Effect of drugs that alter uric acid excretion in man on uric acid clearance in the chicken

1960 ◽  
Vol 198 (3) ◽  
pp. 575-580 ◽  
Author(s):  
Lawrence Berger ◽  
T'sai Fan Yü ◽  
Alexander B. Gutman
Keyword(s):  
Uric Acid ◽  
Tubular Secretion ◽  
Acid Excretion ◽  
Uric Acid Excretion ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
The Mean ◽  
Renal Tubular

In 43 chickens, the mean Cinulin was 4.7 ± 1.8 ml/min. (1.8 ± 0.8 ml/kg/min.), mean Curate 29.0 ± 14.9 ml/min. (11.3 ± 6.0 ml/kg/min.) and mean Turate 1.30 ± 0.69 mg/min. (0.48 ± 0.24 mg/kg/min.). Tubular secretion accounted for a mean of 81% of the total urinary urate. Probenecid, sulfinpyrazone, zoxazolamine and high dosages of phenylbutazone, all uricosuric in man, reduced urate excretion in the chicken, apparently by suppressing tubular secretion of urate; CPAH also was reduced. Salicylate, in doses uricosuric in man, had no effect on chicken urate excretion. Pyrazinamide and sodium r-lactate, agents which decrease urate excretion in man, did not alter urate excretion in the chicken. PAH loading experiments demonstrated that as TPAH increased, Turate decreased. These latter findings suggest competition of urate and PAH for renal tubular transport in the chicken.

AVP-stimulated nucleotide secretion in perfused mouse medullary thick ascending limb and cortical collecting duct

2009 ◽  
Vol 297 (2) ◽  
pp. F341-F349 ◽  
Author(s):  
Elvin Odgaard ◽  
Helle A. Praetorius ◽  
Jens Leipziger
Keyword(s):  
Collecting Duct ◽  
Tubular Secretion ◽  
Hormonal Control ◽  
Similar Response ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Medullary Thick Ascending Limb ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Extracellular nucleotides are local, short-lived signaling molecules that inhibit renal tubular transport via both luminal and basolateral P2 receptors. Apparently, the renal epithelium itself is able to release nucleotides. The mechanism and circumstances under which nucleotide release is stimulated remain elusive. Here, we investigate the phenomenon of nucleotide secretion in intact, perfused mouse medullary thick ascending limb (mTAL) and cortical collecting duct (CCD). The nucleotide secretion was monitored by a biosensor adapted to register nucleotides in the tubular outflow. Intracellular Ca2+ concentration ([Ca2+]i) was measured simultaneously in the biosensor cells and the renal tubule with fluo 4. We were able to identify spontaneous tubular nucleotide secretion in resting perfused mTAL. In this preparation, 10 nM AVP and 1-desamino-8-d-arginine vasopressin (dDAVP) induced robust [Ca2+]i oscillations, whereas AVP in the CCD induced large, slow, and transient [Ca2+]i elevations. Importantly, we identify that AVP/dDAVP triggers tubular secretion of nucleotides in the mTAL. After addition of AVP/dDAVP, the biosensor registered bursts of nucleotides in the tubular perfusate, corresponding to a tubular nucleotide concentration of ∼0.2–0.3 μM. A very similar response was observed after AVP stimulation of CCDs. Thus AVP stimulated tubular secretion of nucleotides in a burst-like pattern with peak tubular nucleotide concentrations in the low-micromolar range. We speculate that local nucleotide signaling is an intrinsic feedback element of hormonal control of renal tubular transport.

A Study of the Hypouricaemic Effect of Tiaprofenic Acid

1988 ◽  
Vol 25 (6) ◽  
pp. 595-600 ◽  
Author(s):  
Vivienne Lyfar ◽  
L Fernandes ◽  
Elizabeth Thornton ◽  
J G H Cook
Keyword(s):  
Uric Acid ◽  
Cell Membrane ◽  
Tiaprofenic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Site Of Action ◽  
Extra Cellular Fluid ◽  
Renal Tubular

Tiaprofenic acid is a non-steroidal anti-inflammatory drug which also has hypouriceamic effect. Studies involving 10 healthy volunteers were designed to investigate the mode of this effect. We postulate that the site of action of tiaprofenic acid is at the cell membrane, the mechanism being an interference with the transport of uric acid from intra- to extra-cellular fluid thus limiting its passage into the plasma. The same mechanism acting on renal tubular cells impedes reabsorption thereby increasing uric acid clearance.

THE EFFECTS OF PORCINE CALCITONIN ON RENAL FUNCTION IN THE RABBIT

1971 ◽  
Vol 50 (3) ◽  
pp. 485-491 ◽  
Author(s):  
L.A. SALAKO ◽  
A. J. SMITH ◽  
R. N. SMITH
Keyword(s):  
Filtration Rate ◽  
Short Circuit ◽  
Renal Plasma Flow ◽  
Short Circuit Current ◽  
Urinary Flow ◽  
Transport Mechanisms ◽  
Acid Clearance ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

SUMMARY Extracts of porcine thyroid containing calcitonin produced increases in urinary flow and urinary electrolyte content when infused or injected into anaesthetized rabbits. This response occurred more rapidly after intraaortic than after intravenous injection and was accompanied by an increase in glomerular filtration rate (inulin clearance) and renal plasma flow (paraaminohippuric acid clearance). Preparations of calcitonin failed to affect the short-circuit current in isolated frog skin. Although an effect of calcitonin on renal tubular transport mechanisms cannot be excluded it seems likely that one mechanism responsible for the diuretic effect of this compound in the rabbit is an increase in renal blood flow.

Mechanisms of the Uricosuric Effect of the Diuretic Tienilic Acid (Ticrynafen) in Man

1977 ◽  
Vol 53 (4) ◽  
pp. 379-386 ◽  
Author(s):  
K. Lau ◽  
R. M. Stote ◽  
M. Goldberg ◽  
Z. S. Agus
Keyword(s):  
Serum Urate ◽  
Mean Value ◽  
Water Diuresis ◽  
Tienilic Acid ◽  
Quantitative Estimates ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
The Mean ◽  
Uricosuric Effect ◽  
Renal Tubular

1. We have studied the effects of the diuretic tienilic acid (Ticrynafen) upon renal tubular transport of urate, in 11 healthy volunteers on a constant dietary intake. 2. Daily administration of tienilic acid for 10 days to six subjects reduced the mean body weight from 67·1 ± 4·7 kg to 64·5 ± 4·7 kg and a reversible fall in serum urate from a mean value of 0·34 ± 0·04 to 0·16 ± 0·01 mmol/l. Fractional urate excretion in the six subjects on the first day of therapy was 30·3 ± 5·6% and then fell to reach a new steady-state mean value of 17·4 ± 2·0%. 3. To evaluate the mechanism of the uricosuria, studies were performed during acute sustained water diuresis in five subjects to assess the effects of tienilic acid, pyrazinamide, probenecid and their combinations. 4. Fractional urate excretion increased markedly with tienilic acid from 11·2 ± 1·3% to 47·5 ± 5·7%. Pyrazinamide, 24·4 mmol (3 g) orally, decreased urate excretion to 5·1 ± 0·7% and markedly blunted the uricosuric effects but not the natriuresis of tienilic acid. Probenecid increased urate excretion to 26 ± 6·0 % and when given with tienilic acid increased urate excretion to 66·4 ± 2·6%. Addition of pyrazinamide to this combination decreased urate excretion to 19·6 ± 4·0%, which was greater than the effect with pyrazinamide alone. 5. We suggest that tienilic acid increased urate excretion by inhibiting reabsorption of both filtered and secreted urate. We have used our results to construct semi-quantitative estimates of the various components of urate transport in man.

Tubular Urate Transporter Gene Polymorphisms Differentiate Patients with Gout Who Have Normal and Decreased Urinary Uric Acid Excretion

2014 ◽  
Vol 41 (9) ◽  
pp. 1863-1870 ◽  
Author(s):  
Rosa J. Torres ◽  
Eugenio de Miguel ◽  
Rebeca Bailén ◽  
José R. Banegas ◽  
Juan G. Puig
Keyword(s):  
Uric Acid ◽  
Tubular Secretion ◽  
Dietary Control ◽  
Nucleotide Polymorphisms ◽  
Transporter Gene ◽  
Acid Excretion ◽  
Uric Acid Excretion ◽  
Control Subjects ◽  
Urate Transporter ◽  
Primary Gout

Objective.Primary gout has been associated with single-nucleotide polymorphisms (SNP) in several tubular urate transporter genes. No study has assessed the association of reabsorption and secretion urate transporter gene SNP with gout in a single cohort of documented primary patients with gout carefully subclassified as normoexcretors or underexcretors.Methods.Three reabsorption SNP (SLC22A12/URAT1, SLC2A9/GLUT9, and SLC22A11/OAT4) and 2 secretion transporter SNP (SLC17A1/NPT1 and ABCG2/BRCP) were studied in 104 patients with primary gout and in 300 control subjects. The patients were subclassified into normoexcretors and underexcretors according to their serum and 24-h urinary uric acid levels under strict conditions of dietary control.Results.Compared with control subjects, patients with gout showed different allele distributions of the 5 SNP analyzed. However, the diagnosis of underexcretor was only positively associated with the presence of the T allele of URAT1 rs11231825, the G allele of GLUT9 rs16890979, and the A allele of ABCG2 rs2231142. The association of the A allele of ABCG2 rs2231142 in normoexcretors was 10 times higher than in underexcretors. The C allele of NPT1 rs1165196 was only significantly associated with gout in patients with normal uric acid excretion.Conclusion.Gout with uric acid underexcretion is associated with transporter gene SNP related mainly to tubular reabsorption, whereas uric acid normoexcretion is associated only with tubular secretion SNP. This finding supports the concept of distinctive mechanisms to account for hyperuricemia in patients with gout with reduced or normal uric acid excretion.

Renal failure in the alligator

1961 ◽  
Vol 200 (4) ◽  
pp. 893-897 ◽  
Author(s):  
Roland A. Coulson ◽  
Thomas Hernandez
Keyword(s):  
Renal Failure ◽  
Uric Acid ◽  
Acid Level ◽  
Renal Damage ◽  
Amino Acid Level ◽  
Prominent Feature ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Blood Uric Acid ◽  
Renal Tubular

Intraperitoneal injection of d-serine into alligators produced renal failure characterized by decreased NH4HCO3 excretion, increased NaCl and NaHCO3 excretion, decreased uric acid clearance, and acidemia. Oliguria or anuria was common in the early stages. Blood uric acid levels as high as 70 mg% were observed. In some respects the loss in renal tubular function resembled that found in alligators kept in the cold. Alligators severely dehydrated or injected with theophylline or insulin also excreted a urine deficient in NH4HCO3 and rich in NaCl. The injection of glycine, a good ammonia precursor, reversed the picture in these alligators but not in those damaged by d-serine. It was concluded that in severe renal damage NH4HCO3 cannot be synthesized, regardless of the amino acid level of the blood, and that salt and base are lost as a consequence. The loss of extracellular salts due to failure of the ammonia mechanism is the most prominent feature in renal failure in the alligator.

Uric Acid in Advanced Renal Failure

1972 ◽  
Vol 43 (3) ◽  
pp. 331-341 ◽  
Author(s):  
G. M. Danovitch ◽  
J. Weinberger ◽  
G. M. Berlyne
Keyword(s):  
Renal Failure ◽  
Uric Acid ◽  
Renal Tubule ◽  
Tubular Secretion ◽  
Acid Excretion ◽  
Acid Transport ◽  
Uric Acid Excretion ◽  
Striking Increase ◽  
Suppression Test ◽  
Diseased Kidney

1. The results of studies of renal uric acid excretion in eleven patients with advanced chronic renal failure are presented. 2. The pyrazinamide suppression test was used to separate secretion from reabsorption of uric acid in the renal tubule. 3. There is a marked increase in the excretion and clearance of uric acid as renal function deteriorates. This was due to a striking increase in tubular secretion of urate and to incomplete reabsorption of filtered urate. 4. The remarkable functional capacity of the remaining nephrons of the chronically diseased kidney with respect to uric acid transport might be due to a uricosuric factor in uraemic serum.

The association of renal tubular inflammatory and injury markers with uric acid excretion in chronic kidney disease patients

2020 ◽  
Vol 52 (5) ◽  
pp. 923-932 ◽  
Author(s):  
Yuqi Zheng ◽  
Haochen Guan ◽  
Xun Zhou ◽  
Ying Xu ◽  
Chensheng Fu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Acid Excretion ◽  
Uric Acid Excretion ◽  
Renal Tubular

Renal tubular transport of nitrofurantoin

1962 ◽  
Vol 202 (6) ◽  
pp. 1136-1140 ◽  
Author(s):  
James A. Buzard ◽  
Raymond C. Bender ◽  
Esther G. Nohle ◽  
Donald T. Humphrey ◽  
Mary F. Paul
Keyword(s):  
Proximal Tubule ◽  
Transport System ◽  
Weak Acid ◽  
Tubular Secretion ◽  
Acid Transport ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Tubular secretion of nitrofurantoin has been demonstrated in the dog and the chicken. This secretion has been localized in the proximal tubule and has been shown to be due to the action of the weak acid transport system. Reabsorption of nitrofurantoin by passive, nonionic diffusion has also been illustrated.

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