I can only discuss chloride clearance from a medical stand point so I am not sure it will be of help to you?
In most clinical states, sodium and chloride excretion vary in parallel [1] . When used to assess volume status, for example, both are typically less than 15 meq/L with hypovolemia and greater than 20 meq/L with euvolemia or volume expansion.
However, as many as 30 percent of volume depleted patients have more than a 15 meq/L difference between the sodium and chloride concentrations in the urine [1] . This may be due to the excretion of sodium with another anion (such as bicarbonate or carbenicillin) or of chloride with another cation, such as ammonium in metabolic acidosis. (See "Urine anion and osmolal gaps in metabolic acidosis").
As a result, it may be helpful to measure the urine chloride concentration in a patient who appears to be hypovolemic but has a higher than expected urine sodium. This most often occurs in metabolic alkalosis due to vomiting. In this setting, the desire to excrete the excess bicarbonate (as NaHCO3) to correct the alkalosis may lead to a high urine sodium concentration despite the presence of volume depletion (show table 1) [1,2] .
In contrast, there is no stimulus to chloride wasting; as a result, the urine chloride concentration will be appropriately low, reflecting both the true volume status and the associated hypochloremia. The possibility of bicarbonate-induced sodium-wasting can be detected simply by measuring the urine pH: a value above 7.0 suggests significant bicarbonaturia and the probable need to measure the urine chloride, whereas a value below 6.5 indicates that there is little bicarbonate in the urine and that the urine sodium concentration alone should be accurate (assuming that some other unmeasured anion is not present). (See "Urine electrolytes in diagnosis of metabolic alkalosis").
The dissociation between urinary sodium and chloride occurs in the opposite direction in metabolic acidosis. In this setting, ammonium excretion is physiologically increased in an attempt to excrete the excess acid. The net effect is that, in a hypovolemic patient with diarrhea, the urine sodium concentration is appropriately low but the excess urinary ammonium will obligate an increase in the urine chloride concentration [3] .
Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES
Sherman, RA, Eisinger, RP. The use (and misuse) of urinary sodium and chloride measurements. JAMA 1982; 247:3121. Kassirer, JP, Schwartz, WB. The response of normal man to selective depletion of hydrochloric acid. Factors in the genesis of persistent gastric alkalosis. Am J Med 1966; 40:10. Kamel, KS, Ethier, JH, Richardson, RM, et al. Urine electrolytes and osmolality: When and how to use them. Am J Nephrol 1990; 10:89.
