Urinary citrate

Less than 5% of thorium was excreted in the urine up to 42 days after intravenous injection of thorium-234 sulfate in rats and guinea pigs (Scott et al. 1952). After intravenous injection, the amount of thorium excreted in the feces was 0.7-24.5% of the level administered for 14-42 days in rats, 0.6 and 14.6% for 2 and 5 days in guinea pigs, and 0.9% for 7 days in rabbits. In dogs injected with thorium-228 citrate, urinary excretion dominated initially, but after 2.5 years, the fecal to urinary ratio approximated 1.0 (Stover 1981 Stover et al. 1960). Thomas et al. (1963) reported the excretion of thorium citrate administered as thorium-234 tracer plus thorium-232 carrier in rats. No differences were found in the rate and route of excretion following various routes of administration (intravenous, intraperitoneal, intratracheal, and intramuscular). In the first 2 days, 25-30% of the thorium was excreted. Most of the thorium was excreted in the feces and not in the urine. At a high exposure level, the feces/urine ratio was 45 and at a low level, it was 1.6. This indicates that at the... 

Urinary tract The susceptibUity factors for topiramate-induced renal stones have been studied in six subjects [321. After 5 days treatment there was a 31% reduction in mean calcium and a 40% reduction in mean citrate urinary concentrations. Dose escalation was associated with a further reduction in citrate concentration. The authors concluded that topiramate causes a profound reduction in urinary citrate concentrations, equivalent to the changes seen in distal renal tubular acidosis. 

Litholytic agents in current use are classified as direct or indirect. Indirect type drugs decrease the C.P. of urine, thus inhibiting calculus formation. An example is citrate which helps prevent insoluble salts from crystallizing in the urinary tract. Potassium citrate is administered in pill form as a preventive drug. Direct type drugs dissolve renal calculi which have already formed. 

Finally, we may add that fluorocitrate interferes with fat metabolism in vivo, because it leads to rapid and marked urinary appearance of ketone bodies.1 Unlike fluoroacetate, intraperi-toneal fluorocitrate (20 mg./kg.) (synthetic), though increasing the citrate in the brain, produces no convulsions in 2 hr. 

Urinary alkalinization- Urates tend to crystallize out of an acid urine therefore, a liberal fluid intake is recommended, as well as sufficient sodium bicarbonate (3 to 7.5 g/day) or potassium citrate (7.5 g/day) to maintain an alkaline urine continue alkalization until the serum uric acid level returns to normal limits and tophaceous deposits disappear. Thereafter, urinary alkalization and the restriction of purine-producing foods may be relaxed. 

Drugs that may affect tetracyclines include antacids containing aluminum, calcium, or magnesium iron salts zinc salts barbiturates bismuth salts carbamazepine cholestyramine colestipol phenytoin rifamycins urinary alkalinizers (eg, sodium lactate, potassium citrate). 

Overall, serum and urinary increment methods have shown that a Ca source (e.g., CaCOs) accompanied by citrate is better absorbed than one that is not (Heaney et ah, 1999). Citrate that is absorbed into circulation is inclined to bind Ca ions and thereby artificially elevate incremental data compared to other salts (Heaney, 2001b). A number of studies utilizing the most sensitive isotopic tracer methods have demonstrated that CCM is highly absorbable compared to other Ca sources (Abrams et ah, 2003 Heaney et ah, 1989b Miller et ah, 1988 Smith et ah, 1987). 

In both sexes, CCM-OJ provided an alkali load that significantly increased urinary pH compared to basal levels and versus milk consumption, and also increased urinary citrate excretion versus basal levels. An elevated urine pH and citrate level are generally considered to reduce Ca oxalate supersaturation and crystallization potential (Odvina, 2006). However, in this study the relative supersaturation measurement for Ca oxalate was not different between the CCM-OJ and milk treatment groups, or between either treatment and the basal levels. Although the alkalizing effect of milk was less than that of CCM-OJ, it also induced a higher urinary pH compared to basal levels (p <. 01 and p <. 05 in women and men, respectively). 

Diethylcarbamazine, a synthetic piperazine derivative, is marketed as a citrate salt. It is rapidly absorbed from the gastrointestinal tract after a 0.5 mg/kg dose, peak plasma levels are reached within 1-2 hours. The plasma half-life is 2-3 hours in the presence of acidic urine but about 10 hours if the urine is alkaline, a Henderson-Hasselbalch trapping effect (see Chapter 1). The drug rapidly equilibrates with all tissues except fat. It is excreted, principally in the urine, as unchanged drug and the N-oxide metabolite. Dosage may have to be reduced in patients with persistent urinary alkalosis or renal impairment. 

Table 3.5.3 Reference values for urinary oxalate, glycolate, citrate, glycerate (given in mmol/mol creatinine), and sulfate (given in mol/mol creatinine), and plasma oxalate, citrate, and sulfate (given in fimol/l)...

Forfar et al. (F7) have examined urinary citrate excretion in one case of idiopathic hypercalcemia. During the active phase of the condition, citrate excretion was 9.5 and 10.6 mg/day rising to 96 mg/day during the recovery phase. The latter represents a low normal value. It would appear that in this particular case, a hypocitruria existed during the active phase of the condition. 

The urinary excretion of citrate in hypervitaminosis D has been reported to be increased above the normal range (H5). 

Urinary pH significantly affects the activity of nitrofurantoin, with loss of potency as the urine becomes more alkaline. For this reason, women with lower UTI who are prescribed nitrofurantoin should be advised not to take alkalinising agents such as potassium citrate (Effercitrate). 

METHENAMINE POTASSIUM CITRATE 1 efficacy of methenamine Methenamine is only effective at a low pH raising the urinary pH 1 its effect Avoid co-administration... 

Perez, G.A., Frindt, G. (1977). The effect of fluorocitrate on urinary calcium and citrate excretion. Experimentia 33 741-2. 

CAIs alter renal function primarily by inhibiting carbonic anhydrase in the proximal tubule, which results in decreased bicarbonate reabsorption. The net effect of the renal actions of acetazolamide therapy is alkaliniza-tion of the urine and metabolic acidosis. Metabolic acidosis results from the initial bicarbonate loss and persists with continued acetazolamide use. Moderate metabolic acidosis develops in most patients. Reabsorption of bicarbonate independent of carbonic anhydrase prevents severe acidosis. Initially, acetazolamide produces diuresis, but urinary output decreases with the development of metabolic acidosis. In addition, decreased urinary citrate excretion follows acetazolamide therapy and has been attributed to the metabolic acidosis it produces. A high urinary pH and low urinary citrate concentration are conducive to precipitation of calcium phosphate in both the renal papillae and the urinary tract. 

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