Riboflavin vitamin urinary excretion

Riboflavin and riboflavin phosphate that are not bound to plasma proteins are filtered at the glomerulus. Renal tubular resorption of riboflavin is saturated at normal plasma concentrations. There is also active tubular secretion of the vitamin urinary excretion of riboflavin after high doses can be two- to threefold greater than the glomerular filtration rate. 

There is no evidence of any significant storage of riboflavin in addition to the limited absorption, any surplus intake is excreted rapidly thus, once metabolic requirements have been met, urinary excretion of riboflavin and its metabolites reflects intake until intestinal absorption is saturated. In depleted animals, the maximum growth response is achieved with intakes that give about 75% saturation of tissues, and the intake to achieve tissue saturation is that at which there is quantitative urinary excretion of the vitamin. 

Under normal conditions, about 25% of the urinary excretion of riboflavin is as the unchanged vitamin, with a small amount as a variety of glycosides of riboflavin and its metabolites. Riboflavin-8-a-histidine andriboflavin-8-a-cysteine arising from the catabofism of enzymes in which the coenzyme is covalently bound are excreted unchanged. 

Two methods of assessing riboflavin status are generally used urinary excretion of the vitamin and its metabolites, and activation of EGR. Criteria of riboflavin adequacy are shown in Table 7.5. 

Clinical signs of riboflavin deficiency are seen at intakes below about 1 mg per day. At intakes below about 1.1 mg per day, there is very little urinary excretion of riboflavin thereafter, as intake increases, there is a sharp increase in excretion. Up to about 2.5 mg per day, there is a linear relationship between intake and excretion. At higher levels of intake, excretion increases sharply, reflecting active renal secretion of excessive vitamin (Section 7.2.5). 

Indices of Vitamin E Nutritional Status Reference Intakes of Vitamin K Indices of Thiamin Nutritional Status Reference Intakes of Thiamin Tissue Flavins in the Rat Urinary Excretion of Riboflavin Metabolites... 

Fourteen cases of acute boric acid ingestion were reported in New York City over 30 months. In these patients excretion of urinary riboflavin (vitamin B2) was determined, and in about two-thirds it was significantly increased. This is not surprising, since riboflavin and boric acid are known to form a water-soluble complex. The range of lethal doses is 1-3 g for babies, 5 g for infants, and 15-20 g for adults. 

In a small study of children on PHT, their mean urinary excretion of riboflavin was low, i.e. 14% of dietary intake. This may indicate riboflavin deficiency (Lewis et at. 1998). Patients on inducer AEDs (PHT, PB, PRD and CBZ) have low plasma riboflavin (Apeland et at. 2003 Krause et at. 1988). Low plasma riboflavin may indicate increased risk of vitamin B2 deficiency. Furthermore, patients with low plasma riboflavin also have elevated plasma flavin nucleotides (Apeland et at. 2003). 

Estimates of riboflavin requirements are based on depletion/repletion studies to determine the minimum intake at which there is significant excretion of the vitamin. In deficiency there is virtually no excretion of the vitamin as requirements are met, so any excess is excreted in the urine. On this basis the minimum adult requirement for riboflavin is 0.5-0.8 mg/day. At intakes between 1.1 and 1.6mg/day urinary excretion rises sharply because tissue reserves are saturated. 

Use of physiological functional indices in relation to riboflavin deficiency (analogous to dark adaptation for vitamin A clotting factors for vitamin K, etc.) has not proved possible, because the analogous riboflavin-sensitive physiological processes are insufficiently specific or easily measurable for use in population studies. Of the biochemical indices, urinary excretion and the flavin-dependent enzyme, erythrocyte glutathione reductase, are generally considered to be the front-runners in the race for acceptance in human studies. These have already been described in the previous section. 

As with most other B vitamins, riboflavin and its cofactors are remarkably nontoxic even at high intakes. The reasons for this are probably associated with limitations on absorption, once the active transport process has become saturated in the gut coupled with very effective urinary excretion of any absorbed vitamin that is in excess of cellular requirements. 

Tucker et al. showed that both sudden severe physical exercise and longer sustained work on a treadmill during training decreases urinary riboflavin excretion during the experimental periods (12) The acute reduction in riboflavin excretion observed by these investigators was attributed to a reduction in renal plasma flow. In order to explain the long-term reduced excretion of the vitamin, they proposed that riboflavin was retained for incorporation into "new muscle tissue". The significance of this study is that if the hypotheses... 

At physiological levels, the cysteinyl flavin did not adequately replace or significantly antagonize the vitamin in deficient or normal rats. Excretion of the N-acetylcysteinyl riboflavin and its metabolites was competitive with riboflavin urinary loss was influenced by the amount administered, either separately or together with vitamin. 

---