Urine Analysis:- Part 4 – Chemical Examination and Interpretations

Urine Analysis

Chemical Examination

Sample for urine analysis

1. Preferably use freshly voided urine.
2. If there is a delay, then refrigerate the urine.
3. The morning sample is concentrated urine.

Precautions for urine analysis

1. Preferably examine the urine within the first 30 minutes.
2. Reject unlabelled urine sample.
3. Avoid fecal or menstrual blood contamination.

Urine Protein

1. A normal healthy person will have daily protein exertion of 100 mg/day. This is a very small proportion of the total plasma protein.
2. It is mostly the albumin because of the smaller size. There is a small fraction of globulin as well.
   1. The proximal tubules reabsorb most of the protein filtered in the glomerular filtrate.
3. So proteinuria may be due to:
   1. As a result of increased filtration from the glomerulus.
   2. Or it is decreased reabsorption from the tubules.

Urine analysis, Proteinuria mechanism

4. Proteinuria is the first indicator of renal disease.
5. The random sample is negative.

Clinical types of proteinuria are:

Prerenal proteinuria:

1. This is caused by  nonrenal diseases and is transient; it is seen in:
   1. Hemoglobinuria.
   2. Myoglobinuria.
   3. Acute phase proteinuria.
   4. This is usually not detected by the routine urine reagent strips.

Renal proteinuria:

1. This is due to renal diseases involving glomeruli or tubules.
2. Albumin appears in the urine in glomerular damage, followed by the WBCs and RBCs.
3. It is seen in:
   1. SLE.
   2. Streptococcal glomerulonephritis.
   3. Strenuous exercise  (reversible condition).
   4. Pre-eclampsia and hypertension. (reversible condition).
   5. Toxic heavy metals.
   6. Severe viral infection.

Postrenal proteinuria:

1. Proteins can be added as the urine passes through the ureter, urinary bladder, and urethra.
   1. Bacterial and fungal infection of the lower urinary tract,
   2. Menstrual contamination also contains proteins.
   3. Prostatic fluid and spermatozoa.

Orthostatic or postural proteinuria:

1. This is a persistent benign condition frequently seen in young patients.
2. It appears when the person is upright and disappears when the patient lies down.
3. Procedure to confirm the diagnosis:
   1. These patients are advised to empty their bladders before going to bed.
   2. Take the first urine sample when patients get up.
   3. Take another sample when patients are upright for several hours.
      1. The first sample will be negative.
      2. The second sample will be positive in orthostatic proteinuria.

Microalbuminuria:

1. This is seen in diabetic nephropathy.
   
2. This microalbuminuria indicates diabetic complications.
3. The further complication of diabetes can be prevented by controlling diabetes.
4. This is also associated with an increased risk of cardiovascular diseases.
5. Microalbuminuria is reported as albumin excreted as µg/min or in mg/24 hours.
6. The level is significant from 20 to 200 µg/min Or 30 to 300 mg/24 hours.
   1. The albumin/creatinine ratio is >3.4 mg/mmol in these cases.
   2. The first-morning specimen is recommended.

Bence Jones proteinuria (BJ):

1. It is seen in multiple myeloma patients.
2. These are monoclonal light-chain immunoglobulins.
3. This is a low molecular weight protein and is excreted in the urine.

Procedure to detect BJ protein:

1. Heat the urine, and these proteins coagulate at 40 to 60 °C.
2. Dissolve when the temperature reaches 100 °C.
   1. Reading the result: Urine turbid at 40 to 60 °C and clear at 100 °C is considered positive.

Urine analysis, Urine BJ protein test

Type and degree of proteinuria:

Normal urine protein :

1. In 24 hours of urine, 150 mg or 20 mg/dL. ( another source = it is 0 to 0.1 gm).
2. Another source:  Protein in the urine is <10 mg/dL or 100 mg/24 hours.
   1. This protein consists of mainly low molecular weight serum proteins, so the major protein is the albumin seen in the urine.
   2. Other proteins include serum and tubular microglobulins, Tamm Horsfall protein produced by the tubules, and proteins from the prostate and vaginal secretions.

How to check proteinuria:

1. Mostly urine strips are used as a screening for proteinuria. These strips are specific for albumin.
2. False-positive results are seen in the following:
   1. In alkaline urine.
   2. In highly buffered urine.

Reagent test strip test for protein in the urine:

Urine protein reagent strips

Various urine tests for proteins and their characteristics:

Clinical types of proteinuria and etiology:

Glucose

1. Because of the diagnosis of diabetes mellitus, a glucose test in the urine is very commonly advised.
2. The blood glucose and urine glucose tests are part of a routine check-up.
3. Early diagnosis of diabetes mellitus helps improve the prognosis and complications of diabetes mellitus.

Glucose metabolism:

1. Glucose filtered in the glomerular filtrate is almost all absorbed by the proximal convoluted tubules; therefore, there will be a negligible amount of glucose in the urine.
2. Tubular absorption of glucose is an active process that depends upon the body’s needs.
3. In diabetes mellitus, tubular transport of glucose ceases, and glucose appears in the urine.

Urine Glucose and the Role of Kidneys

5. In hyperglycemia, the tubular transport of glucose stops, and glucose starts appearing in the urine.
6. For testing diabetes mellitus, take after the 2 hours of the meal.
   1. The first-morning sample does not give a real picture of the last evening meal. Void the first sample and then collect the next sample.
   2. The renal glucose threshold is 160 to 180 mg/dL.

Normal glucose in the urine:

1. A random sample is negative (qualitatively is negative).
2. In 24 hours, urine glucose is 0 to 0.3 grams.
3. Another source, glucose in random urine, is <30 mg/dL.
4. Glucose in urine during pregnancy is called gestational diabetes.
   1. This is usually seen around the 6 months of pregnancy.
   2. Hormones secreted by the placenta during pregnancy are believed to block insulin’s action and lead to hyperglycemia.

Renal glycosuria:

1. It is seen when the blood glucose level is normal, and glucose appears in the urine.
   1. Renal tubules’ absorption of glucose by the tubules is compromised.
   2. It is usually seen in end-stage kidney diseases, osteomalacia, and Fanconi’s syndrome.
2. Glucose false tests are seen in the urine’s high specific gravity and contain a large amount of ascorbic acid.

Hyperglycemia of nondiabetic origin is seen in:

1. It is seen in the following conditions:
   1. Pancreatitis.
   2. Pancreatic cancer.
   3. Acromegaly.
   4. Cushing’s syndrome.
   5. Hyperthyroidism.
   6. Pheochromocytoma.
   7. The above conditions produce hormones like glucagon, epinephrine, cortisol, thyroxine, and growth hormone.
   8. These hormone acts against insulin and leads to glycogenolysis.

Urine glucose and the effect of hormones

Glucose in the urine can be checked by:

1. Reagents strips, glucose oxidase reaction.
2. Copper reduction method.

Glucose-oxidase reagent strips:

1. This test is specific for the β-isomer of glucose.
   1. It converts glucose in the presence of oxygen to gluconic acid and hydrogen peroxide.
   2. The serum glucose concentration is proportional to the oxygen consumed in the reaction or the H2O2 produced.
   3. In the second step, peroxidase catalyzes the reaction between H2O2 and chromogen to form the oxidized colored compound, indicating the presence of glucose in the urine.
2. The result is reported as follows:
   1. Trace, 1+, 2+, 3+, 4+
   2. These colors also provide quantitative measurements ranging from 100 mg/dL to 2000 mg/dL or 0.1% to 2%.

Urine analysis: Glucose-oxidase principle

Chemical Examination of Urine by glucose oxidase method

Copper reduction method (Benedict’s reaction):

1. This test was used in the early days.
2. An alkaline cupric sulfate solution oxidizes all reducing sugars like glucose, galactose, fructose, maltose, xylulose, arabinose,  and ribose.
   1. It forms a brick-red to yellow precipitate of Cu₂O.
3. This test is based on reducing copper sulfate (CuSO4) to cuprous oxide in the presence of alkali and heat.
   1. The color depends upon the amount of Cu₂O.
4. Reading:
   1. The color changes from blue = Negative ( CuSO4).
   2. Green, yellow, orange/red = Positive 4+ (CuO).
   3. Greenish = 1+ to Yellow = 4+
   4. The positive reaction of 1+ = Roughly 50 mg/dL.
   5. The positive reaction of 4+ = 2 or more g/dL.

Principle of Benedict’s reaction:

Benedict’s reaction principle

Procedure for Benedict’s Reaction

Comparison of Benedict reaction and Oxidase method:

Ketones Bodies

1. Ketone bodies are absent in the normal person.
2. These are seen in patients with uncontrolled diabetes mellitus.
3. These can also be seen in person on a low carbohydrate diet.
4. These are seen in people on a high-fat diet.

Chemical examination of urine: ketone bodies metabolism and their presence in diabetic patients

Indications for the ketone bodies:

1. Diabetic acidosis.
2. Starvation.
3. Vomiting.
4. Malabsorption syndrome.
5. Pancreatic disorders.
6. Insulin dosage monitoring.
7. Strenuous exercise.
8. Inborn error of amino acid metabolism.

Ketones are the intermediate products of fat metabolism, and these are:

1. acetone.
2. Acetoacetate.
3. β-hydroxybutyric acid.

ketone bodies formation

4. Normally no ketone bodies are found in the urine because all the metabolized fats are completely broken down to CO2 and H2O.
5. When the carbohydrate source of energy is unavailable, body fat stores are mobilized to supply energy, and ketones are found in the urine.
6. Ketone bodies formation in diabetic patients.
   1. In diabetic patients, ketonuria shows a deficiency of insulin.
   2. It needs to adjust the dose of insulin in diabetic patients.

Ketone bodies in diabetic patients

7. The increased amount of ketones in the blood leads to electrolyte imbalance and dehydration.
8. If this is not corrected, it leads to acidosis, and ultimately the patient goes into a coma.

ketone bodies in diabetes mellitus

9. These ketone bodies’ ratio is different, acetoacetate 20%, acetone 2%, and β-hydroxybutyrate 78%.

Ketone bodies formation and ratio

Normal ketone bodies:

1. These are negative in the random sample.
2. Qualitatively is also negative.

Urobilinogen in the urine

1. It is a colorless compound, and it forms in the intestine by the bacterial enzyme from the reduction of bilirubin action.
2. Normal urine contains small traces of urobilinogen.
3. Because of the fewer number of intestinal bacteria, infants have decreased urobilinogen in the urine.
4. It is decreased after the antibiotics therapy because of the decreased number of intestinal bacteria.
5. Urobilinogen is a bile pigment like bilirubin, and hemoglobin degradation forms it.
6. It is formed in the intestine from the bilirubin by the action of the intestinal bacteria.
7. Most of the urobilinogen is reabsorbed into the blood circulation (enterohepatic circulation), and some of this is excreted through the kidney into the urine.
8.  It is oxidized to urobilin in the feces and gives a characteristic brown color to stool.
   1. So usually, a urine test for urobilinogen is positive. There is normally <1 mg/dL or Ehrlich unit in the urine. So it is necessary to test for bilirubin and urobilinogen to diagnose liver diseases.
9. Absent urobilinogen in the urine and feces is diagnostic of biliary duct obstruction.

Urobilinogen in different conditions:

Sample of the urine:

1. A fresh urine sample is needed ( because it is light-sensitive).
2. An ideal sample for detecting or quantitating is 2- hour early afternoon specimen.
3. Keep in mind the diurnal variation.

Indications for urobilinogen in the urine:

1. Early detection of liver diseases.
2. Hemolytic diseases.
3. Hepatitis and Cirrhosis.
4. In carcinomas.

Differential diagnosis of urobilinogen in the urine:

The fate of Urobilinogen and excretion in the urine

Ehrlich aldehyde reaction:

1. This is the test for urobilinogen.
2. Perform this test on the fresh urine sample because it is unstable and breakdown into urobilin on keeping the urine.
3. This test detects urobilinogen at least at the level of 0.1 mg/dL.
4. Procedure:
   1. The reagent strip is impregnated with p-dimethylamino benzaldehyde, and there is an acid buffer.
      1. This method may give a false-positive result due to the presence of porphobilinogen.
   2. Another method uses the Diazonium compound, and it forms red color.
   3. Result:  Red color in positive cases.

The normal urobilinogen in the urine

1.  Its level with this method is 0.1 to 1.0 mg/dL.
2. The level of 2 mg/dL is the cut-off point for the result to be abnormal.
3. These are 0 to 4 mg / 24 hours.
4. Random urine = 0.1 to 1 Ehrlich U/dL or <1 mg/dL.
   1. 2 hours urine = 0.1 to 1.0 Ehrlich U/2 hours or <1 mg/2 hours.
   2. 24 hours urine = 0.5 to 4.0 Ehrlich U/24 hours or 0.5 to 4.0 mg/24 hours.

Increased level of urobilinogen is seen in:

1. Hemolytic anemia.
2. Pernicious (megaloblstic) anemia.
3. Malarial attack.
4. Excessive bruising.
5. Pulmonary infarction.
6. Cirrhosis.
7. Acute hepatitis.
8. Cholangitis.

A decreased level of urobilinogen is seen in:

1. Complete or partial obstruction of the biliary tract.
2. Cholelithiasis.
3. Biliary duct inflammation.
4. Cancer of the head of the pancreas.
5. Antibiotic therapy will suppress intestinal bacterial flora.

Bilirubin in the urine

1. Bilirubin in the urine is called bilirubinuria.
2. This will appear in the urine before the appearance of jaundice.
3. Bilirubin is a pigmented yellow compound, a degradation product of hemoglobin.
4. The following diagram gives the concept of the formation of bilirubin. When there is increased production, then it may appear in the urine.

Bilirubin metabolism

5. Conjugated bilirubin appears in the urine when the normal degradation cycle is disrupted by obstruction of the bile duct-like gall stones or cancer.
   1. Another possibility is when the liver cells are damaged and allow the leakage of bilirubin directly into the circulation.
   2. Hepatitis and cirrhosis are common causes of liver cell damage and result in bilirubinuria.
   3. Increased hemolysis does not produce bilirubinuria.
6. Bilirubin in the urine is detected only if the urine sample is fresh because bilirubin decomposes rapidly in bright light.
7. If the urine is left in the lab, bilirubin is converted into biliverdin, a green compound by the light not detected by the bilirubin strips.

Normal bilirubin level in urine:

1. Urine bilirubin is negative (0 to 0.2 mg/dL (0 to 0.34 µmol/L).
2. Bilirubin can be detected in urine by the Foam test.

The procedure of foam test for bilirubin:

1. Place a small urine volume in the test tube, cap it, and shake it vigorously.
2. Result:
   1. The foam at the top is white means bilirubin is negative.
   2. If the foam is orange in color means bilirubin is present.

Other methods to detect bilirubin in the urine are:

1. Diazo reaction in the form of tablets or Dipsticks.
2. Fouchet’s test.
3. Ferric chloride test.

Comparison of Fouchet’s, Ferric chloride, and Diazo reaction for Bilirubin:

1. Increased bilirubin in the urine is seen in the following:
   1. Hepatitis and liver diseases.
   2. Obstructive biliary tract disease.
   3. Liver or biliary tract tumors.
   4. Septicemia.
   5. Hyperthyroidism.

Hemoglobinuria

Hemoglobinuria causes are:

1. It may result from the hemolysis of RBCs in the urinary tract. This happens in dilute and alkaline urine.
2. This can also occur in intravascular hemolysis, where hemoglobin filters out through the glomeruli. No RBCs will be seen in the urine.

Pathogenesis of hemoglobinuria:

1. Under normal conditions, the complex of hemoglobin+haptoglobin complex can not filter out of the glomeruli.
2. This happens when the free hemoglobin exceeds the haptoglobin e.g.
   1. Hemolytic anemia.
   2. Transfusion reactions.
   3. Infection.
   4. Severe burns.
   5. Strenuous exercise.
   6. Malarial infection.

Normal hemoglobinuria

• This is negative.

Myoglobinuria

1. Myoglobin is a heme-containing protein found in muscle tissue.
2. This is seen in the case of rhabdomyolysis.
3. The heme portion of the myoglobin is toxic to the renal tubules; increased concentration will lead to renal failure.
4. The blood hemolytic transfusion reaction may cause damage to the kidneys and leads to renal failure.

Causes of hemoglobinuria are:

1. Crush syndrome.
2. Muscle wasting diseases.
3. Trauma.
4. Alcoholism.
5. Convulsion.
6. Extensive exertion.
7. Heroin abuse.

Ammonium sulfate (NH4)2SO4) concentration test:

1. It is done to differentiate hemoglobinuria and myoglobinuria:

Urine ammonium sulfate test for the D/D of hemoglobinuria and myoglobinuria

Phosphorus

1. Most of the body’s phosphorus is combined with the calcium in the bones.
2. About 15% is present in the blood, making the main intracellular anions.
3. The human body contains 620 g of phosphorus, mainly in the form of phosphate.
4. The urine HPO₄-2^_: H2PO4^– ratio varies over a wide range, from 1: 100 at pH 4.5 and  90:10 at pH 8.0.
5. Urine for phosphorus for 24 hours collections needs acid-washed detergent-free containers.

Indication for urinary 24 hours phosphorus:

1. In hyperparathyroidism.
2. In hypoparathyroidism.
3. In case of renal loss.

Phosphorus has many functions in the body:

1. It has a role in glucose and lipid metabolism.
2. It helps in the storage and transfers the energy in the body.
3. It generates bony tissue.
4. It maintains the acid-base balance in the body.

Normal phosphorus in urine:

1. Serum level = 2.4 to 4.1 mg/dL (0.78 to 1.34 mmol/L).
2. Urine = 1 gram / 24 hours.
3. This also depends on the diet.
4. Inorganic phosphate = 20 to 40 meq/L.

Creatinine/Creatine

1. Creatine is synthesized in the liver, pancreas, and kidneys from the amino acids arginine, glycine, and methionine.
2. It is transported from blood to muscles, the brain, and other organs,  converted to phosphocreatine, and acts as an energy reservoir like ATP.
3. Creatinine is the waste product of creatine and phosphocreatine.
4. Most of the creatinine is produced in the muscles, so it is proportional to the muscle mass.
5. Creatinine enters the blood and is excreted through the kidney.

Indications for creatinine:

1. To evaluate kidney diseases.
2. During 24- hours of urine collection refrigerates the urine, and no preservative is needed.

Normal creatinine in urine:

1. 1.0 to 1.6 gm/24 hours.
2. Or 15 to 25 mg/ kg body weight / 24 hours.

Nitrites/Nitrates

1. Some of the bacteria from the urinary tract convert Nitrates into nitrite.
2. Bacteria containing the enzyme reductase will convert nitrate to nitrite.
   1. NO3 →NO2 in the presence of a reductase enzyme.
   2. This test is negative in yeast and gram-positive bacteria.
3. The reductase enzyme is found in gram-negative bacteria like Enterobacteriaceae.
4. This is available as urine reagent strips and detects urinary tract infections.
5. Most infections start in the urinary bladder, and from there, it travels to the ureters, tubules, and renal pelvis and reaches the kidneys.
6. This is useful for detecting the initial urinary bladder infection called cystitis.
7. Cystitis will lead to pyelonephritis as a complication of cystitis, and the result is:
   1. Renal tissue damage.
   2. Impairment of renal functions.
   3. Hypertension.
   4. Sometimes lead to septicemia.
8. So the detection of bacteriuria in the early stages and the treatment in time will save from all these complications.

Indications for Nitrate test:

1. Cystitis.
2. Pyelonephritis.
3. Monitoring of the patients who are at high risk for urinary tract infection.
4. Monitoring of antibiotic therapy.
5. Screening of the urine culture specimens.
6. These are negative.
   1. A negative result does not rule out bacteriuria.
7. A gram-positive pathogen does not produce a nitrate-reducing substance like:
   1. Staphylococcus.
   2. Enterococcus.
   3. Streptococcus.

Sodium

1. Sodium is the primary regulator for retaining or excreting water and maintaining acid-base balance.
2. Sodium also maintains the normal electrolytes’ intracellular and extracellular balance. This will take place along with potassium under the effect of aldosterone.

Indication for urinary sodium:

1. Electrolytes imbalance.
2. Acute renal failure.
3. Hyponatremia.
4. Oliguria.
5. Na⁺ excreted for diagnosis of renal and adrenal imbalance. No preservative is needed for the collection for 24 hours ; only refrigerate during the collection.

Increased sodium in urine is seen in:

1. Addison’s disease (adrenal failure, primary and secondary).
2. Renal tubular acidosis.
3. Diabetic acidosis.
4. Tubulointerstitial disease.
5. Salt-losing nephritis.
6. Barrter’s syndrome

A decrease in urinary sodium is seen in the following:

1. Excessive sweating and diarrhea.
2. Prerenal azotemia.
3. Cushing’s syndrome.
4. Primary aldosteronism.
5. Congestive heart failure.
6. Nephrotic syndrome with acute oliguria.

Normal sodium in urine:

1. Adult = 40 to 220 meq/24 hours urine (40 to 220 mmol/day)
2. Child = 41 to 115 meq/24 hours urine (41 to 115 mmol/day)
3. Value is salt intake dependent.

Potassium

1. Potassium acts as a body buffer system and serves an important role in the maintenance of electrolyte balance.
2. The potassium study is helpful for the study of renal and adrenal disorders.
3. Potassium in the urine is in the form of KCL, K2SO4, and K2PO4 salts.
4. K⁺ values <20 meq/L are associated with nonrenal causes.
   1. K⁺ >20 meq/L are associated with renal causes.

Indications for K⁺ estimation:

1. To evaluate the electrolyte imbalance.
2. Renal disorders.
3. Adrenal glands disorder.
4. For collecting urine for 24 hours, no preservative is needed; only refrigerate the sample during collection.

Normal potassium in urine:

1. Adult = 25 to 125 meq/24 hours urine (25 to 125 mmol/day).
2. Child = 10 to 60 meq/24 hours urine (10 to 60 mmol/day)
3. Values are diet-dependent.

Increased urinary K⁺ is seen in:

1. Diabetic and renal tubular acidosis.
2. Primary renal diseases.
3. Cushing’s syndrome.
4. Starvation.
5. Primary and secondary aldosteronism.
6. Fanconi’s syndrome.
7. The onset of metabolic alkalosis.

The decreased urinary K⁺ value is seen in the following:

1. Addison’s disease.
2. In patients with K⁺ deficiency.
3. Pyelonephritis and glomerulonephritis.

Calcium

1. The parathyroid gland hormones maintain calcium hemostasis.
2. An adequate amount of calcium is excreted in the stool, and a small amount is in the urine.
3. Calcium absorption is dependent upon dietary calcium intake.

Indications for calcium in the urine:

1. To evaluate the calcium intake.
2. To evaluate the rate of absorption from the intestine.
3. To find resorption from the bone.
4. To evaluate the renal loss.

Normal calcium in urine:

1. Normal diet = 100 to 300 mg/24 hours (2.50 to 7.50 mmol/day)
2. Low calcium diet = 50 to 150 mg/24 hours (1.25 to 3.75 mmol/day)
3. Another source:
   1. 5 to 12 meq/L
   2. < 150 mg/ 24 hours on a low calcium diet.
   3. Or o.3 g/24 hours of urine.

Increased calcium in urine is a result of the following:

1. Increased intestinal absorption.
2. A lake of renal tubular reabsorption.
3. Resorption or loss of calcium from the bones.
4. Or there is a combination of the above mechanism.
5. Calcium is present in urine as CaCl2, CaSO4, and CaPO4 salts.
6. Urinary calcium does not have much value in the differential diagnosis of diseases.

Increased urine calcium is seen in:

1. Hyperparathyroidism in 30 to 80% of the cases.
2. Paget’s disease.
3. Renal tubular acidosis.
4. Vitamin D intoxication.
5. Fanconi’s syndrome.
6. Idiopathic hypercalciuria.
7. Osteoporosis.
8. Osteitis deforms.
9. Sarcoidosis.
10. Bone metastasis in osteolytic type.
11. Multiple myeloma.
12. Thyrotoxicosis.

A decrease in urinary calcium is seen in the following:

1. Hypoparathyroidism.
2. Vitamin D deficiency.
3. Metastatic carcinoma of the prostate.
4. Preeclampsia.
5. Malabsorption syndrome:
   1. Celiac disease.
   2. Steatorrhea.
   3. Sprue disease.
6. Renal osteodystrophy.
7. Renal failure, acute nephrosis, and nephritis.
8. Vitamin-D resistant Rickets.

Chloride

1. Chloride is most often associated with sodium balance and fluid changes.
2. Mostly urinary excretion of chloride is parallel to the dietary intake.
3. This also reduces dietary salt intake, especially in patients with cardiovascular diseases,  hypertension, kidney diseases, and liver diseases.

Indications for chloride:

1. It is advised in electrolyte imbalance.
2. In the case of dehydration.
3. In metabolic alkalosis.
4. For collecting the urine, no preservative is needed; only refrigerate the samples.

Normal chloride in urine:

1. Children’s values are much lower than adult values.
2. The values vary with the salt intake and perspiration.
3. The values vary from different lab values.
   

   Age	Value in 24 hours of urine
   Child <6 years	15 to 40 meq/day (15 to 40 mmol/day)
   Children 10 to 14 years	64 to 176 meq/day (64 to 176 mmol/day
   Adult	140 to 250 meq/day (140 to 250 mmol/day)

Magnesium

1. Magnesium excretion through the urine controls the blood magnesium level.
2. Urinary excretion of magnesium is dependent upon dietary intake.
3. If somebody takes 200 to 500 mg/day, then urinary excretion of magnesium is 75 to 150 mg/24 hours (3 to 6 mmol/day).

Indications for magnesium:

1. It is advised in magnesium metabolism.
2. Electrolytes balance.
3. Advised in nephrolithiasis.
4. For collecting the 24-hour urine sample, 20 mL of 6N HCL is needed in a metal-free container. Also, refrigerate the sample.

Normal magnesium in urine:

1.  Urine = 75 to 150 mg/24 hours
2. urine = 3.0 to 6.0 meq/24 hours (3.0 to 6.0 mmol/day)
3. 2 to 12 meq/L

Increased urine magnesium is seen in:

1. 1. Chronic glomerulonephritis.
   2. Increased level of blood alcohol.
   3. Bartter’s syndrome.

Decreased urine magnesium is seen in:

1. Magnesium deficiency.
2. Malabsorption.
3. Chronic renal diseases.
4. Hypoparathyroidism.
5. Hypercalciuria. It is seen in long-term parenteral therapy.
6. Decreased renal function like Addison’s disease.

Amino acids

1. Free amino acids are found in the urine and acid filtrate of the protein-containing fluids.
2. This test is advised when there are suspected genetic abnormalities, patients with mental retardation, reduced growth, or unexplained symptoms.

Indications for an amino acid in urine:

1. This is advised for the screening of the inborn error of metabolism.
2. Advised for genetic abnormalities.
3. For collecting the 24 hours of urine, no preservative is needed; only refrigerate while collecting the samples.

Normal amino acids in urine:

1. Negative.

Urine analysis summary

The details are seen in part 1, complete urine analysis.

Questions and answers: