V. Odor

Freshly voided urine in a normal healthy person or the urine which has not been permitted to spoil, has a not unpleasant odor described as aromatic odor. If urine does not have such an odor soon after it is passed it may be in a pathologic state.

Causes of abnormal odor

1. A putrid or strongly ammoniacal odor points to decomposition by bacteria, probably occurring in the urinary bladder.

2. An unpleasant odor is due to excretion of methyl mercaptan

1. after partaking of food like asparagus

2. methyl mercaptan is some times formed from abnormal metabolism of aminoacid methionine in cases of hepatic failure and excreted in urine.

3. Fruity odor found when a large amount of acetone is excreted in urine in diabetic ketoacidosis. This may help in diagnosis.

4. A peculiar “mousy” odor is found in inherited disorder “phenylketonuria”, in which ‘phenyl-acetyl glutamine’ is excreted and account for the odor.

VI. Turbidity

Normal urine is almost always perfectly clear and transparent when voided. On standing, there is likely to separate out a faintly cloudy flocculation, believed to be mucoprotein or nucleoprotein, which is present only in traces, together with some epithelial cells.

Mucus

It appears as a flocculent precipitate, which gradually sinks to the bottom of the urine. Mucus occurs in greater amounts in

1. in inflammatory conditions of urinary tracts,

2. after prostatic massage, or

3. when the urine contains semen or vaginal discharge.

Types of turbidities

1.Urates: ammonium urate may precipitate, from alkaline urine whereas other urates are found only in acid urines. Ammonium urates dissolve on acidification, whereas other urates on warming.

2. Phosphates: calcium PO4 and NH4-Mg-PO4 (or so called Triple phosphates) are found only in alkaline urine or they may form a cloudy precipitate from an alkaline urine on warming. They dissolve on acidification.

Note:

1. it is essential that a urine sample is slightly acidified, when making a test for heat-coagulable proteins.

2. Furthermore, the iso-electric points (pI) of most proteins that may appear in urine are slightly acidic.

3. Cellular deposits: a sediment in urine that may account for turbidity and does not dissolve on adding acid or on heating is most likely made up of cellular matter, “organised deposit” eg. Pus cells leukocytes, R.B. Cells, epithelial cells or microorganisms etc.

Inorganic constituents

1. Chlorides

Normal value: next to urea, clorides make up the chief solid constituents of urine, generally amounting to 6.0 to 9.0gm per day of Cl, and equivalent to 10-15gms of NaCl, which is the predominant chloride present. However, the daily excrtetion varies with the dietary intake.

Clinical significance

1. Decrease of urinary chlorides:

1. Markedly decreased by excessive sweating by loss of chlorides in sweat.

2. During fasting, chloride excretion may fall to a trace, even though the concentration of blood chlorides is approximately normal. This shows the remarkable capacity of the kidneys to conserve electrolytes for the maintenance of the osmotic pressure of the body fluids.

3. Excretion of chlorides in urine is also decreased, when blood chlorides levels are lowered by loss through diarrohoea and excessive vomiting.

4. Oedema – patients with oedema from practically any cause (nephrotic syndrome, nephritis, malnutration, or cardiac decompensation) show decreased urine chlorides rather independent of blood chlorides concentration.

5. Diabetes insipidus – urine chlorides may be extremely low in cases of severe D.insipidus.

6. Infections – during pneumonia and other infectious diseases, hypochloraemia, results from the withdrawal of blood chlorides into exudates, and the excretion of chlorides in urine falls. Upon resolution of exudates, excretion of chlorides increases.

7. Urinary excretion of chlorides is decreased in Adrenocortical hyperfunction (Cushing’s syndrome).

(b) Increase of urinary chlorides

1. Excessive water drinking and the resulting diuresis cause increased chloride excretion.

2. Addison’s disease – Excessive amounts of sodium and chloride are excreted in the urine in cases of adrenal cortical insufficiency

3. Use of diuretics.

II. Phosphates

Phosphate ions rank next to Cl- - among the anions in urine.

Normal value: the amount varies widely depending on the diet. Usually it is 0.8 to 1.3g of P per day (average about 1.1g).

Most of the urinary PO4 is present as

1. inorganic PO4

2. organic PO4 – only 1 to 4% of the total.

Source: Urinary PO4 arises largely from the breakdown of phospholipids, nucleoproteins, nucleotides and phosphoproteins of foods and tissues. Reaction of intestinal contents determine the quantity of PO4 absorbed into the blood and excreted in urine. An acid condition increases the intestinal absorption.

Clinical significance

(a) Increase:

1. Urinary phosphate excretion is increased in diseases of bones such as rickets, osteomalacia, and periostosis.

2. Parathyroid hyperfunction – In hyperparathyroidism increased amounts of phosphates are excreted.

3. Acidosis – In acidosis, PO4 excretion may rise (unless the kidney is incapable of secreting it, as may be in nephritis).

(b) Decrease: Low urinary PO4 is likely to be associated with:

1. Diarrhoea – as intestinal contents are hurried through the G.I.tract.

2. In acute infections.

3. In nephritis – because failure of the kidneys to function adequately.

4. In parathyroid hypofunction – hypoparathyroidism.

5. Pregnancy – due to utilization of maternal PO4 in the formation of foetal bones.

6. During insulin administration as there is increased requirement of PO4 for the formation of hexose-phosphate.

7. Certain inherited disorders like Galactosaemia, hereditary fructose intolerance.

III. Sulfur Compounds in Urine

Forms of sulfur compounds

Sulfur is excreted in urine in three forms:

1. Inorganic SO4 – 80 to 85%

2. Organic esters or “ethereal sulfates” – 5%

3. Neutral sulfur – (organic sulfate) – 15 to 20%.

Source: Most of urinary sulfur arises from metabolism of proteins, specially from sulfur-containing aminoacids cysteine, cystine and Methionine.

Note: Methionine indirectly contributes through cysteine. A small amount obtained from S-containing vitamins like thiamine, Biotin, Lipoic acid. Food proteins contain on an average 1% of sulfur. Excretion of S in urine varies with:

1. protein intake in diet and

2. rate of tissue protein break down.

Normal value and clinical significance: total urinary sulfur varies from 0.8 to 1.4gm per 24hrs (average =1.0gm). urinary N:S ratio = 13 to 16 on a high meat diet and during fasting.

1. Inorganic SO4

Makes greater proportion – 0.7 to 1.0gm per day, and constitutes 80 to 85% of total S excreted.

Decrease – The SO4 sulfur excretion may be diminished in conditions of renal functional impairment.

Increase: it is increased

1. on high protein diets, and

2. in excessive tissue Proteins breakdown

2. Ethereal sulfur

Range from 0.06 to 0.12 gm/day. It consists ofNa and K salts of sulfuric acid esters of phenols such as indoxyl, skatoxyl, phenol and cresol. These ethereal SO4 represent detoxication compounds of phenols and are formed in liver. Some of the phenolic substances originate through:

1. Bacterial action in the gut,

2. Some appears to be formed in tissue metabolism.

Indoxyl and skatoxyl are formed practically entirely by putrefactive decomposition of tryptophan in the gut and phenol and cresol from tyrosine. Both substances are esterified with H2SO4 in liver and excreted in urine as the Na and K salts. K-salt of indoxyl sulphuric acid is called as Indican and is excreted in urine.

Clinical importance: Excretion of Indican in urine is taken as a rough index of intestinal putrefaction.

1. Clinically in intestinal obstruction due to putrefaction, and absorption of these products in carcinoma liver, cholera, thyphus, excretion of ethereal SO4 increases. In cholera and thypus, sufficient indican is excreted to cause urine to assume a bluish tinge on standing.

2. Bacterial decomposition of tryptophan in pus anywhere in the body in pathological conditions increase the excretion of indican.

3. Neutral Sulfur Fraction

Ranges from 0.08-0.16 gm/day. It is composed of heterogenous mixture of sulfur compounds. These include cystine, methionine, urochrome, thiosulfates, oxy-proteic acids, thiocyanates, bile acids and taurine and its derivatives.

Clinical significance: Increase – Urinary sulfur (neutral fraction) is increased in:

1. Inherited disorders like cystinuria, Homocystinuria.

2. Melanuria in melanoma

3. In obstractive jaundice – due to excretion of bile acids

4. In hepato cellular jaundice

5. Cyanide poisoning – as cyanide is converted to thiocyanates

6. In chloroform anaesthesia.

IV. Sodium (Na) and Potassium (K)

The kidney plays the vital role in regulation of excretion of Na and K.

Normal value: Daily urinary output approximates their intake in diet. Under usual dietary conditions, a normal healthy adult excretes in the urine about 3-5gms (130-215mEq) of Na; and 2-4gms (50-100mEq) of K daily. Na:K ratio = is approx 5:3

Clinical significance: 1. Fasting or inadequate protein in take, in excessive tissue protein catabolism, with liberation of Intra-cellular fluid components, results in an increase in urinary K and a change in Na:K ratio (in fasting, there is lack of NaCl intake). 2. Mineralo corticoid, aldosterance, increases the reabsorption of Na and excretion of K. In primary aldosteronism (Conn’s syndrome) the excretion of K will increase. 3. Effect of acidification of urine: K enters the urine from the plasma by glomerular filtration and also by active tubular secretion, the latter mechanism apparently competing withh that for urine acidification. The amount of K in urine is thus influenced by the requirement of urine acidification. K excretion will be increased if acidification is low e.g. in alkaline ash diet, and in alkalosis. K excretion will be dicreased if acidification is high eg in highly acid diet, and in acidosis. 4. Abnormal loss, through extrarenal channels of Na e.g in excessive sweating, diarrhoea etc, or of K (in diarrhoea) results in decreased urinary excretion of these elements.

V. Calcium and Magnesium

Ordinarily the greater proportions of Ca and Mg are excreted in the faces. Generally, the urinary excretion of Ca lies between 0.1gm (100mg) and 0.3gm (300mg) and of Mg between 0.1gm (100mg) and 0.2gm (200mg) per day. Absorption depends on reaction of the intestinal contents – increased alkalinity of intestinal contents causes precipitation of increased amounts of Ca and Mg phosphates which are lost in the faeces, with less being absorbed in blood and excreted in urine. Reverse occurs with increased acidity of intestinal contents.

Influence of Diet

Urinary excretion of both Ca and Mg normally is primarily dependant on the nature of the diet and there is wide variation. Under usual dietary conditions, in normal healthy subjects, urinary excretion accounts for about 15-30% of the total Ca and about 20-50% of the total Mg elimination, the remainder being excreted in faeces. At low or moderate levels of Ca intake (0.1-0.5gm daily) about 30-50% is eliminated in the urine, whereas at high levels of intake (1.0gm), about 10-25% is eliminated. The renal threshold for excretion of Ca lies between 6.5-8.0mg/100ml of plasma, little being eliminated at lower plasma Ca concentration.

Clinical Significance of Urinary Calcium

There is an increased urinary Ca if the plasma ionised Ca is high.

Increase: Increased urinary excretion seen:

1. In hyperparathyroidism – 300-700mg per day may be lost. However, normal values are sometimes found, especially so if some impairment of renal function develops.

2. In hyperthyroidism

3. In hypervitaminosis D

4. In multiple myeloma, may be 300-750mg per day

5. Renak stones – an increase in urinary Ca occurs fairly frequently in patients with renal stones who do not hhave hyperparathyroidism

6. In renal tubular acidosis – in which neutral or alkaline urine low in NH3 but high in Na, K and Ca is passed

7. Hyperchloraemic acidosis – enhances loss of Ca from bone, can be seen in Fanconi’s syndrome, galactosaemia, alkaptonuria, Wilson’s desease, nephrogenic diabetes insipidus

8. Drugs – certain drugs e.g. steroids, diuretics, cholestyramine can increase excretion of urinary Ca.