The Mechanism of the Excretion of Vitamin C by the Human Kidney 1

Ralli, Elaine P.; Friedman, Gerald; Rubin, Saul H.

doi:10.1172/jci101006

Cited by 64 publications

(19 citation statements)

References 19 publications

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“…This appears to be the situation in the case of glucose and of diodrast to which this type of analysis has been applied. However it does not seem reasonable that individual tubular function should be closely correlated to individual glomerular function in the case of glucose but not in the case of other substances such as ascorbic acid (21,22), various amino acids (23), and phosphate (especially in acidosis) (24), where excretion of appreciable amounts well below saturation levels is the rule.…”

Section: Discussionmentioning

confidence: 99%

The Renal Mechanism for Urate Excretion in Man 1

Berliner¹,

Hilton²,

Yu³

et al. 1950

J. Clin. Invest.

136

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The renal mechanisms by which urate is excreted have not yet been defined and there still is disagreement on several major points.Previous studies are in accord on one point, that the normal urate clearance in man is only a small fraction of the glomerular filtration rate, usually of the order of 8-10o. Differing explanations for the relatively low clearance have been offered. Patently, the difference between the clearance of urate and the clearance of inulin must be due either to non-filterability of a large fraction of the plasma urate, to tubular reabsorption of a major fraction of the filtered urate, or to some combination of these two.Some observers have reported non-filterability of the plasma urate, presumably due to proteinbinding or polymerization, but the magnitude of the bound fraction, 4-24%o (1), and 23% (2) has not been nearly sufficient to account for the difference between the clearances of urate and inulin. In a number of other studies (3)(4)(5) Despite this evidence of filterability in sitro and, at least in lower vertebrates, in s'ivo, several investigators have held that this is not the situation in man and that the actual amount filtered at the glomerulus is close to the amount excreted. Berglund and Frisk (9) advanced this theory to explain the fairly constant clearance of urate over a moderate range of plasma urate concentrations and a fairly constant ratio of urate to creatinine clearance in a series of patients with a wide range of renal functional impairment. The same hypothesis has been more recently supported by Wolfson and his associates (2, 10, 11), for reasons similar to those of Berglund and Frisk. In addition, it was suggested that the very low cerebro-spinal fluid urate concentration was due to non-filterability in vivo. The latter position, however, is not tenable since the composition of spinal fluid departs in several respects from that of a plasma ultrafiltrate, the concentration of a number of filterable substances in the spinal fluid being appreciably lower than that in plasma water (12, 13). These authors hypothesize that non-filterability of urate is due to polymerization and that urate is excreted by filtration only or by filtration with a small amount diffusing back passively.The most extensive work on the mechanism of uric acid excretion is probably that of Talbott (14) who reported a number of simultaneous determinations of inulin and urate clearances and the effect of various agents on the clearance ratio. Benedict's method (17). No correction for non-uric acid chromogen was made in any of these experiments since all critical data were obtained at times when the plasma concentration and urinary excretion of urate had been greatly increased by the administration of solutions of pure urate. At such times the non-uric acid chromogen is a negligible fraction of the total. Complete diffusibility of the plasma urate has been assumed in all calculations. Toxic reactionsNausea and vomiting occurred in about half of the patients who received infusions of the lithium carbon...

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Section: Discussionmentioning

confidence: 99%

The Renal Mechanism for Urate Excretion in Man 1

Berliner¹,

Hilton²,

Yu³

et al. 1950

J. Clin. Invest.

136

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“…AA is reabsorbed through SVCT1 transporter in proximal convoluted tubule [6]. The difference between the amount of AA filtered and reabsorbed constitutes renal excretion [8]. Together, intestinal absorption and renal excretion controls the serum level of vitamin C and thus its bioavailability.…”

Section: Vitamin C Bioavailabilitymentioning

confidence: 99%

Vitamin C in Disease Prevention and Cure: An Overview

et al. 2013

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The recognition of vitamin C is associated with a history of an unrelenting search for the cause of the ancient haemorrhagic disease scurvy. Isolated in 1928, vitamin C is essential for the development and maintenance of connective tissues. It plays an important role in bone formation, wound healing and the maintenance of healthy gums. Vitamin C plays an important role in a number of metabolic functions including the activation of the B vitamin, folic acid, the conversion of cholesterol to bile acids and the conversion of the amino acid, tryptophan, to the neurotransmitter, serotonin. It is an antioxidant that protects body from free radical damage. It is used as therapeutic agent in many diseases and disorders. Vitamin C protects the immune system, reduces the severity of allergic reactions and helps to fight off infections. However the significance and beneficial effect of vitamin C in respect to human disease such as cancer, atherosclerosis, diabetes, neurodegenerative disease and metal toxicity however remains equivocal. Thus further continuous uninterrupted efforts may open new vistas to understand its significance in disease management.

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“…As described by Ralli et al [11] in the 1930s, vitamin C is excreted by the kidneys by filtration and active tubular reabsorption. The metabolism of vitamin C to oxalate was later described in the 1960s by other investigators [12,13].…”

Section: Discussionmentioning

confidence: 97%

Vitamin C Induced Oxalate Nephropathy

2017

American Journal of Kidney Diseases

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Although a multitude of syndromes have been thoroughly described as a result of vitamin deficiencies, over consumption of such substances may also be quite dangerous. Intratubular crystallization of calcium oxalate as a result of hyperoxaluria can cause acute renal failure. This type of renal failure is known as oxalate nephropathy. Hyperoxaluria occurs as a result of inherited enzymatic deficiencies known as primary hyperoxaluria or from exogenous sources known as secondary hyperoxaluria. Extensive literature has reported and explained the mechanism of increased absorption of oxalate in malabsorptive syndromes leading to renal injury. However, other causes of secondary hyperoxaluria may also take place either via direct dietary consumption of oxalate rich products or via other substances which may metabolize into oxalate within the body. Vitamin C is metabolized to oxalate. Oral or parenteral administration of this vitamin has been used in multiple settings such as an alternative treatment of malignancy or as an immune booster. This article presents a clinical case in which ingestion of high amounts of vitamin C lead to oxalate nephropathy. This article further reviews other previously published cases in order to illustrate and highlight the potential renal harm this vitamin poses if consumed in excessive amounts.

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The Mechanism of the Excretion of Vitamin C by the Human Kidney 1

Cited by 64 publications

References 19 publications

The Renal Mechanism for Urate Excretion in Man 1

The Renal Mechanism for Urate Excretion in Man 1

Vitamin C in Disease Prevention and Cure: An Overview

Vitamin C Induced Oxalate Nephropathy

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