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II. Ammonia

Ordinarily, 2.5-4.5% of the total urinary N is composed of NH4-salts. On the average, this represents about 0.7gm/day.

Note:since both urinary NH3 and urea are derived from the –NH2 grs of aminoacids, for a given quantity of N2 excreted, an increase in the amount of one leads to a decrease in the other.

Clinical significance

Decrease:

1. quantity of urinary NH3 per day decreases grossly in alkalosis.

2. Administration of alkalies or base forming foods decreases the excretion of NH3.

3. Nephritis – urinary NH3 may be markedly decreased in cases of severe nephritis, in which the capacity of the kidneys to form it is impaired. This reduces the capacity of the kidneys to conserve base and contributes to developments of acidosis

Increase

1. in cases of severe diabetic acidosis.

2. Administration of acid forming foods also increase NH3 output.

3. Copious water drinking increases the ammonia output.

4. The quantity of NH3 in the urine may be enormously increased through hydrolysis of urea by the bacteria in the bladder in cystitis or in other parts of urinary tract.

Note:bacterial production of NH3 from urea in normal urine may take place if the samples are stored without preservative due to bacterial contamination (“alkaline” fermentation).

III. Uric acid

Normal value: the quantity of uric acid in human urine is generally from 0.5-1.0gm per 24 hours, though it is subjected to wide variations.

Clinical significance

1. Diet: on a purine free diet uric acid excretion may fall to 0.1gm/day, while on a high purine diet the daily excretion may rise to 2gms/day.

2. Pathological variations:

(i) In gout – the uric acid excretion in urine tends to decrease prior to an attack of gout and to increase during the crisis and recovery, sometimes to twice the normal values.

(ii) Conditions involving the breakdown of large quantities of nuclear material such as is found in destruction of leukocytes as in leukaemias – may cause the excretion of large amounts of uric acid (10gms or more).

3. Administration of cortisone or ACTH increases urate excretion.

4. In Wilson’s disease – increased excretion of uric acid occurs due to accumulation of copper in the kidneys leads to damage to proximal renal tubules.

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