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Results for “Renal excretion”

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At least 19 recordsLinked to original sources
PubMed1994

Renal excretion and renal tubular transport of p-aminohippurate (PAH) in methimazole treated, hypothyroid rats of different ages.

Thyroid hormone deficiency following treatment with methimazole for 7 days does not reduce PAH secretion in renal tubular cells as expected from data in thyroid hormone treated rats. This treatment with methimazole causes an increase in renal excretion of PAH in rats of various age groups, statistically significant in 5-, 10- and 20-day-old rats. In 20-day-old, methimazole treated rats the increase in renal excretion of PAH is obviously caused by a higher transport rate in renal tubular cells, proved also in 33-day-old rats. An increased filtered fraction of PAH in 5- and 10-day-old rats could be the reason for the rise in renal excretion of PAH after repeated treatment with methimazole. The mechanism of renal effects of methimazole treatment remains unclear.

Animals↗
PubMed1995

Calmodulin inhibitors and calcium channel blockers influence dideoxycytidine renal excretion.

Renal handling of 2',3'-dideoxycytidine (ddC), a new anti-HIV dideoxynucleoside which undergoes renal and non-renal clearance, was determined in CF-1 male mice. Since calmodulin inhibitors (CIs) and calcium channel blockers (CCBs) have been shown to influence the flux of pyrimidine nucleosides across mammalian membranes and since the plasma concentration (and hence the efficacy) of therapeutic nucleosides is usually affected by the rate of renal elimination, we decided to determine the impact of the CIs loperamide (LOP) and trifluoperazine (TFP) as well as the CCB verapamil (VER) on the renal excretion of ddC. The ratio of ddC clearance to inulin clearance suggests that ddC undergoes secretion into renal tubules. Pre-exposure of mice to the calmodulin inhibitors loperamide (LOP) and trifluoperazine (TFP) resulted in a decrease in ddC renal secretion while pre-treatment with the calcium channel blocker verapamil increased ddC secretion.

Animals↗
PubMed2005

Uric acid renal excretion and renal insufficiency in decompensated severe heart failure.

OBJECTIVE: To evaluate uric acid renal excretion, hyperuricemia, renal dysfunction, and prognosis in patients with decompensated severe heart failure, as there are few data available. METHODS: One hundred and twenty-two patients, hospitalized for heart failure decompensation, in NYHA class IV, were classified into 3 groups as follows. Pilot group [ejection fraction (EF)</=0.45, n=16], group 1 (EF</=0.45, n=90), and group 2 (EF>0.45 and valvular dysfunction, n=16). The patients in groups 1 and 2 underwent assessment of creatinine and uric acid clearance before and after pyrazinamide, to estimate uric acid tubular secretion. Uric acid clearance <6.8 mL/min and secretion <170 microg/min were considered reduced. In groups 1 and pilot (n=106), mortality was analyzed by Cox regression model, and the prognostic value of hyperuricemia was assessed by ROC curve. RESULTS: In groups 1 and 2, respectively, serum uric acid was 511.7 and 422.5 micromol/L, and creatinine clearance was 46.7 and 61.4 mL/min. Uric acid clearance (3.2 vs. 3.9 mL/min) and tubular secretion (116 vs. 128 microg/min) were not different, but lower than normal values. In groups 1 and pilot, the 12-month mortality was 46.4% (CI 95%: 36.7%-56.0%). At end of follow-up, mortality was associated with impaired creatinine clearance (p<0.001), but not with hyperuricemia (p=0.236). CONCLUSIONS: In patients with decompensated severe heart failure, the tubular secretion and the clearance of uric acid were reduced. Renal dysfunction was associated with mortality, but hyperuricemia was not.

Female↗
PubMed1985

Factors contributing to variability in drug pharmacokinetics. IV. Renal excretion.

The renal excretion of drugs is mainly controlled by three factors: glomerular filtration, tubular secretion and tubular reabsorption. Only relatively polar drugs are excreted in appreciable amounts by the kidneys. Factors affecting renal excretion of drugs include: kidney function, protein binding, urine pH and urine flow. Impaired renal function may lead to a clinically significant accumulation of drugs eliminated by the kidneys, if more than 50% of the dose is normally excreted unchanged in the urine and the renal function is less than 50% of the normal value. Successful removal of a drug by dialysis requires that it possesses a polar character, low protein binding and a small to moderate volume of distribution.

Biotransformation↗
PubMed1978

Renal excretion of contrast medium after endoscopic retrograde investigations.

Endoscopic retrograde investigations are often performed as diagnostic procedures. The investigation of urine after such procedures in 21 patients has shown that appreciable amounts of contrast medium can be excreted renally. No such excretion could be shown when the contrast medium was injected into the gut lumen. The fact that contrast medium can be absorbed into the liver the pancreas during endoscopic retrograde procedures should influence the decision to perform these studies in patients with known allergies.

Cholangiography↗
PubMed1975

Renal excretion of fluoride in renal failure and after renal transplantation.

We have compared the renal excretion of fluoride in a variety of patients with chronic renal failure maintained with and without protein restriction before and during regular dialysis treatment and after transplantation. The patients tended to continue to excrete normal dietary loads of fluoride quite well until renal function was seriously reduced. From a regression of function on excretion the mean level of creatinine clearance when a normal dietary load of fluoride 0.0526 plus or minus 0.019 mmol/2 h (1.0 plus or minus 0.36 mg/24h) has a 90% chance of being excreted lies around 16 ml/min, a level when most patients with renal failure will be symptomatic. Acute loading of such patients with additional fluoride in the form of sodium fluoride from 40 mg to 60 mg/day showed a twofold to threefold increase of serum fluoride concentrations, slight increases in urinary fluoride excretion, and heavy tissue absorption, suggesting that prior fluoride loading of the skeleton had not taken place. These effects contrasted with those in one patient with normal renal function and with those in one patient with skeletal saturation due to prolonged loading. After renal transplantation fluoride excretion increased but reached normal levels within three months of satisfactory function, suggesting that fluoride loading in renal failure and during regular dialysis therapy had not been excessive.

Calcium↗
PubMed1979

[Study of the effect of dopamine on renal excretion in chronic renal failure (author's transl)].

The effects of dopamine on renal excretory function were studied in 20 patients with chronic renal failure (plasma creatinine higher than 30 mg/i). Effects were marked at a dose of 2 micrograms/kg/mn and were no greater at a dose of 5 micrograms/kg/mn (10 subjects in each case). In general, creatinine clearance increased by 28%, urea excretion by 45%, urine output by 77% and urinary sodium output by 164%. In ten patiens with terminal renal failure (plasma creatinine greater than 100 mg/i), the effects of dopamine were maintained. In these individuals, furosemide (250 mg by single intravenous injection) resulted in a higher total urine and urinary sodium output but had a less favourable effect upon creatinine.

Adult↗
PubMed1989

Quantitative evaluation of renal excretion on the dynamic DTPA renal scan.

In order to evaluate the renal excretion quantitatively, the authors analyzed the Tc-99m DTPA renogram using mean transit time (MTT) with deconvolution analysis and compared it to the perfusion index. One hundred thirteen studies consisting of 25 normal, 11 obstruction, 35 transplant-norm, 12 transplant-obstruction, and 30 transplant-rejection were evaluated. In the non-transplant obstruction, MTT is significantly long (3.40 +/- 0.85 minutes vs 2.02 +/- 0.42 minutes) and has high sensitivity (100%) and specificity (93%, 23/25) for the diagnosis of obstruction. In the transplant-obstruction, if the field of view includes both transplant and liver or spleen as a blood pool image, MTT has high sensitivity for the diagnosis (10/11) and for the follow up of obstruction (12/12), with the same specificity, but low sensitivity for rejection (25%). Perfusion index is of value in the diagnosis of rejection (73% specificity, 77% sensitivity) but is useless for the detection of obstruction (25% specificity, 75% sensitivity). The authors conclude that MTT is a useful marker for diagnosis and serial quantitative evaluation of renal obstruction. Also, they suggest the use of multiple techniques based on different principles for the complete evaluation of the renal scan.

Humans↗
PubMed1977

Iodipamide kinetics: capacity-limited biliary excretion with simultaneous pseudo-first-order renal excretion.

Iodipamide was infused into three dogs with bile fistulas to achieve various steady-state blood levels. When using ultracentrifugation techniques, iodipamide was found to be highly bound to plasma protein. The total blood clearance was low relative to hepatic blood flow. For either the whole blood concentration or the unbound concentration of iodipamide, the biliary excretion was shown to be capacity limited with a transport maximum, Tm, of approximately 1.0mumole/kg/min. The steady-state renal excretion rate, plotted against the whole blood concentration of iodipamide, resulted in a concave ascending curve, which could lead to the false conclusion that iodipamide was undergoing active renal tubular reabsorption. However, when corrected for plasma protein binding, a linear relationship was obtained, suggesting that the renal excretion of iodipamide is a pseudo-first-order process. The Michaelis-Menten parameters for the extrarenal elimination, when calculated using the whole blood concentration of iodipamide, led to a similar discrepancy compared to the parameter estimates obtained from biliary excretion rate data. This discrepancy can be eliminated when one uses the unbound concentration of iodipamide in the parameter estimates.

Animals↗
PubMed1991

Renal excretion of citrate in patients with chronic renal failure or nephrolithiasis.

Using a specific citrate lyase method, renal excretion of citrate was studied in 32 normal Chinese males, 30 nondialysed uremic male patients and 35 male subjects who had a history of nephrolithiasis. Patients with uremia or nephrolithiasis were found to have a lower urinary citrate excretion. Tubular reabsorption of citrate was markedly decreased in uremic patients, but in stone patients, the increased renal tubular reabsorption of citrate was only found in patients with hypocitraturia, whose renal citrate excretion was below 650 mumol/day and whose urinary magnesium was also low. Hypocitraturia was found in 45% (16/35) of the patients with renal stones whether their filtered load of citrate was normal or subnormal. Urinary citrate excretion was correlated with renal creatinine clearance in both normal subjects and in patients with renal stones or chronic renal failure. However, urinary phosphate correlating with urinary citrate was only found in normal subjects and in patients with kidney stones. In normal subjects, we found a positive correlation between urinary citrate and phosphate, but in stone patients, we found a negative correlation. Hypercalciuria and hyperoxalaturia were noted in some stone formers, who had, moreover, a lower urinary citrate and ascorbate excretion level. Mean urinary ascorbate excretion in patients with renal stones was markedly below that in normal subjects. Thus, we suggest that low urinary citrate excretion may be prevalent in patients with renal stones or chronic renal failure, and that hypocitraturia can be found in some stone formers, whose tubular reabsorption of citrate may be increased.

Adult↗
PubMed1981

Autoradiographic localization of 35-S-furosemide at different stages of its renal excretion.

The renal localization of 35-S-activity was studied by autoradiography at different times (1/2 min intervals) following the rapid injection of a bolus of 70 micrograms 35-S-furosemide into the renal portal system of hens. After removal, both kidneys were freeze-sectioned, freeze-dried and subjected either to apposition autoradiography according to Ullberg or to microautoradiography. There was extensive labelling over cortical areas of the ipsilateral kidney, in the periphery of lobuli, the site of proximal tubular cells. This labelling was maximal at 1 and insignificant already at 4 min post injection. At this time, however, there was a distinct patchy labelling corresponding to collecting ducts. At 7 min post-injection no specific labelling was found. The findings suggest that furosemide in the peritubular blood is accumulated in proximal tubules, rapidly transferred (tubular secretion) to their lumina and carried distally by the tubular fluid, subsequently resulting in high concentrations of the diuretic in the lumina of collecting ducts. Thus the findings are in keeping with the view that active tubular secretion of furosemide in the hen contributes significantly to a high luminal concentration of the drug in more distal parts of the tubules, the likely site of diuretic action.

Animals↗
PubMed2001

Effect of endotoxin on P-glycoprotein-mediated biliary and renal excretion of rhodamine-123 in rats.

The effects of Klebsiella pneumoniae endotoxin on the biliary excretion and renal handling of rhodamine-123 were investigated in rats at different times after intraperitoneal injection (1 mg/kg of body weight). The typical substrates for P glycoprotein, i.e., cyclosporine, colchicine, and erythromycin, inhibited the biliary clearance of rhodamine-123, whereas a substrate for organic cation transporter, cimetidine, did not inhibit clearance, suggesting that rhodamine-123 is transported mainly by P glycoprotein. The biliary, renal, and tubular secretory clearances of rhodamine-123 and the glomerular filtration rate significantly decreased 6 h after injection of endotoxin but returned to control levels by 24 h. These results suggest that endotoxin-induced decreases in P-glycoprotein-mediated biliary excretion and renal handling of rhodamine-123 were probably due to impairment of P-glycoprotein-mediated transport ability. Pretreatment with pentoxifylline (50 mg/kg) significantly inhibited endotoxin-induced increases in tumor necrosis factor alpha (TNF-alpha) levels in plasma, which ameliorated the endotoxin-induced reduction of the biliary excretion of rhodamine-123. It is likely that endotoxin-induced impairment of the transport of rhodamine-123 is caused, in part, by overproduction of TNF-alpha. The effect of endotoxin on the expression of P-glycoprotein mRNA in liver and kidneys of rats was investigated by using a reverse transcriptase PCR. The expression of Mdr1a mRNA in both liver and kidney decreased 6 h after endotoxin injection and returned to control levels after 24 h, whereas the expression of Mdr1b mRNA in liver increased at both times and that in kidney decreased at 24 h. These findings suggest that K. pneumoniae endotoxin dramatically decreases P-glycoprotein-mediated biliary and renal excretion of rhodamine-123 probably by decreasing the expression of Mdr1a, which is likely due to increased plasma TNF-alpha levels.

ATP Binding Cassette Transporter, Subfamily B↗