RENAL FUNCTION TESTYousaf khanRenal Dialysis LecturerIPMS KMU

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

URINE ANALYSIS Urine examination is an extremely

valuable and most easily performed test for the evaluation of renal functions.

It includes physical or macroscopic examination, chemical examination and microscopic examination of the sediment.

MACROSCOPIC EXAMINATION

Colour Normal- pale yellow in colour due to

pigments urochrome,urobilin, Cloudiness may be caused by excessive cellular material or protein, crystallization or precipitation of salts upon standing at room temperature or in the refrigerator.

If the sample contains many red blood cells, it would be cloudy as well as red.

COLOR OF URINE

Normal Deep yellow---- conc. Of urochrome pigmentRed Blood, Hemoglobulinuria, myoglobinuria, beetroot

( chukandar) orange rifampicinyellow Concentrated urine, ( dehydration, jaundice, B complex,

sulfasalazine)Green Methylene blueBlack Severe hemoglobinuri, methyldopaBrown Bilirubin, phenothiazides

VOLUME Normal- 800 ml -2.5 L/day Oliguria- Urine Output < 300ml/day

Seen in Acute glomerulonephritisRenal Failure

Polyuria- Urine Output > 2.5 L/daySeen in Increased water ingestionDiabetes mellitus and insipidus.

Anuria- Urine output < 100ml/daySeen in renal shut down

SPECIFIC GRAVITY Normal ranges 1.002 – 1.025 Varies with quantity of urineLow SG CRF diabetes insipidus Absence of ADH Renal tubular demageHigh SG Dehydration diabetes mellitus Albuminuruia Acute nephritis

PH: Urine pH ranges from 4.5 to 8 Normally it is slightly acidic lying between 6 –

6.5. After meal it becomes alkaline. On exposure to atmosphere, urea in urine

splits causing NH4+ release resulting in

alkaline reaction.

CHEMICAL EXAMINATIONGlucose: Diabetes Impaired Renal tubular False positive or negative – large dose of

vitamin C, tetracycline or levodopaKetones: Diabetic- diabetic ketoacidosis StarvationProtein: Normal protein loss from urine is less than

150mg /24 hrs.

MICROSCOPIC EXAMINATIONWhite cell: More than 10 or more wbc per cm- UTI Stone, tubulointestinal nephritis, tuberculosis, papillary

necrosisRed cell: 2-5 per high power field – hematuriaCast: Cylindrical structure- kidney tubule-coagulation of protein Hyaline cast: concentrated urine, fever, diuretic therapy, after

exercise Granular cast: found in chronic glomerulonephritis, diabetic

nephropathy and malignant hypertension White cell cast: acute pyelonephritis Red cell cast: glomerulonephritis Epithelial cast: acute tubular necrosis and interstitial nephritis

Hyaline cast

Red cell cast

White cell casts

Granular cast

Crystals: Uric acid: acid urine, acute uric acid nephropathy Calcium phosphate in alkaline urine Calcium oxalate: hyperoxaluria, acid urine

Uric acid

Calcium phosphate Calcium

oxalate

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 Most useful clinical test Creatinine is the product of muscle metabolism 50% renal function is lost before creatinine is raise Normal range is 0.8-1.3 mg/dl in men and 0.6-1 mg/dl in

womenIncreases serum creatinine independent of GFR

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

Decrease serum creatinine• Advance age• Liver disease

SERUM UREA Produce by liver and end product of protein catabolism Freely filtered by the glomerulus and 30-40 %

reabsorbed.Increase serum urea Dehydration Catabolic state High protein diet Glucocorticoid TetracyclineLow serum urea Liver disease Malnutrition Low protein diet Old age

GLOMERULAR FUNCTION TESTS Measure the amount of plasma ultra filtered

across glomerular capillaries Ability of kidney to filter fluids and various

substance Normal GFR is in the range of 115- 125

ml/mint. GFR indicate both acute and chronic

condition Inulin clearance and creatinine clearance are

used to measure the GFR.

Stage Description (GFR)

At increased risk

Risk factors for kidney disease (e.g., diabetes, high

blood pressure, family history, older age, ethnic

group)

More than 90

1 Kidney damage with normal kidney function 90 or above

2 Kidney damage with mild loss of kidney function 89 to 60

3a Mild to moderate loss of kidney function 59 to 44

3b Moderate to severe loss of kidney function 44 to 30

4 Severe loss of kidney function 29 to 15

5 Kidney failure Less than 15

CREATININE CLEARANCE:

GFR= Ccr = {Ucr * Urinary flow rate(ml/min)} / Pcr

Cockroft Gault Formula

CLINICAL MANIFESTATIONS OF RENAL DISEASE Azotemia: Elevation of blood urea nitrogen

and creatinine levels Decreased glomerular filtration rate (GFR) Intrinsic renal disease or extrarenal causes. Prerenal azotemia is encountered-

hypoperfusion of the kidneys – Decrease GFR in the absence of parenchymal damage.

Postrenal azotemia results when urine flow is obstructed below the level of the kidney. Relief of the obstruction is followed by correction of the azotemia

Azotemia gives rise - uremia. Uremia is characterized not only by failure of

renal –But metabolic and endocrine alteration Secondary cause uremic gastroenteritis,

peripheral neuropathy and uremic pericarditis Azotemia has three classifications, depending on

its causative origin Decrease in the glomerular filtration rate (GFR) of

the kidneys and increases in blood urea nitrogen (BUN) and serum creatinine concentrations.

The BUN-to-creatinine ratio (BUN:Cr) is a useful measure in determining the type of azotemia. A normal BUN:Cr is equal to 15

Prerenal azotemia decrease in blood flow (hypoperfusion),

hemorrhage, shock,volume depletion, congestive heart failure, adrenal insufficiency, and narrowing of the renal artery.

The BUN:Cr in prerenal azotemia is greater than 20.

Primary renal azotemia  intrinsic disease of the kidney, generally the

result of renal parenchymal damage. The BUN:Cr in renal azotemia is less than 15Postrenal azotemia Blockage of urine flow in an area below the

kidneys results in postrenal azotemia The BUN:Cr in postrenal azotemia is initially >15

NEPHRITIC SYNDROME Glomerular injury and is dominated by the

acute onset hematuria (red blood cells and red cell casts

in urine), proteinuria of mild to moderate degree, azotemia, edema, hypertension; it is the classic presentation.

NEPHROTIC SYNDROME Glomerular syndrome proteinuria (excretion of greater than 3.5 g

of protein/day in adults), hypoalbuminemia, severe edema, hyperlipidemia, lipiduria (lipid in the urine).

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS Rapidly progressive glomerulonephritis is

associated with severe glomerular injury loss of renal function in a few days or weeks. Microscopic hematuria, dysmorphic red blood cells and red cell casts

in the urine sediment, Mild to moderate proteinuria.

ACUTE KIDNEY INJURY Oliguria or anuria (no urine flow), Recent onset of azotemia. It can result from glomerular injury (such as

rapidly progessive glomerulonephritis), interstitial injury, vascular injury (such as thrombotic microangiopathy), or acute tubular injury.

Chronic kidney disease, prolonged symptoms and signs of uremia, is the

result of progressive scarring in the kidney from any cause and may culminate in end-stage kidney disease, requiring dialysis or transplantation.

URINARY TRACT INFECTION Bacteriuria and pyuria (bacteria and

leukocytes in the urine). The infection may be symptomatic or

asymptomatic, and it may affect the kidney (pyelonephritis) or the bladder (cystitis) only.

Nephrolithiasis (renal stones) is manifested by renal colic, hematuria (without red cell casts), and recurrent stone formation

IMAGING TECHNIQUES Ultrasound Plain X-ray abdomen Radionuclide studies CT scan MRI Arteriography and Venography Excretion urography Antegrade urography Retrograde urography Renal biopsy

ULTRASOUND Renal size, shape, Hydronephrosis Renal Mass Poly cystic kidney Kidney stone

Normal Kidney

Hydronephrosis

Renal Mass

Poly cystic kidney disease

Plain X-ray: Renal calcification or radiodense calculi Outline of ureters and bladder

Radionuclide Studies:99mTc- DTPA Access GFR when urine collection is difficult or expected

inaccurate Helpful in the diagnosis of renal artery stenosis Localized the site of obstruction

99mTc-DMSA Determine the contribution of each kidney to overall renal

function. Localized infection such as renal abscess

CT SCAN: CT scan shows kidney, ureters and surrounding tissue in

detail and is useful in the diagnosis of renal tumors.

MRI: Differentiation between cystic and solid renal masses. MR

angiography of renal arteries is increasingly used to screen for renal arterial disease.

Arteriography and Venography Excretion urography (IVP ) Antegrade urography Retrograde urography Renal BIPSY

INDICTION OF RENAL BIOPSY Adult nephritic syndrome Persistent proteinuria > 1g/24 hr Persistent microscopic and macroscopic

hematuria Systemic disease with renal involvement

such as amyloidosis Chronic renal failure with normal size of

kidney Unexplained kidney failure Childhood nephritic syndrome