliferation
of epithelial cells in the glomeruli with consequent
mild increase in glomerular permeability and decrease
in GFR.
• The characteristic features are:
– mild proteinuria
– Haematuria
– oedema
– mild hypertension
– Fluid retention
 Syndrome accompanying tubular pathology : When
the ARF is caused by destruction of the tubular cells of
the nephron as occurs in acute tubular necrosis
• Oliguric phase: lasts for an average from 7 to 10 days is
characterised by urinary output of less than 400 ml per
day. There is accumulation of waste products of protein
metabolism in the blood and resultant azotaemia,
metabolic acidosis, hyperkalaemia, hypernatraemia
and hypervolaemia
• Diuretic phase: there is improvement in urinary output
and the pH urine is of low or fixed specifc gravity.
• Phase of recovery: Full recovery with healing of tubular
epithelial cells occurs in about half the cases, while
others terminate in death.
 Pre-renal syndrome :
• The ARF occurring secondary to disorders in which
neither the glomerulus nor the tubules are damaged,
results in pre-renal syndrome.
• Typically, this pattern is seen in marginal ischaemia
caused by renal arterial obstruction, hypovolaemia,
hypotension or cardiac insuffciency.
• Due to depressed renal blood flow, there is decrease
in GFR causing oliguria, azotaemia (elevation of BUN
and creatinine) and possible fluid retention and
oedema.
CHRONIC RENAL FAILURE
• Chronic renal failure is a syndrome characterised by
progressive and irreversible deterioration of renal
function due to slow destruction of renal parenchyma,
Eventually terminating in death when sufficient number
of nephrons have been damaged

• Acidosis is the major problem in CRF with

development of biochemical azotaemia and clinical
uraemia syndrome.
 ETIOLOGY
Diseases causing glomerular pathology

Primary glomerular pathology Systemic glomerular pathology

Chronic glomerulonephritis lupus erythematosus

memb ranous serum sickness nephritis

Glomerulonephritis
membranoproliferative diabetic
glomerulonephritis nephropathy

Lipoid nephrosis (minimal

change disease)
anti-glomerular basement
membrane nephritis
 Diseases causing tubulointerstitial pathology:

vascular infections toxins obstructive

HTN Chronic Drugs (aspirin, Calculus

pyelonephritis acetaminophen)
Nephrosclerosis Lead Blood clots

ischemia Cadmium Tumours

uranium Strictures

Enlarged
prostate
 Stages of CRF
• Decreased renal reserve :
– damage to renal parenchyma is marginal and the
kidneys remain functional.
– The GFR is about 50% of normal
– BUN and creatinine values are normal and the
patients are usually
• Renal insufciency:
– about 75% of functional renal parenchyma has been
destroyed
– GFR is about 25% of normal
– elevation in BUN and serum
creatinine
– Polyuria and nocturia occur due to tubulointerstitial
damage
– Sudden stress may precipitate uraemic syndrome
• Renal failure:
– about 90% of functional renal tissue has been
destroyed
– The GFR is approximately 10% of normal
– Tubular cells are essentially nonfunctional
– As a result, the regulation of sodium and water is
lost resulting in oedema, metabolic acidosis,
hypocalcaemia, and signs and symptoms
of uraemia
• End-stage kidney (chronic kidney disease):
– The GFR at this stage is less than 5% of normal and
results in complex clinical picture of uraemic
syndrome with progressive primary (renal) and
secondary systemic (extra-renal) symptoms
 Clinical features
Primary renal manifestations Secondary extra-renal
manifestations
Metabolic acidosis Anemia

Hyperkalaemia Skin changes

Sodium and water imbalance Cardiovascular system

Hyperuricaemia Fluid overload

azotaemia Pulmonary oedema

Osteomalacia, osteodystrophy