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PubMed1992

Methimazole protection of rats against chemically induced kidney damage in vivo.

Because methimazole has antioxidant properties, the effects of methimazole treatment on cephaloridine, S-(1,2-dichlorovinyl)-L-cysteine (DCVC), 2-bromohydroquinone (2-BHQ) and cis-diaminedichloroplatinum (II) (cisplatin)-induced nephrotoxicity were investigated. Rats given cephaloridine (1 g/kg), cisplatin (5 mg/kg), DCVC (100 mg/kg) or 2-BHQ (157 mg/kg) i.p. exhibited significant elevations in blood urea nitrogen concentrations, which correlated with appearance of distinct renal histopathological changes. Cephaloridine, DCVC or 2-BHQ-induced nephrotoxicity was reduced only when methimazole (20-40 mg/kg) was given 30 min before the nephrotoxicant, whereas cisplatin-induced nephrotoxicity was reduced when methimazole was given 30 min before and up to 4 hr after cisplatin. Because the renal organic acid transport system plays an important role in the nephrotoxicity of cephaloridine, cisplatin and DCVC, the role of the organic acid transport system in the renal uptake of methimazole was investigated. With rat kidney cortical slices, methimazole uptake was time- and concentration-dependent; however, the organic acid transport substrates, probenecid (1 mM) and p-aminohippuric acid (7.5 mM), were ineffective in blocking methimazole uptake. Furthermore, cephaloridine (1 mM) uptake by kidney cortical slices was not affected by methimazole (5 mM). Rats given methimazole (40 mg/kg) 30 min before cephaloridine (2 g/kg) had serum and kidney cephaloridine concentrations similar to rats given cephaloridine only, but the methimazole-pretreated rats were significantly protected against cephaloridine-induced oxidation of renal nonprotein thiols. These results show that methimazole does not inhibit the transport of cephaloridine into the kidneys, but may protect against cephaloridine-induced renal damage by acting as an antioxidant within the kidneys.

Animals↗
PubMed2005

Transport of prostaglandin E1 across the blood-brain barrier in rats.

The transport of prostaglandin E(1) (PGE(1)) across the blood-brain barrier (BBB) was characterized using an in-situ rat brain perfusion technique. The uptake of [(3)H]PGE(1) was not affected by shortchain monocarboxylic acids (butyric acid and valeric acid). On the other hand, uptake of [(3)H]PGE(1) was significantly inhibited by medium-chain monocarboxylic acids such as hexanoic acid, enanthic acid and octanoic acid. These medium-chain monocarboxylic acids showed a more potent inhibitory effect on [(3)H]PGE(1) uptake with increasing number of carbon atoms. In contrast, there was no decrease in [(3)H]PGE(1) transport by any dicarboxylic acids with 5-8 carbon atoms. Valproic acid decreased [(3)H]PGE(1) uptake, whereas p-aminohippuric acid, a substrate for the organic anion transporter family, did not inhibit [(3)H]PGE(1) transport. Bromocresol green, an inhibitor of prostaglandin transporter (PGT), strongly decreased [(3)H]PGE(1) transport across the BBB. In addition, digoxin and taurocholate, substrates for organic anion transporting polypeptide subtype 2 (Oatp2), significantly inhibited [(3)H]PGE(1) uptake. RT-PCR analysis revealed that PGT mRNA and Oatp2 mRNA are expressed in a capillary-rich fraction from rat brain. Thus, it is suggested that PGE(1) transport across the BBB is mediated by some specific transport systems, possibly by the members of the Oatp family.

Alkaline Phosphatase↗
PubMed1988

Contraluminal transport systems in the proximal renal tubule involved in secretion of organic anions.

The transport of organic anions in the proximal tubule occurs primarily through the epithelial cells. This process involves movement across both the luminal and contraluminal membranes via specialized transport systems. Although some of the organic anions are taken up into the cell from the lumen, they can also be accumulated in tubule cells from the interstitial compartment by a variety of transporters. The relative affinities of anions for the different luminal and contraluminal transporters in concert with their conjugate driving forces determine the net directional movement, i.e., organic anion absorption or secretion. By use of the approach of stopped-flow microperfusion, it has been possible to characterize the contraluminal anion transporters in the rat. The following three different systems have been identified: 1) an exchange system for sulfate and oxalate; 2) a cotransport system for Na+ and dicarboxylates; and 3) an exchange system (the so-called p-aminohippuric acid transport system) for hydrophobic anions and long-chain fatty acids. By use of a wide variety of different analogues, the substrate specificities for these different systems were determined. Substrates with two negative ionic charges or with one negative ionic charge and one or more negative partial charges interact with all three systems, depending on the distance between the two charged groups. Polyhalogenated substrates are preferred by the dicarboxylate system. Those substrates which interact only with the p-aminohippurate transport system possess a hydrophobic area and one negative ionic charge or two negative partial charges.

Amino Acids↗
PubMed1980

Some pathways of xenobiotic metabolism in the adult and neonatal marmoset (Callithrix jacchus).

1. An oral dose of [carboxyl-14C]benzoic acid was excreted as hippuric acid or benzoylglucuronide by the adult marmoset Callithrix jacchus, and the relative proportions of the metabolites were dose-dependent over the range 1-100mg/kg body weight, the proportion of glucuronideincreasing with increasing dose level. 2. [14C]Aspirin was rapidly absorbed by the marmoset, giving peak blood levels within 1 h of dosing. Unchanged aspirin (trace to 5% dose) was excreted up to 3 h after dosage. Salicylic acid was the major metabolite, relatively little asalicyluric acid was excreted; glucuronic acid conjugates accounted for about 30% of the urinary metabolites and gentisic acid about 2%. 3. p-aminobenzoic acid administered to adult marmosets was excreted as p-acetamidobenzoic acid, the major urinary metabolite, unchanged p-aminobenzoates, p-aminobenzoyl glucuronide and p-aminohippuric acid each representing about 10% of the urinary metabolities; one-fifth of the p-aminohippurate was acetylated. 4. After oral administration of [35S]sulphadiazine to marmosets, peak blood levels of 35S occurred within 5 h dosing, and immediately fell to near-zero values at 24 h. Sulphadiazine and N-acetylsulphadiazine comprised 36% and 34% respectively of the urine 35S while the N1-glucuronide (tentative identification) accounted for 22%. Minor metabolites were the N4-glucuronide and N4-sulphate of sulphadiazine. 5. The extent of acetylation of sulphadimidine by marmosets corresponded to that of fast acetylators in man. 6. The metabolism of [14C]benzoate and of p-aminobenzoic acid in the neonatal marmoset was compared with that in similarly dosed neonatal rats.

Animals↗
PubMed1976

Active transport of phenol red by rat lung slices.

32S-phenol red was taken up by rat lung slices incubated in oxygenated Krebs-Ringer phosphate-glucose solution (pH 7.4) at 37 degrees C by a process showing the characteristics of active transport. Uptake against a concentration gradient occurred by a saturable process that was inhibited by low temperature, anaerobic conditions and certain metabolic inhibitors. Phenol red uptake was depressed in the presence of certain anionic dyes, such as chlorphenol red, bromphenol blue, bromthymol blue and bromcresol green, and by various other organic acids, including disodium cromoglycate, probenecid, cephalothin and benzylpenicillin. In contrast, isoniazid and p-aminohippuric acid had no effect on phenol red uptake, suggesting that a specificity exists in the rat lung for transport of anionic compounds. Interestingly, in the presence of paraquat, an organic cation,phenol red uptake was increased. The extent of uptake of phenol red by lung slices was dependent on levels of Na, K and Ca ion in the incubation medium as well as on the thickness of the tissue slice. Phenol red was bound to lung homogenates; however, the characteristics of the binding were such that binding alone could not account for accumulation by lung slices.

Animals↗
PubMed1990

Carrier-mediated uptake of nicotinic acid by rat intestinal brush-border membrane vesicles and relation to monocarboxylic acid transport.

The intestinal transport of [14C]nicotinic acid was investigated at 27 degrees C by using brush-border membrane vesicles (BBMV) isolated from the rat small intestine. The osmolarity sensitive uptake by BBMV showed a remarkable overshoot phenomenon in the presence of an inward-directed H+ gradient (pHin = 7.5, pHout = 6.0). In contrast, the imposition of a Na+ gradient ([Na+]in = 0 mM, [Na+]out = 100 mM) had no stimulatory effect on the uptake of [14C]nicotinic acid. The remarkable pH-dependence of the initial uptake showing an increase of the uptake rate with decreasing the extravesicular pH disappeared completely in the presence of a structural analogue, isonicotinic acid, at pH below 6.5. In the presence of a H+ gradient, the initial uptake of [14C]nicotinic acid was saturable with the apparent Kt of 4.43 mM and Jmax of 2.55 nmol/mg protein/15 s. The uptake was increased by the imposition of an inside-positive membrane potential and was significantly inhibited by monocarboxylic acids such as benzoic acid, salicylic acid, acetic acid, propionic acid, valproic acid and L-lactic acids as well as two isomers (isonicotinic acid and picolinic acid). The uptake was not inhibited by nicotinamide, nicotinyl alcohol, D-glucose, p-aminohippuric acid, glycyl-L-proline, succinic acid and an exchange transport inhibitor. From these results it was concluded that nicotinic acid is transported through the intestinal brush-border membrane by a carrier-mediated system and the system can recognize some acidic drugs with a monocarboxylic group. The pH dependent intestinal uptake of nicotinic acid can be ascribed to the proton-coupled and active carrier-mediated transport mechanism rather than a simple diffusion of the undissociated nicotinic acid to follow a pH-partition hypothesis.

Animals↗
PubMed2000

In-vivo and in-vitro evidence of a carrier-mediated efflux transport system for oestrone-3-sulphate across the blood-cerebrospinal fluid barrier.

The efflux transport of oestrone-3-sulphate, a steroid hormone sulphate, across the blood-cerebrospinal fluid barrier has been examined following its intracerebroventricular administration. [3H]Oestrone-3-sulphate was eliminated from cerebrospinal fluid (CSF) with an apparent efflux clearance of 205 microL min(-1) per rat. There was 25% of unmetabolized [3H]oestrone-3-sulphate in the plasma 5 min after intracerebroventricular administration, indicating that at least a part of [3H]oestrone-3-sulphate is transported from CSF to the circulating blood across the blood-CSF barrier. This efflux transport was inhibited by co-administration of excess oestrone-3-sulphate (25 mM 10 microL = 0.25 micromol) into rat cerebral ventricle. To characterize the oestrone-3-sulphate transport process, an in-vitro uptake experiment was performed using isolated rat choroid plexus. Oestrone-3-sulphate uptake by isolated rat choroid plexus was found to be a saturable process with a Michaelis-Menten constant (Km) of 18.1 +/- 6.3 microM, and a maximum uptake rate (Vmax) of 48.0 +/- 15.1 pmol min(-1) microL(-1) of tissue. The oestrone-3-sulphate transport process was temperature dependent and was inhibited by metabolic inhibitors such as 2,4-dinitrophenol and rotenone, suggesting an energy dependence. This uptake process was also inhibited by steroid hormone sulphates (1 mM dehydroepiandrosterone sulphate and 1 mM oestrone sulphate), bile acids (1 mM taurocholic acid and 1 mM cholic acid) and organic anions (1 mM sulphobromophthalein and 1 mM phenolsulphonphthalein), whereas 1 mM p-aminohippuric acid, 1 mM p-nitrophenol sulphate, 0.1 mM methotrexate and the cardiac glycoside, 2.5 microM digoxin, had little effect. In conclusion, these results provide evidence that oestrone-3-sulphate is transported from CSF to the circulating blood across the blood-CSF barrier via a carrier-mediated efflux transport system.

2,4-Dinitrophenol↗
PubMed2000

Effect of a keto acid-amino acid supplement on the metabolism and renal elimination of branched-chain amino acids in patients with chronic renal insufficiency on a low protein diet.

The aim of our study was to evaluate the effect of a low-protein diet supplemented with keto acids-amino acids on renal function and urinary excretion of branched-chain amino acids (BCAA) in patients with chronic renal insufficiency (CRI). In a prospective investigation 28 patients with CRI (16 male, 12 female, aged 28-66 yrs, CCr 18.6 +/- 10.2 ml/min) on a low-protein diet (0.6 g of protein /kg BW/day and energy intake 140 kJ/kg BW/day) for a period of one month were included. Subsequently, this low protein diet was supplemented with keto acids-amino acids at a dose of 0.1 g/kg BW/day orally for a period of 3 months. Examinations performed at baseline and at the end of the follow-up period revealed significant increase in the serum levels of BCAA leucine (p < 0.02), isoleucine (p < 0.03), and valine (p < 0.02) while their renal fractional excretion declined (p < 0.02, p < 0.01 resp.). Keto acid-amino acid administration had no effect on renal function and on the clearance of inulin, para-aminohippuric acid. Endogenous creatinine and urea clearance remained unaltered. A significant correlation between fractional excretion of sodium and leucine (p < 0.05) and a hyperbolic relationship between inulin clearance and fractional excretion of BCAA (p < 0.01) were seen. Moreover, a significant decrease in proteinuria (p < 0.02), plasma urea concentration and renal urea excretion and a rise in albumin level (p < 0.03) were noted. We conclude that in patients with CRI on a low protein diet the supplementation of keto acids-amino acids does not affect renal hemodynamics, but is associated--despite increases in plasma concentrations--with a reduction of renal amino acid and protein excretion suggesting induction of alterations in the tubular transport mechanisms.

Adult↗
PubMed1995

Mechanism of valproic acid uptake by isolated rat brain microvessels.

In an effort to characterize putative transport systems of valproic acid (VPA) at the blood-brain barrier, the effects of various substrates and inhibitors of known anion transporters on the equilibrium vessel-to-medium concentration (vessel/medium) ratio of VPA were investigated using isolated rat brain microvessels. The equilibrium vessel/medium ratio of VPA was decreased by the presence of high millimolar concentration of unlabeled VPA, indicating that a saturable transport system was involved in VPA transport from medium to microvessels. Short-chain monocarboxylates such as propionic acid, pyruvic acid, and L-lactic acid did not alter the vessel/medium ratio, whereas medium-chain fatty acids and unsaturated metabolites of VPA significantly inhibited the net transport of VPA. Dicarboxylates, tricarboxylate, and p-aminohippuric acid did not affect VPA accumulation in the brain microvessels. Several anionic drugs including salicylic acid, penicillin G, cefazolin, and probenecid significantly reduced the vessel/medium ratio of VPA. In addition, disulfonate inhibitors of inorganic anion exchangers, SH-group modifying reagent, and metabolic inhibitor showed remarkable inhibitory effects on the net transport of VPA between brain microvessels and medium. These results suggest that VPA may be actively transported through the antiluminal membrane via a carrier-mediated system shared by other anionic drugs.

Animals↗
PubMedDate not supplied

Absorption of aerosolized drugs from the rat lung.

To investigate the absorption of aerosolized drugs from the rat lung, anesthetized animals were allowed to inhale through a tracheal cannula liquid aerosols of drug solutions generated with an air-jet nebulizer. The aerosols had a mass median aerodynamic diameter of 2.81 +/- 0.08 micron and a geometric standard deviation of 2.53 +/- 0.05. At various times after aerosol inhalation, the lungs were removed and assayed for the amount of compound that had not been absorbed. The times (min) necessary for 50% absorption were: antipyrine, 0.25; salicylic acid, 0.67; barbital, 0.93; amitrole, 1.3; urea, 1.4; procainamide, 2.3; guanidine, 3.1; erythromycin, 6.3; benzylpenicillin, 20.5; p-aminohippuric acid, 21.7; mannitol, 26.5; and N-acetylprocainamide ethobromide, 34.5. Comparison with previously reported absorption rates measured after intratracheal injection of 0.1 ml of drug solution showed that drug inhaled as an aerosol was absorbed roughly two times more rapidly than when administered by intratracheal injection. The results suggest that drug absorption may be more rapid from the alveolar region than from the tracheobronchial region of the lung.

Absorption↗
PubMed1988

Carrier-mediated transport of cefixime, a new cephalosporin antibiotic, via an organic anion transport system in the rat renal brush-border membrane.

The renal excretion mechanism of cefixime, a newly developed and p.o. effective cephalosporin antibiotic, was investigated by using the renal brush-border membrane vesicles from the rat kidney cortex. The initial uptake rate of cefixime into an osmotically sensitive vesicular space showed concentration and temperature dependencies, indicating the presence of a carrier-mediated transport mechanism for cefixime. Kinetic parameters for apparently saturable and nonsaturable components were evaluated as follows: maximum uptake rate was 7.32 +/- 1.07 nmol/30 sec/mg of protein; Michaelis constant was 7.35 +/- 2.04 mM; and the first-order rate constant was 0.34 +/- 0.02 nmol/30 sec/mg of protein per mM. The uptake was not affected by an inward-directed gradient of Na+, K+, Li+, Rb+ or H+. In contrast, the initial uptake rate was enhanced by an inside-positive membrane potential imposed by valinomycin. Although amino acids, dipeptides and organic cations had no effects on the uptake of cefixime, organic anions such as probenecid and p-aminohippuric acid and anion transport inhibitors such as 4,4'-diisothiocyano-stilbene-2,2'-disulfonic acid and furosemide reduced the uptake significantly. Twenty beta-lactam antibiotics including both zwitter-ionic and anionic derivatives inhibited significantly the uptake of cefixime. Furthermore, by adding probenecid in the extravesicular medium, an efflux of cefixime from the brush-border membrane vesicles was enhanced significantly at the initial stage. Benzylpenicillin, cephalothin and cephradine also enhanced an efflux of cefixime to the same extent as observed by the addition of probenecid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Transport of the new quinolone antibacterial agents of lomefloxacin and ofloxacin by rat erythrocytes, and its relation to the nicotinic acid transport system.

Transport mechanism of quinolonecarboxylic acid derivatives (quinolones), lomefloxacin and ofloxacin, in rat erythrocytes was investigated. The uptake of lomefloxacin by erythrocytes was apparently nonsaturable over the concentration range of 0.1-1.0 mM at 27 degrees C and pH 7.4. In the case of ofloxacin, however, the erythrocytes took up ofloxacin in a concentration dependent manner at 20 degrees C and pH 7.4, with a maximum rate (Jmax) of 28.8 +/- 0.98 pmol/10(6) cells/s and a Michaelis constant (Kt) of 0.92 +/- 0.15 mM. An increase in the medium osmolarity caused a decrease in the [14C]lomefloxacin uptake, indicating that the drug is transported into the intracellular space of erythrocytes. The uptake of [14C]lomefloxacin by the erythrocytes was independent of pH but increased above pH 6.0, and, moreover, was dependent on temperature with an activation energy of 16.6 kcal/mol. The uptake of [14C]lomefloxacin was competitively inhibited by a water-soluble vitamin, nicotinic acid, with an inhibition constant (Ki) of 16.1 mM, but not inhibited by 10 mM of L-alanine, glucose, p-aminohippuric acid (PAH), N-methyl-nicotinamide (NMN) or tetraethylammonium chloride (TEA). These lines of evidence suggest that the transport system of lomefloxacin and ofloxacin in rat erythrocytes is common with that of a water-soluble vitamin, nicotinic acid, to which quinolones are structurally analogous.

Animals↗
PubMed1994

Influence of the renin-angiotensin system and atrial natriuretic peptide on renal functional reserve.

We studied the renin-angiotensin system (RAS) and atrial natriuretic peptide (ANP) after amino acid loading in order to elucidate whether or not glomerular hyperfiltration is mediated by these hormones. Eight healthy controls without kidney disease (group 1), 8 renal graft recipients (group 2) and 8 patients after nephrectomy (group 3) were studied. Furthermore, we investigated the influence of amino acid loading on RAS and ANP and glomerular filtration during acute application of captopril in healthy controls. Clearances in insulin (CIn) and para-aminohippuric acid (CPAH) were determined during an infusion of 0.9% saline and during amino acid loading. CIn increased in healthy controls from 96.5 +/- 3.3 to 111.9 +/- 4.4 ml/min (p < 0.01), CPAH rose from 577 +/- 28.7 to 618.9 +/- 38 ml/min (p = NS). During the combined application of amino acid infusion and 25 mg captopril, CIN increased to 125.0 +/- 16.4 ml/min/1.73 m2 (p < 0.01) and there was no significant increase in CPAH which was 595 +/- 77 ml/min/1.73 m2. There was no significant change in renal vascular resistance, but filtration fraction increased from 17 +/- 1 to 19 +/- 1% under amino acid infusion and increased further under the application of captopril to 21 +/- 2% (p < 0.05). In renal graft recipients, CIn had a tendency to increase during amino acid infusion from 78.4 +/- 5.8 to 84.7 +/- 6.5 ml/min (p = NS). In patients after nephrectomy, CIn did not increase (84.5 +/- 6 ml/min) but CPAH did from 345.7 +/- 26.3 to 409 +/- 24.1 ml/min (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Expression of human organic anion transporters in the choroid plexus and their interactions with neurotransmitter metabolites.

The purpose of the present study was to elucidate the expression of human organic anion transporter 1 (hOAT1) and hOAT3 in the choroid plexus of the human brain and their interactions with neurotransmitter metabolites using stable cell lines. Immunohistochemical analysis revealed that hOAT1 and hOAT3 are expressed in the cytoplasmic membrane and cytoplasm of human choroid plexus. Neurotransmitter metabolites, namely, 5-methoxyindole-3-acetic acid (5-MI-3-AA), homovanillic acid (HVA), vanilmandelic acid (VMA), 3,4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindole-3-acetic acid (5-HI-3-AA), N-acetyl-5-hydroxytryptamine (NA-5-HTT), melatonin, 5-methoxytryptamine (5-MTT), 3,4-dihidroxymandelic acid (DHMA), 5-hydroxytryptophol, and 5-methoxytryptophol (5-MTP), but not methanephrine (MN), normethanephrine (NMN), and 3-methyltyramine (3-MT), at 2 mM, inhibited para-aminohippuric acid uptake mediated by hOAT1. On the other hand, melatonin, 5-MI-3-AA, NA-5-HTT, 5-MTT, 5-MTP, HVA, 5-HI-3-AA, VMA, DOPAC, 5-hydroxytryptophol, and MN, but not 3-MT, DHMA, and NMN, at 2 mM, inhibited estrone sulfate uptake mediated by hOAT3. Differences in the IC(50) values between hOAT1 and hOAT3 were observed for DHMA, DOPAC, HVA, 5-HI-3-AA, melatonin, 5-MI-3-AA, 5-MTP, 5-MTT, and VMA. HOAT1 and hOAT3 mediated the transport of VMA but not HVA and melatonin. These results suggest that hOAT1 and hOAT3 are involved in the efflux of various neurotransmitter metabolites from the cerebrospinal fluid to the blood across the choroid plexus.

Cell Line↗
PubMed1986

Effect of captopril on 99mTc-diethylenetriaminepentaacetic acid renograms in two-kidney, one clip hypertension.

In an effort to improve on the noninvasive detection of renal artery stenosis, we investigated the effect of angiotensin converting enzyme inhibition on computer-assisted 99mTc-diethylenetriaminepentaacetic acid (DTPA) renal flow studies in a canine model of two-kidney, one clip hypertension and compared these findings with clearances of inulin and p-aminohippuric acid in the stenotic and contralateral kidney before and after converting enzyme inhibition. The 99mTc-DTPA renal flow study with the converting enzyme inhibitor captopril (1.5 mg/kg bolus with 1.5 mg/min infusion) showed an increased sensitivity in the detection of unilateral renal artery stenosis over the use of the 99mTc-DTPA study alone. Captopril induced striking alterations that were most evident in the 15-minute 99mTc-DTPA renal flow study, in which all nine curves exhibited severely blunted uptake and excretion of the radionuclide. These changes were reversed during a recovery study without converting enzyme inhibition and were not seen when blood pressure was lowered with nitroprusside to a level similar to that observed during converting enzyme inhibition. The changes shown by the 99mTc-DTPA study during converting enzyme inhibition correlated with a decrease in the glomerular filtration rate of the stenotic kidney. Captopril infusion significantly decreased the glomerular filtration rate of the stenotic kidney (16.0 +/- 3.1 vs 11.0 +/- 2.5 mg/min, p less than 0.03) but not of the contralateral kidney (32.4 +/- 2.6 vs 28.4 +/- 2.8 mg/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Hyperuricemia in patients with hyperthyroidism due to Graves' disease.

The effects of hyperthyroidism on uric acid metabolism were investigated. First, the serum uric acid level was measured in 92 patients with hyperthyroidism due to Graves' disease, eight patients with subacute thyroiditis, six patients with hypothyroidism, and 70 sex- and age-matched controls. Second, the correlation between serum thyroxine (T4) and serum uric acid was obtained in hyperthyroid Graves' disease patients before and during antithyroid drug therapy. Finally, uric acid clearance (CUA) was determined in untreated patients with hyperthyroidism due to Graves' disease. Serum uric acid was significantly elevated in patients with hyperthyroidism, and the elevation correlated well with serum T4 before treatment as a group and during treatment in each patient. A significant elevation of serum uric acid was not present in patients with a transient mild thyrotoxicosis due to subacute thyroiditis. Serum uric acid was significantly decreased in patients with hypothyroidism. Renal excretion of uric acid clearly increased in hyperthyroid patients, and CUA also increased. The increase in CUA corresponded to the increase in renal plasma flow (RPF), which was measured by p-aminohippuric acid clearance. The fractional excretion of uric acid as determined by CUA/glomerular filtration rate (GFR) was similar and within the normal range in hyperthyroid patients and normal controls. A significant inverse correlation between CUA and serum uric acid concentration was present in hyperthyroid patients as in normal controls, indicating that the renal handling of uric acid in the tubule affected uric acid excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗