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Renal Excretion and Tubular Transport of Organic Anions and Cations

Françoise Roch‐Ramel, Kamel Besseghir, Heini Murer

10.1002/cphy.cp080248

Source: Supplement 25: Handbook of Physiology, Renal Physiology

Originally published: 1992

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Organic Anions
1.1 Introduction
1.2 Renal Excretion and Tubular Transport of Organic Anions
1.3 Mechanisms Involved in Tubular Transport of Organic Anions
1.4 Conclusions on the Renal Transport of Organic Anions
2 Organic Cations
2.1 Introduction
2.2 Renal Excretion and Tubular Transport of Organic Cations
2.3 Mechanisms Involved in Tubular Transport of Organic Cations
3 General Conclusions
Figure 1. Figure 1.

Upper part: rate of filtration, secretion, and excretion of p‐aminohippurate as function of free plasma p‐aminohippurate concentration in humans. Lower part: clearance of p‐aminohippurate as function of total (free + bound) p‐aminohippurate plasma concentration.

From Pitts, Physiology in Kidney and Body Fluids, ref. 469; reproduced with permission
Figure 2. Figure 2.

Fractional excretion of p‐aminohippurate in a few mammalian species.

From data in references 462,469,488,627,688,692
Figure 3. Figure 3.

Overall fractional excretion (FEPAH) and fractional deliveries (FDPAH) of p‐aminohippurate to various sites of nephron, as measured in free‐flow micropuncture experiments in rats. In early proximal tubule, FDPAH was equal to filtered load of p‐aminohippurate, and increased toward the late proximal, following p‐aminohippurate secretion, to reach final values at the beginning of distal tubule, after secretion in pars recta. Plasma concentrations of p‐aminohippurate were about 3μM (striated columns) and 0.7 mM (white columns).

From data in references 627,688,692, as recalculated in reference 523 for this latter work
Figure 4. Figure 4.

Fractional excretion of ascorbate, m‐hydroxybenzoate, and nicotinate in various species as function of their plasma concentration.

From references 120,205,402,403
Figure 5. Figure 5.

Fractional excretion and fraction deliveries of ascorbate in rats, as measured in micropuncture experiments. At low plasma concentrations (white columns), fractional delivery of ascorbate remained below unity. At high plasma concentrations of ascorbate (striated columns), fractional delivery of ascorbate was higher than 1, indicating net secretion.

From reference 393
Figure 6. Figure 6.

Fractional excretion of urate in various species in function of plasma urate concentration.

From data in references 74,164,182,434,579
Figure 7. Figure 7.

Urinary pH dependency of fractional excretion of salicylic acid in humans.

From reference 238
Figure 8. Figure 8.

Urinary flow rate dependency of excretion of salicylic and m‐hydroxybenzoic acids in dogs.

From references 402,686
Figure 9. Figure 9.

Biphasic response of renal clearance at high and low loads of competitive inhibitor. Left: data obtained in chimpanzees 183, where uric acid renal excretion was measured in the presence of increasing doses of the competitive inhibitor of urate transport pyrazinoate. At low doses of pyrazinoate, urate excretion decreased; at higher doses of pyrazinoate, urate excretion increased and exceeded that of controls. Right: data obtained in chickens, where renal excretion of choline was measured in the presence of increasing doses of the competitive inhibitor triethylethanolamine or triethylcholine 6. At low doses, the competitive inhibitor increased choline excretion; at higher doses, it decreased choline renal excretion.

From reference 499 with permission
Figure 10. Figure 10.

Mechanisms that may be involved in organic anion transport across the proximal tubular cell (see text for explanations). X− = α‐ketoglutarate; Y− = lactate, pyruvate, β‐hydroxybutyrate, acetoacetate, succinate, α‐ketoglutarate, urate, hydroxyl ions, chloride, bicarbonate, etc.
Figure 11. Figure 11.

Mechanisms that may be involved in organic cation transport across the proximal tubular cell (see text for explanations). X+ = choline.


Figure 1.

Upper part: rate of filtration, secretion, and excretion of p‐aminohippurate as function of free plasma p‐aminohippurate concentration in humans. Lower part: clearance of p‐aminohippurate as function of total (free + bound) p‐aminohippurate plasma concentration.

From Pitts, Physiology in Kidney and Body Fluids, ref. 469; reproduced with permission


Figure 2.

Fractional excretion of p‐aminohippurate in a few mammalian species.

From data in references 462,469,488,627,688,692


Figure 3.

Overall fractional excretion (FEPAH) and fractional deliveries (FDPAH) of p‐aminohippurate to various sites of nephron, as measured in free‐flow micropuncture experiments in rats. In early proximal tubule, FDPAH was equal to filtered load of p‐aminohippurate, and increased toward the late proximal, following p‐aminohippurate secretion, to reach final values at the beginning of distal tubule, after secretion in pars recta. Plasma concentrations of p‐aminohippurate were about 3μM (striated columns) and 0.7 mM (white columns).

From data in references 627,688,692, as recalculated in reference 523 for this latter work


Figure 4.

Fractional excretion of ascorbate, m‐hydroxybenzoate, and nicotinate in various species as function of their plasma concentration.

From references 120,205,402,403


Figure 5.

Fractional excretion and fraction deliveries of ascorbate in rats, as measured in micropuncture experiments. At low plasma concentrations (white columns), fractional delivery of ascorbate remained below unity. At high plasma concentrations of ascorbate (striated columns), fractional delivery of ascorbate was higher than 1, indicating net secretion.

From reference 393


Figure 6.

Fractional excretion of urate in various species in function of plasma urate concentration.

From data in references 74,164,182,434,579


Figure 7.

Urinary pH dependency of fractional excretion of salicylic acid in humans.

From reference 238


Figure 8.

Urinary flow rate dependency of excretion of salicylic and m‐hydroxybenzoic acids in dogs.

From references 402,686


Figure 9.

Biphasic response of renal clearance at high and low loads of competitive inhibitor. Left: data obtained in chimpanzees 183, where uric acid renal excretion was measured in the presence of increasing doses of the competitive inhibitor of urate transport pyrazinoate. At low doses of pyrazinoate, urate excretion decreased; at higher doses of pyrazinoate, urate excretion increased and exceeded that of controls. Right: data obtained in chickens, where renal excretion of choline was measured in the presence of increasing doses of the competitive inhibitor triethylethanolamine or triethylcholine 6. At low doses, the competitive inhibitor increased choline excretion; at higher doses, it decreased choline renal excretion.

From reference 499 with permission


Figure 10.

Mechanisms that may be involved in organic anion transport across the proximal tubular cell (see text for explanations). X− = α‐ketoglutarate; Y− = lactate, pyruvate, β‐hydroxybutyrate, acetoacetate, succinate, α‐ketoglutarate, urate, hydroxyl ions, chloride, bicarbonate, etc.



Figure 11.

Mechanisms that may be involved in organic cation transport across the proximal tubular cell (see text for explanations). X+ = choline.

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Article Title: Renal Excretion and Tubular Transport of Organic Anions and Cations
 

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Françoise Roch‐Ramel, Kamel Besseghir, Heini Murer. Renal Excretion and Tubular Transport of Organic Anions and Cations. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 2189-2262. First published in print 1992. doi: 10.1002/cphy.cp080248