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CHAPTER 27

KIDNEY FUNCTION TESTS

1. FUNCTIONS OF THE KIDNEY

2. FORMATION OF URINE

3. RENAL THRESHOLD SUBSTANCES

4. CLASSIFICATION OF KFTs

5. PATIENTS HISTORY

6. ANALYSIS OF BLOOD

7. URINE EXAMINATION

8. UREA CLEARANCE TEST

9. CREATININE CLEARANCE TEST

10. INULIN CLEARANCE TEST

11. CYSTATIN C ESTIMATION

12. PARA AMINO HIPPURATE (PAH) TEST

13. FILTRATION FRACTION

14. CONCENTRATION TEST

15. DILUTION TEST

16. PHENOL SULPHA PTHALEIN (PSP) TEST

17. AMMONIUM CHLORIDE LOAD TEST

18. INTRAVENOUS PYELOGRAPHY

19. RADIOACTIVE RENOGRAM

20. RADIOACTIVE SCANNING

21. CHOICE OF KIDNEY FUNCTION TESTS

22. MICROALBUMINURIA

23. ALBUMIN: CREATININE RATIO

24. NEPHROTIC SYNDROME

25. ACUTE RENAL FAILURE

26. CHRONIC RENAL FAILURE

 KIDNEY FUNCTION TESTS

FUNCTIONS OF THE KIDNEY

1. Maintenance of homeostasis:

The kidneys are largely responsible for the regulation of

water, electrolyte and acid base balance in the body.

2. Excretion of metabolic waste products:

The end products of protein & nucleic acid metabolism

are eliminated from the body through the urine; these include
urea, creatinine, uric acid, sulphate & phosphate.

3. Retention of substances vital to the body:

The kidneys reabsorb and retain several substances of

biomedical importance in the body e.g. glucose and amino
acids.

4. Hormonal function:

The kidneys function as endocrine organs by producing

hormones:

a) Erythropoietin, a peptide hormone, stimulates

haemoglobin synthesis and formation of erythrocytes.

b) Calcitriol, the biochemically active form of vitamin D,

is produced in the kidney.

c) The hormone renin, liberated by the kidney, stimulates

the formation of angiotensin II, which in turn leads to aldosterone
production.
 FORMATION OF URINE

1. Nephron is the functional unit of the kidney.

2. Each kidney is composed of one million nephrons.

3. The nephron consists of Bowman’s capsule, proximal

convoluted tubule, loop of Henle, distal convoluted tubule
& collecting tubule.

4. The blood supply to kidneys is relatively large.

5. 1200 ml of blood passes through the kidneys every

minute.

6. From this, about 120 to 125 ml is filtered per minute by

the kidneys & this is known as the glomerular filtration rate.

7. With a normal GFR, the glomerular filtrate formed in an

adult is about 180 litres per day, out of which only 1.5 litres
is excreted as urine.

8. Thus, more than 99% of the glomerular filtrate is

reabsorbed by the kidneys.

9. The process of urine formation involves two steps –

glomerular filtration and tubular reabsorption.
 GLOMERULAR FILTRATION

1. This is a passive process that results in the formation of

ultra-filtrate of the blood.

2. All the constituents of plasma with molecular weight less

than 70,000 are passed into the filtrate.

3. Therefore, the glomerular filtrate is almost similar in

composition to the plasma.

TUBULAR REABSORPTION

1. The renal tubules retain water and most of the soluble

constituents of the glomerular filtrate by reabsorption.

2. This may occur either by passive or active process.

3. The excreted urine has an entirely different composition

compared to the glomerular filtrate from which it is
derived.
 RENAL THRESHOLD SUBSTANCES

1. There are certain substances in the blood whose excretion

in urine is dependent on their concentration.

2. Such substances are referred to as renal threshold substances.

3. At the normal concentration in the blood, they are completely

reabsorbed by the kidneys, with a result that their excretion in urine
is almost negligible.

4. Renal threshold of a substance is defined as the concentration

in blood beyond which it is excreted into urine.

5. Renal thresholds for some important substances:

a) Glucose: 180 mg/dl.

b) Ketone bodies: 3 mg/dl.

c) Calcium: 10 mg/dl.

d) Bicarbonate: 30 mEq/lt.

6. While calculating the renal threshold of a particular compound,

it is assumed that both the kidneys are optimally functioning,
without any abnormality, but this is not always true; in which
case the renal threshold is altered.

7. For instance, renal glucosuria is associated with reduced renal

threshold for glucose due to diminished tubular reabsorption.

8. The term tubular maximum (Tm) is used to indicate the

maximum capacity of kidneys to absorb a particular substance; for
instance, the tubular maximum for glucose (TmG) is 350
mg/min.
CLASSIFICATION OF KFTs

1. Patient’s history.

2. Analysis of blood.

3. Urine examination.

4. Tests based on glomerular filtration:

a) Urea clearance test.

b) Creatinine clearance test.

c) Inulin clearance test.

d) Cystatin C estimation.

5. Tests for renal plasma flow:

a) Para amino hippurate test.

b) Filtration fraction.

6. Tests based on tubular function:

a) Concentration test.

b) Dilution test.

c) PSP excretion test.

d) Ammonium chloride load test.

7. Miscellaneous tests:

a) Intravenous pyelography.

b) Radioactive renogram.

c) Radioactive scanning.
 PATIENT’S HISTORY

Proper history taking is important, particularly in respect

of oliguria, nocturia and frequency of urination.

ANALYSIS OF BLOOD

1. Kidney function can be assessed by the measurement of

blood urea, serum creatinine and serum uric acid.

2. In kidney dysfunction the levels of all three compounds

are elevated. Serum uric acid normally rises first,
followed by blood urea & finally serum creatinine.

3. Estimation of serum creatinine is a better indicator

than blood urea to assess kidney function.

4. In kidney diseases there is marked fall in serum albumin

and rise in serum cholesterol levels.
 URINE EXAMINATION

1. Examination of urine for volume, pH, colour, appearance, odour,

specific gravity and abnormal constituents such as protein,
glucose, ketone bodies, bile salts, bile pigments and
blood helps in assessing renal function.

2. Microscopic examination of urinary deposit for pus cells,

RBCs and casts also helps in diagnosis.

QUESTIONS

1. Classify kidney function tests.

2. Renal threshold substances.

3. Functions of kidney.
 TESTS BASED ON GLOMERULAR FILTRATION

UREA CLEARANCE TEST

DEFINITION

1. Urea clearance is defined as the number of ml. of plasma

which are completely cleared of urea by the kidney per minute.

2. Urea is the end product of protein metabolism.

3. After being filtered by the glomeruli, it is partially

reabsorbed by the renal tubules, hence urea clearance is less
than the GFR.

CALCULATION

1. Maximum urea clearance:

a) If the urine volume exceeds 2 ml/min, the clearance

calculated is known as maximum urea clearance and its value
is 75 ml/min.

b) Maximum urea clearance is calculated by the formula:

UxV

Where:

U: Concentration of urea in the urine in mg/dl.

V: Volume of urine in ml/min.

P: Plasma urea level in mg/dl.

 2. Standard urea clearance:

a) If the urinary volume is less than 2 ml/min, the clearance

calculated is known as standard urea clearance and its value
is 54 ml/min.

b) Standard urea clearance is calculated by the formula:

Ux√V

Where:

U: Concentration of urea in the urine in mg/dl.

V: Volume of urine in ml/min.

P: Plasma urea level in mg/dl.

DISADVANTAGES

1. Blood urea level is influenced by the protein content of

the diet, hence urea clearance is not as sensitive as creatinine
clearance in assessing renal function.

2. Urea is reabsorbed by the renal tubules, hence impaired

tubular function affects urea clearance.
 DIAGNOSTIC APPLICATIONS

1. Expression of result as percentage:

a) Cm (%) = U V x 100
P 75

b) Cs (%) = U √ V x 100
P 54

2. Urea clearance and status of kidneys:

Urea Clearance Status of Kidneys

1. > 70% Normal functioning

2. 40% to 70% Mild functional impairment

3. 20% to 40 % Moderate impairment

4. 5% to 20% Severe impairment

5. < 5% Terminal uremia

 CREATININE CLEARANCE TEST

DEFINITION

Creatinine clearance is defined as the number of ml. of

plasma which are completely cleared of creatinine by the
kidney per minute.

CALCULATION

1. Creatinine clearance is calculated by the formula:

UxV

Where:

U: Concentration of creatinine in the urine in mg/dl.

V: Volume of urine in ml/min.

P: Plasma creatinine level in mg/dl.

2. Normal creatinine clearance:

a) Males: 95 to 140 ml/min.

b) Females: 85 to 125 ml/min.

 ADVANTAGES

1. Creatinine is a normal metabolite of the body.

2. The test does not require intravenous administration

of any test material.

3. Estimation of creatinine is simple.

4. Extra renal factors rarely interfere with the test.

5. Conversion of creatine phosphate to creatinine is

spontaneous and non-enzymatic.

6. As the production of creatinine is continuous, the

blood level does not fluctuate and blood may be collected at
any time.

7. The test is not affected by diet or exercise.

DISADVANTAGES

1. Creatinine blind area:

a) Very early stages of decrease in GFR may not be

identified by creatinine clearance.

b) This is known as creatinine blind area.

 2. Overestimation of GFR:

a) Creatinine is filtered at the glomerulus but neither

reabsorbed nor metabolized by the kidneys.

b) Tubular secretion by the organic secretory pathways in

the proximal tubule accounts for 10 to 20% of urinary
creatinine in patients with a normal GFR.

c) The creatinine clearance is said to overestimate the GFR

by 10 to 20 ml/min, and a progressively higher number as the
GFR falls.

d) The net effect is progressive overestimation of the GFR

in more severe disease.

DIAGNOSTIC APPLICATIONS

1. Decrease in creatinine clearance (< 75% normal) indicates

decreased GFR, reflecting renal damage.

2. Creatinine clearance test is valuable in the detection of

impairment in kidney function, often before the clinical manifestations are
observed.
 INULIN CLEARANCE TEST

1. Inulin is a homopolysaccharide, a polymer of fructose.

2. Inulin is not metabolised in the body.

3. Following intravenous administration, inulin is excreted

entirely through glomerular filtration and is neither secreted nor
reabsorbed by the renal tubules.

4. Inulin clearance is calculated by the formula:

UxV

Where

U: Concentration of inulin in the urine in mg/dl.

V: Volume of urine in ml/min.

P: Plasma inulin level in mg/dl.

5. Normal inulin clearance level is 100 to 150 ml/min.

 CYSTATIN C ESTIMATION

1. Cystatin C is a non-glycosylated protein, made up of 120

amino acids.

2. Cystatin C is found in high concentration in biological fluids

such as breast milk, tears and saliva.

3. Cystatin C is the most abundant extracellular cysteine protease

inhibitor.

4. Normal serum level of cystatin C is 0.6 to 1 mg/lt.

5. Cystatin C is produced at a constant rate, completely filtered at

the glomerulus, taken up by the proximal tubular cells and then
catabolized.

6. Only small amounts of cystatin C are lost in the urine under

normal conditions.

7. Cystatin C is an excellent GFR marker.

8. Serum cystatin C level progressively increases as GFR decreases.

9. Serum cystatin C level is not dependent on age, sex, muscle

mass or inflammatory process.

10. Since there is no tubular secretion of cystatin C, it is extremely

sensitive to minor changes in GFR in the earliest stages of
chronic kidney disease (creatinine blind area).

11. Serum level of cystatin C is a better test for GFR than serum
creatinine.
 TESTS FOR RENAL PLASMA FLOW

PARA AMINO HIPPURATE TEST

1. PAH (para amino hippurate) is filtered at the glomerulus

and secreted by the renal tubules.

2. At concentrations of less than 2 mg/dl, PAH is removed

completely during a single circulation of blood through the
kidneys.

3. PAH clearance measures the renal plasma flow (RPF).

4. Renal plasma flow is 574 ml/min.

FILTRATION FRACTION

1. Filtration fraction is obtained by dividing the glomerular

filtration rate (GFR) by the renal plasma flow (RPF).

2. This can be obtained by dividing the inulin clearance by the

PAH clearance:
𝐶𝑔𝑓𝑟
FF = 𝐶𝑟𝑝𝑓

𝐶𝑖𝑛
FF = 𝐶𝑝𝑎ℎ

125
FF = 574

FF = 0.21

3. The normal range of filtration fraction is 0.16 to 0.21.

4. The filtration fraction is increased in hypertension and
congestive cardiac failure.

5. The filtration fraction is decreased in glomerulonephritis.

QUESTIONS

1. Urea clearance test.

2. Creatinine clearance test.

3. Inulin clearance test.

4. Cystatin C estimation.

5. Para amino hippurate test.

6. Filtration fraction.
 TESTS BASED ON TUBULAR FUNCTION

CONCENTRATION TEST

1. This test is based on the ability of the kidneys to concentrate

urine.

2. The patient is given the evening meal at 7 pm, and it must

have fluid content of less than 200 ml.

3. The patient is not allowed any fluids after the evening meal
till the test is over.

4. Urine specimens are collected next morning at 8 am, 9 am

and 10 am and specific gravity of each specimen is calculated.

5. The normal range of specific gravity is 1.003 to 1.030.

6. If the tubular function is normal, the specific gravity of

atleast one of the specimens should be greater than 1.025.

7. Impaired tubular function is shown by a specific gravity

of 1.020 or less.
 DILUTION TEST

1. This test is based on the ability of the kidneys to eliminate

water.

2. The patient is given evening meal at 8 pm, and takes nothing

by mouth after that till the test is over.

3. On the morning of the test the patient empties his bladder at

8 am, which is discarded.

4. The patient is given 1200 ml of water to drink within half an

hour.

5. Urine is collected at 9 am, 10 am, 11 am and 12 noon, and

the volume and specific gravity of the 4 specimens is measured.

6. The normal specific gravity of urine is 1.003 to 1.030.

7. If the renal function is normal more than 1000 ml. of urine

is excreted in 4 hours and the specific gravity of atleast one
specimen should be 1.003.

8. If the renal function is impaired, less than 1000 ml of water

is excreted in 4 hours and the specific gravity does not fall to
1.003.

PHENOL SULPHA PTHALEIN TEST

 1. 94% of PSP (phenol sulpha pthalein) is excreted by tubular
action and only 6% by glomerular filtration.

2. PSP test measures tubular activity and is also a measure of

renal plasma flow.

3. When 1 ml. of PSP is injected intravenously, normal kidneys

will excrete 30 to 50% of the dye during the first 15 minutes.

4. Excretion of less than 23% of the dye during 15 minutes

indicates impaired renal function.

AMMONIUM CHLORIDE LOAD TEST

1. Ammonium chloride load test is also known as urinary

acidification test.

2. The patient is given ammonium chloride at a dose of

0.1 gm/kg body weight.

3. The ammonium chloride dissociates into NH4+ and Cl-.

4. In the liver NH4 is immediately converted to urea and the Cl-

ions are counter balanced by H+ to produce HCL, a powerful acid.

5. HCL is then excreted through the urine, so as to produce

acidification.

6. Urine is collected hourly, from 2 to 8 hours after ingestion.

7. The pH and acid excretion of each sample is noted.

8. Atleast one sample should have a pH of 5.3 or less and

ammonia excretion should be 30 to 90 mmol/hour.
9. In chronic renal failure, the ammonia excretion is less.

10. In renal tubular acidosis, pH 5.3 is not achieved.

11. Liver disease is a contra-indication to perform the test.

MISCELLANEOUS TESTS

INTRAVENOUS PYELOGRAPHY

1. When injected intravenously, certain radio-opaque organic

compounds of iodine are excreted by the kidneys in sufficient
concentration to cast a shadow of the renal pelvis, ureters and
bladder on an X ray film.

2. This test gives information regarding the size, shape and

functioning of the kidneys.

3. The commonly used dyes are iodoxyl and diodone.

4. This test is done for investigation of patients with:

a) Renal stones.

b) Repeated urinary infections.

c) Renal pain.

d) Haematuria.

e) Prostate enlargement.

f) Renal tumours.

RADIOACTIVE RENOGRAM
 1. I131 labeled hippuran is given intravenously and the
radioactivity from each kidney is recorded graphically.

2. This test gives information regarding any major asymmetry

in function between the two kidneys.

RADIOACTIVE SCANNING

1. Hg203 labeled chlormerodrin is given intravenously and a

renal scan is obtained.

2. Renal scanning is helpful in detecting abnormalities in the

size, shape and position of the kidneys.

3. Renal scan helps in detection of renal tumours and renal

infarcts.

CHOICE OF KIDNEY FUNCTION TESTS

1. Early symptoms of kidney failure are polyuria, pedal edema,
puffiness of face, hypertension, unexplained anemia, fatigue,
lassitude and tiredness.

2. The assessment of kidney function starts with the routine urine

examination, followed by serum creatinine and/or blood urea
estimations & finally the specific tests to measure the tubular
and glomerular functions.

3. In glomerular dysfunction:

a) Blood urea and serum creatinine levels are increased.

b) Urine volume is decreased.

c) Urine specific gravity is increased.

d) Inulin clearance, creatinine clearance and urea clearance

are decreased.

e) Proteinuria is present.

4. In tubular dysfunction:

a) Serum uric acid is increased.

b) Urine volume is increased.

c) Urine specific gravity is decreased.

d) Dilution test is abnormal.

e) Aminoaciduria is present.

QUESTIONS
1. Concentration test.

2. Dilution test.

3. PSP test.

4. Ammonium chloride load test.

5. Intravenous pyelography.

DISORDERS OF ALTERED RENAL FUNCTION

 MICROALBUMINURIA

1. Normal urinary albumin excretion per day is 3 to 30 mg.

2. Microalbuminuria is also called minimal albuminuria or

pauci-albuminuria.

3. Microalbuminuria is identified when small quantity of

albumin (30 to 300 mg/day) is detected in the urine.

4. Macroalbuminuria is excretion of more than 300 mg of

albumin in the urine per day.

5. Microalbuminuria is an early indication of nephropathy in

patients with diabetes mellitus and hypertension, hence all patients who
are known diabetics and hypertensives should be screened for
microalbuminuria.

6. Microalbuminuria is an early indicator of onset of

nephropathy.

7. The test should be done atleast once a year.

ALBUMIN: CREATININE RATIO

1. Albumin: creatinine ratio (ACR) is the comparison of the

amount of albumin in the urine sample against its
concentration of creatinine.

2. A ratio of albumin (mcg/lt) to creatinine (mg/lt) of less

than 30 is normal.

3. A ratio of 30 to 300 signifies microalbuminuria & values

above 300 are considered as macroalbuminuria.

NEPHROTIC SYNDROME
 INTRODUCTION AND CAUSE

1. Nephrotic syndrome is a collection of symptoms due to

kidney damage, characterized by proteinuria, low serum albumin and
oedema.

2. About 5 per 100,000 people per year are affected.

3. Primary causes:

a) Focal segmental glomerulosclerosis.

b) Membranous glomerulonephritis, membranoproliferative

glomerulonephritis & rapid progressive glomerulonephritis.

c) Minimal change disease.

4. Secondary causes:

Nephrotic syndrome may occur as a complication of:

a) Diabetes mellitus.

b) Systemic lupus erythematosus, sarcoidosis & syphilis.

c) Hepatitis B, Sjogren’s syndrome and HIV.

d) Amyloidosis and multiple myeloma.

e) Vasculitis and cancer.

PATHOPHYSIOLOGY
 1. Cause of hypoproteinemia:

In nephrotic syndrome, the glomeruli are affected by

inflammation or hyalinization that allows proteins such as
albumin, anti-thrombin and immunoglobulins to pass through the
cell membrane and appear in the urine.

2. Causes of hyperlipdaemia:

a) Hypoproteinemia stimulates protein synthesis in the

liver, resulting in over-production of lipoproteins.

b) Lipid catabolism is decreased due to lower levels of

lipoprotein lipase.

3. Causes of edema:

a) The underfill hypothesis states that the loss of albumin

in urine leads to lower plasma albumin; this decreases
plasma colloid osmotic pressure, which is the cause of
edema.

b) The overfill hypothesis states that primary renal sodium

retention is the cause of edema.

CLINICAL FEATURES
 1. The first sign of nephrotic syndrome in children is usually
swelling of the face.

2. There is puffiness around the eyes, characteristically in the

morning, pitting oedema over the legs, followed by swelling of the
entire body (anasarca).

3. Pleural effusion and ascites.

4. Fatigue and loss of appetite.

5. A thrombotic complication such as deep vein thrombosis

or pulmonary embolism may be the first clue to nephrotic syndrome.

INVESTIGATIONS

1. Urinalysis: Proteinuria (> 3 grams of proteins/day) and

lipiduria.

2. Urine sediment examination shows presence of cells and

casts.

3. Hypoalbuminemia (serum albumin <2.5 gm/dl).

4. Lipid profile: High level of serum total cholesterol,

specifically LDL along with VLDL is indicative of nephrotic
syndrome.

5. Increase in serum creatinine level.

6. Ultrasound examination of the kidneys: To examine the

structure

7. Kidney biopsy: Kidney biopsy is a more specific and

invasive test; a study of the anatomical pathology may allow
identification of the type of glomerulonephritis.
COMPLICATIONS

1. Thrombosis due to decreased blood anti-thrombin III level,

due to leakage.

2. Infections: Peritonitis, lung infections, urinary infections

and meningoencephalitis.

3. Hypovolemia, leading to acute kidney failure.

4. Pulmonary oedema.

5. Atherosclerosis, due to increase in serum cholesterol level.

6. Nephrotic syndrome may trigger the onset of hypothyroidism

or aggravate pre-existing hypothyroidism, because of urinary
loss of free and protein-bound thyroid hormones.

7. Patients with nephrotic syndrome lose 25 OH cholecalciferol

in the urine, which may lead to hypocalcemia.

8. Anemia is seen in nephrotic syndrome due to excessive urinary

loss of iron, transferrin, erythropoietin and transcobalamin.

9. Malnutrition and growth retardation.

TREATMENT

1. Diet with the correct energy intake and balance of proteins:

 a) Patients are usually recommended lean cuts of meat, fish
and chicken.

b) Protein consumption should not be more than 1 gram/kg

body weight/day.

2. Restrict the ingestion of sodium to 1 to 2 gm/day, which

means that salt cannot be used in cooking and salty food should also
be avoided.

3. The intake of cholesterol should be less than 300 mg/day,

which will require switch to foods that are low in saturated fats.

4. In cases of severe hyperlipdaemia the use of statins and

fibrates (hypolipidaemic drugs) may be necessary.

5. Heparin may be used for thrombosis.

6. Anti-bacterials can be taken for infectious complications.

7. Furosemide and spironolactone (diuretics) are given for

oedema.

8. Captopril (ACE inhibitor) & losartan (angiotensin receptor

blocker) can reduce proteinuria.

9. Prednisone (corticosteroid) decreases risk of infection and

also helps in resolution of oedema.

10. Immuno-modulators such as rituximab (monoclonal

antibody) and mycophenolate (purine synthesis inhibitor)
are used in severe cases.

11. Cyclophosphamide & cyclosporine (immuno-suppressors)

are only indicated in severe cases.

12. Dialysis and kidney transplant in cases of renal failure.

 PROGNOSIS

1. The prognosis for nephrotic syndrome under treatment is

generally good, although this depends on the underlying
cause, age of the patient and their response to treatment.

2. The prognosis is usually good in children with minimal

change disease because it responds very well to steroids and
does not cause chronic renal failure.

3. Other causes, such as focal segmental glomerulosclerosis,

frequently lead to end stage renal disease.

4. Without treatment, nephrotic syndrome has a very bad

prognosis especially rapidly progressing glomerulo-
nephritis, which leads to acute kidney failure after a few months.

ACUTE RENAL FAILURE

INTRODUCTION
 1. Acute renal failure / acute kidney injury is defined as an
abrupt decline in renal function, clinically manifesting as a
reversible, acute increase in nitrogen waste products (measured
by BUN and serum creatinine levels).

2. Acute renal failure is increasingly common in hospital in-

patients, elderly patients and critically ill patients; it carries a high
mortality.

RIFLE CLASSIFICATION OF ARF

Class Criteria

1. Risk Increase in serum creatinine x 1.5 or decrease in GFR by 25%

2. Injury Increase in serum creatinine x 2 or decrease in GFR by 50%

3. Failure Increase in serum creatinine x 3 or decrease in GFR by 75%

4. Loss Complete loss of kidney function > 4 weeks

5. End stage Complete loss of kidney function > 3 months

CAUSES

The causes of acute renal failure can be classified as pre-

renal, renal and post-renal.
 1. Pre-renal:

a) These are conditions in which the plasma volume / body

fluids are reduced.

b) Examples: Dehydration, severe vomiting, diarrhoea,

hematemesis, haemorrhage, shock and ulcerative colitis.

2. Renal:

a) All forms of kidney diseases.

b) Examples: Acute glomerulonephritis, chronic

pyelonephritis, hydronephrosis & renal tuberculosis.

3. Post-renal:

a) There is an increase in blood urea level when there is

obstruction to urine flow.

b) Examples: Enlargement of prostate, stones in urinary tract,

stricture of the urethra and tumours of urinary bladder.

CLINICAL FEATURES

1. Livedo reticularis, digital ischaemia, butterfly rash and

systemic vasculitis.
 2. Iritis, dry conjunctivae and retinopathy.

3. Jaundice, hypertension and edema.

4. Hearing loss and mucosal ulceration.

5. Atrial fibrillation, pericarditis and cardiac failure.

6. Renal artery thrombosis and prostatic hypertrophy.

7. Pulmonary edema and hemoptysis.

INVESTIGATIONS

1. Increase in BUN and serum creatinine are the hallmarks

of renal failure.

2. Complete blood count.

3. Urinalysis.

4. Renal ultrasound.

5. Aortorenal angiography.

6. Renal biopsy.

TREATMENT

1. Furosemide: For correction of fluid overload.

2. Bicarbonate administration: For correction of severe acidosis.

 3. Blood transfusion: For correction of haematologic
abnormalities.

4. Dialysis.

5. Kidney transplant.

CHRONIC RENAL FAILURE

INTRODUCTION
 1. In chronic renal failure there is loss of kidney function over
a period of months or years.

2. In chronic renal failure there is a gradual rise in serum creatinine

level (over several months or years) as opposed to a sudden
increase in serum creatinine (several days or weeks), seen in
acute renal failure.

STAGING OF CRF

Stage Criteria

1. Stage 1 Kidney damage with normal GFR (>90 ml/min)

2. Stage 2 Mild reduction in GFR (60 to 89 ml/min)

3. Stage 3 Moderate reduction in GFR (30 to 59 ml/min)

4. Stage 4 Severe reduction in GFR (15 to 29 ml/min)

5. Stage 5 Kidney failure (GFR <15 ml/min)

CAUSES

1. Diabetes mellitus.
2. Hypertension.

3. Glomerulonephritis.

4. Kidney artery stenosis.

5. Focal segmental glomerulosclerosis.

6. IgA nephropathy.

7. Drug or toxin induced nephritis.

8. Renal stones.

9. Benign prostatic hyperplasia.

10. Polycystic kidney disease.

CLINICAL FEATURES

1. Muscle weakness, edema and hypertension.

2. Anemia, fatigue and somnolence.

3. Pericarditis, encephalopathy and peripheral neuropathy.

4. Anorexia, nausea, vomiting and diarrhoea.

5. Pruritis and ecchymosis.

6. Malnutrition, erectile dysfunction and amenorrhea.

7. Platelet dysfunction with tendency to bleed.

INVESTIGATIONS

1. Increase in serum creatinine and blood urea levels.

2. Decrease in serum albumin level.

3. Complete blood count.

4. Urinalysis.

5. Renal ultrasound, renal pyelography, CT scan & MRI.

6. Renal radio-nucleotide scanning.

7. Renal biopsy.

TREATMENT

1. Low salt and low protein diet.

2. Epoetin alfa (erythropoiesis stimulating agent) for anemia.

3. Furosemide (diuretic) for volume overload.

4. Dialysis.

5. Kidney transplant.

QUESTIONS

1. Microalbuminuria.
2. Albumin: Creatinine ratio

3. Nephrotic syndrome.

4. Acute renal failure.

5. Chronic renal failure.