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Increases in urea synthesis and the ornithine-urea cycle capacity in the giant African snail, Achatina fulica, during fasting or aestivation, or after the injection with ammonium chloride.

The objectives of this study are to determine whether a full complement of ornithine-urea cycle (OUC) enzymes is present in the hepatopancreas of the giant African snail Achatina fulica, and to investigate whether the rate of urea synthesis and the OUC capacity can be up-regulated during 23 days of fasting or aestivation, or 24 hr post-injection with NH(4)Cl (10 micromol g(-1) snail) into the foot muscle. A. fulica is ureotelic and a full complement of OUC enzymes, including carbamoyl phosphate synthetase III (CPS III), was detected from its hepatopancreas. There were significant increases in the excretion of NH(4)(+), NH(3) and urea in fasting A. fulica. Fasting had no significant effect on the tissue ammonia contents, but led to a progressive accumulation of urea, which was associated with an 18-fold increase in the rate of urea synthesis. Because fasting took place in the presence of water and because there was no change in water contents in the foot muscle and hepatopancreas, it can be concluded that the function of urea accumulation in fasting A. fulica was unrelated to water retention. Aestivation in arid conditions led to a non-progressive accumulation of urea in A. fulica. During the first 4 days and the last 3 days of the 23-day aestivation period, experimental snails exhibited significantly greater rates of urea synthesis compared with fasted snails. These increases were associated with significant increases in activities of various OUC enzymes, except CPS III, in the hepatopancreas. However, the overall urea accumulation in snails aestivated and snails fasted for 23 days were comparable. Therefore, the classical hypothesis that urea accumulation occurred to prevent water loss through evaporation during aestivation in terrestrial pulmonates may not be valid. Surprisingly, there were no accumulations of ammonia in the foot muscle and hepatopancreas of A. fulica 12 or 24 hr after NH(4)Cl was injected into the foot muscle. In contrast, the urea content in the foot muscle of A. fulica increased 4.5- and 33-fold at hour 12 and hour 24, respectively, and the respective increases in the hepatopancreas were 4.9- and 32-fold. The exogenous ammonia injected into A. fulica was apparently detoxified completely to urea. The urea synthesis rate increased 148-fold within the 24-hr experimental period, which could be the greatest increase known among animals. Simultaneously, there were significant increases in activities of glutamine synthetase (2.5-fold), CPS III (3.1-fold), ornithine transcarbamoylase (2.3-fold), argininosuccinate synthetase+lyase (13.6-fold) and arginase (3.5-fold) in the hepatopancreas 12 hr after the injection of NH(4)Cl. Taken altogether, our results support the view that the primary function of urea synthesis through the OUC in A. fulica is to defend against ammonia toxicity, but suggest that urea may have more than an excretory role in terrestrial pulmonates capable of aestivation.

Amino Acids↗

Urea handling by the medullary collecting duct of the rat kidney during hydropenia and urea infusion.

Previous micropuncture studies of distal tubule fluid and ureteral urine have indicated a varying degree of urea reabsorption in the collecting duct. In the present experiments the microcatheterization technique was used to directly determine urea, Na, K, total solute and fluid reabsorption along the length of the medullary collecting duct in anesthetized hydropenic rats and in rats given low dose urea infusion (Purea 18.9 mM/l). In hydropenic rats, the remaining fraction of filtered urea did not change significantly along the collecting duct, as indicated both by regression analysis of all samples and by comparison of paired samples from the corticomedullary junction and papillary tip. During low dose urea infusion, urine osmolality increased in proportion to the increase in urea concentration and again there was no net urea reabsorption between the beginning and end of the duct. However, during urea infusion, analysis of samples from the beginning, mid-zone, and end of the collecting duct indicated that urea entry occurred in the proximal portion of the duct (beginning to mid-zone, P less than 0.01) and that urea reabsorption occurred in the distal portion (mid-zone to end, P less than 0.01). The lack of significant net urea reabsorption along the duct despite the excretion of moderately concentrated urine, has despite the excretion of moderately concentrated urine, has implications for the concept of medullary urea recycling and for models of the urinary concentrating mechanism. The finding of functional heterogeneity with respect to urea handling in the collecting duct in vivo, with both reabsorption are secretion being demonstrated, raises the possibility that internal recycling of urea in the medullary collecting duct itself may contribute to maintenance of a high papillary interstitial urea concentration.

Animals↗

The effects of dietary sucrose and the concentration of plasma urea and rumen ammonia on the degradation of urea in the gastrointestinal tract of cattle.

1. The rates of entry of urea into plasma, of urea degradation in the gastrointestinal tract, and the partition of that degradation between the rumen and post-ruminal tract were determined by use of [14C]urea and NaH14CO3 in Hereford steers receiving hay diets with or without sucrose. The concentrations of plasma urea and rumen ammonia were varied by infusions of urea into the rumen or abomasum. 2. For all diets, plasma urea concentration was related to urea entry rate, to degradation of urea in the whole gastrointestinal tract, and to its degradation in the post-ruminal tract, but the relationship with its degradation in the rumen was poor. 3. Degradation of urea in the rumen was related in a multiple regression in a curvilinear manner in three groups of diets (pasture-hay alone, pasture-hay--lucerne (Medicago sativa) mixtures, diets with sucrose), and negatively to rumen ammonia concentration for pasture-hay diets, and diets with sucrose. 4. Ruminal clearance of urea (rate of urea degradation per plasma urea concentration) was negatively related to the rumen ammonia concentration for steers given diets with sucrose, of pasture-hay with or without urea infusions. Provision of sucrose in the diet significantly increased clearance. 5. Enhanced urea degradation in the rumen associated with dietary sucrose supplements accounted for 0.4 of additional microbial N synthesis in the rumen. 6. The partition of transfer of urea to the rumen via saliva and through the rumen wall is discussed.

Ammonia↗

[Kidney retention of urea in sheep on a hypoprotein diet: study by retrograde perfusion of urea in the kidney pelvis].

In order to study the role of the renal pelvis on urea sparing in sheep fed low protein diets, the pelvis was perfused through the ureter with 1M and 3M urea solutions. Eight ewes were used: four on a regular diet (total nitrogen 188.7 g.kg-1 dry matter) and the other four on a low protein diet (total nitrogen 109.4 g.kg-1 dry matter). On each animal, perfusions were performed on one kidney; the other one was kept as a control. Fractional excretion of urea (TEu) and urea (Cu), inulin, para-aminohippurate and osmolar clearances, were determined during five experimental periods of 30 min each (T = control, 1M = perfusion with 1M urea solution, R1 = first period of recovery, 3M = perfusion with 3M urea solution, R2 = second period of recovery). 1. During control periods sheep on low protein diet have a greater capacity of urea retention than sheep on regular diet, under antidiuretic conditions (inulin U/P = 200). The following data (means +/- S.D.) are all reduced in animals on low protein diet: TEu by 36% (0.38 +/- 0.19 vs. 0.59 +/- 0.28 for normal protein sheep, p less than 0.05), Cu by 55% (0.50 +/- 0.19 vs. 1.15 +/- 0.49 ml.min-1.kg-1 for normal sheep, p less than 0.01) and amount of urea excreted by 80% (2.1 +/- 0.7 vs. 10.4 +/- 2.7 mg.min-1 for normal sheep, p less than 0.01). 2. The linear regression analysis of the relationship between tubular reabsorption of urea and its filtered amount shows that the capacity of urea retention is significantly higher in low protein sheep and that the difference between the two groups is greater as the filtered amount increases. Following 1M and 3M perfusions, the capacity of urea reabsorption by the perfused kidneys is significantly decreased in low protein animals whereas there is no change in the normal ones. The result is that perfused kidneys of the low protein sheep increase the amount of urea excreted during these periods: urine concentration of urea (Uu) increases by 55% during R1 and by 144% during R2, TEu increases by 60% during R1 and by 147% during R2 and Cu increases by 40% during R1 and by 95% during R2, without any variation of urine flow rate. These changes could be understood, provided that an important transfer of the perfused urea to the renal medulla in the low protein sheep would reduce the concentration gradients which enhance urea passive reabsorption from the collecting ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Urea-selective concentrating defect in transgenic mice lacking urea transporter UT-B.

Urea transporter UT-B has been proposed to be the major urea transporter in erythrocytes and kidney-descending vasa recta. The mouse UT-B cDNA was isolated and encodes a 384-amino acid urea-transporting glycoprotein expressed in kidney, spleen, brain, ureter, and urinary bladder. The mouse UT-B gene was analyzed, and UT-B knockout mice were generated by targeted gene deletion of exons 3-6. The survival and growth of UT-B knockout mice were not different from wild-type littermates. Urea permeability was 45-fold lower in erythrocytes from knockout mice than from those in wild-type mice. Daily urine output was 1.5-fold greater in UT-B- deficient mice (p < 0.01), and urine osmolality (U(osm)) was lower (1532 +/- 71 versus 2056 +/- 83 mosM/kg H(2)O, mean +/- S.E., p < 0.001). After 24 h of water deprivation, U(osm) (in mosM/kg H(2)O) was 2403 +/- 38 in UT-B null mice and 3438 +/- 98 in wild-type mice (p < 0.001). Plasma urea concentration (P(urea)) was 30% higher, and urine urea concentration (U(urea)) was 35% lower in knockout mice than in wild-type mice, resulting in a much lower U(urea)/P(urea) ratio (61 +/- 5 versus 124 +/- 9, p < 0.001). Thus, the capacity to concentrate urea in the urine is more severely impaired than the capacity to concentrate other solutes. Together with data showing a disproportionate reduction in the concentration of urea compared with salt in homogenized renal inner medullas of UT-B null mice, these data define a novel "urea-selective" urinary concentrating defect in UT-B null mice. The UT-B null mice generated for these studies should also be useful in establishing the role of facilitated urea transport in extrarenal organs expressing UT-B.

Amino Acid Sequence↗

Minimal sampling protocol for accurate estimation of urea production: a study with oral [13C]urea in fed and fasted piglets.

BACKGROUND & AIMS: An oral [13C]urea protocol may provide a simple method for measurement of urea production. The validity of single pool calculations in relation to a reduced sampling protocol was assessed. METHODS: In eight fed and five fasted piglets, plasma urea enrichments from a 10 h sampling protocol were measured following an intragastric [13C]urea bolus. Blood [13C]bicarbonate was measured to trace gut [13C]urea oxidation. Two-compartment and regression (single pool) computations were performed. Pool sizes were compared to urea distribution over total body water (TBW). Shorter protocol duration was tested in regression simulations. RESULTS: Differences in urea kinetics between fed and fasted piglets did not reach statistical significance. Mean (+/-SE) urea pool from TBW times plasma urea concentration was 2.2+/-0.16 mmol kg(-1). Two-compartment modelling yielded similar results for pool size (despite the oxidation of a small amount of urea tracer). Urea appearance rate was 306+/-18 micromol kg(-1)h(-1). Regression calculations overestimated urea appearance rate vs. compartmental model (P<0.05). When samples <2 h were discarded, results were comparable to compartmental calculations even if protocol length was 6 h (325+/-24 micromol kg(-1)h(-1), NS). CONCLUSIONS: Regression calculations using plasma enrichments sampled between 2 and 6 h after oral [13C]urea administration provide accurate rates of urea production, and are not affected by tracer oxidation.

Administration, Oral↗

The 13C-urea breath test to detect Helicobacter pylori infection: a validated simple methodology with 50 mg 13C-urea.

BACKGROUND: Several modifications of the 13C-urea breath test have been published. For reasons of cost efficiency and practicability, the urea dose and measurement duration should be reduced while still maintaining excellent diagnostic accuracy. AIMS: To establish a validated simple protocol for the urea breath test with 50 mg 13C-urea and to compare this protocol with the conventional urea breath test with 100 mg 13C-urea. METHODS: Conventional urea breath test with 100 mg 13C-urea was performed on 152 dyspeptic patients. Full-cream cow's milk was used as the test meal. Breath tests were repeated using 50 mg 13C-urea and the breath samples were collected at baseline and at 10 (protocol t10), 15 (protocol t15) and 30 min (protocol t30). Helicobacter pylori status was assessed by rapid urease test, histology and conventional urea breath test with 100 mg 13C-urea. RESULTS: With protocol t15, the best combination of sensitivity (99.1%), specificity (97.3%) and accuracy (98.7%) was obtained with a cut-off of 2.5 per thousand. There was an extremely high correlation coefficient between the three protocols and conventional 13C-urea breath test (all P < 0.001). CONCLUSIONS: A urea breath test with 50 mg 13C-urea using a simple test meal and a 15-min sampling interval with a low cut-off seems to be cost-effective and convenient. In a well-standardized laboratory, this modification is not associated with any loss of diagnostic accuracy.

Adolescent↗

High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNA.

UNLABELLED: Urea and NaCl are elevated in the renal inner medulla. We now find that a high concentration of urea or NaCl increases reactive oxygen species (ROS) in mouse renal inner medullary (mIMCD3) cells in culture. Previously, high NaCl, but not high urea, was found to cause DNA double-strand breaks. We now tested whether high urea or NaCl causes oxidative damage to DNA or cellular proteins. We find that high urea increases mIMCD3 cell DNA single-strand breaks and 8-oxoguanine lesions. High NaCl does not cause detectable 8-oxoguanine lesions. High urea or NaCl also greatly increases carbonylation of proteins in mIMCD3 cells. Carbonylation occurs within 5 min and with as little as 5 mM urea, a normal plasma level. It increases as urea is raised over the range in uremia. A high raffinose level increases ROS and carbonylation. High sorbitol and glycerol levels do not increase ROS or carbonylation. Carbonyl content is high in mouse renal inner medullas where interstitial NaCl and urea concentrations are normally high. There, numerous proteins are carbonylated, and carbonylation occurs in both collecting ducts and thin limbs. CONCLUSIONS: (i) Oxidative stress, associated with high urea, causes 8-oxoguanine DNA lesions in mIMCD3 cell DNA. (ii) High urea or NaCl carbonylates proteins in mIMCD3 cells and in renal inner medullary cells in vivo. (iii) In mIMCD3 cells a normal plasma concentration of urea causes carbonylation, and carbonylation increases over the uremic range of urea concentration, indicating that urea can contribute directly to the carbonylation found in uremia.

Animals↗

Urea kinetic analysis of automated peritoneal dialysis allows calculation of a CAPD-equivalent Kt/V(urea).

BACKGROUND: Based on evidence of increased mortality with decreasing urea clearance, the Dialysis Outcomes Quality Initiative (DOQI) recommended a weekly Kt/Vurea of 2.0 or higher for patients receiving continuous ambulatory peritoneal dialysis (CAPD). DOQI recommendations for automated peritoneal dialysis (APD) are based on efforts to determine the clearance providing urea mass removal equivalent to CAPD. We have adapted a variable volume direct quantitation urea kinetic model (UKM) in an effort to assess DOQI APD guidelines. METHODS: The daily urea mass removed with a weekly Kt/Vurea of 2.0 was calculated using standardized CAPD patient profiles. Using this value and defining the pre-APD plasma urea nitrogen (PUN) as C0 and equal to the CAPD steady-state PUN, the UKM reiteratively calculated the urea clearance from an APD treatment that provided a urea mass removal equivalent to CAPD. A total weekly Kt/Vurea was calculated for various levels of continuous urea clearance (defined as Kprt/Vurea) and plotted against Kprt/Vurea (weekly). The impact of dialytic time (t), drain volume of the daytime dwell (delta), and ultrafiltration volume (phi) were assessed, and all profiles were performed with C0 equal to the corresponding blood urea nitrogen of 60, 70, and 80 mg/dL. RESULTS: The relationship between requisite weekly Kt/Vurea and Kprt/Vurea (weekly) was linear. Weekly Kt/Vurea declined with increasing Kprt/Vurea, t, delta, and phi. The effect of phi on the weekly Kt/Vurea was independent of Kprt/Vurea, and the magnitude of the effect of t and delta on the weekly Kt/Vurea decreased with increasing continuous clearance. Weekly Kt/Vurea values were independent of V and C0. The latter observation allowed extrapolation of CAPD clearance and urea generation relationships to APD: CAPD-equivalent weekly Kt/Vurea = [700 x (UD + Ur)]/(C0 x V), where UD and Ur are the daily urea mass (mg) in dialysate and urine, respectively. CONCLUSIONS: The APD urea clearance, which provides urea mass removal equivalent to CAPD, varies as a function of a combination of patient and treatment variables. However, a CAPD-equivalent weekly Kt/Vurea can be calculated by collecting appropriate dialysis and urine samples and estimating patient V. The results can be evaluated in the context of evidence-based CAPD guidelines, increasing the precision of adjustment and monitoring of the APD prescription.

Blood Urea Nitrogen↗

Analysis of regulatory factors for urea synthesis by isolated perfused rat liver. I. Urea synthesis with ammonia and glutamine as nitrogen sources.

Urea synthesis was studied using the isolated liver perfusion with ammonium cholride and glutamine as nitrogen sources. The rate of urea formation increases with ammonium cholorde concentration up to 5mM, and the rate remained constant in the range between 5 and 20mM of ammonium chloride as the substrate. The concentration of ammonia in the medium to support the half-maximum velocity of urea formation was 0.7mM. The rate of urea formation was stimulated by the addition of 2.5mM ornithine, and the greater part of the ornithine which was taken up into the liver was accumulated as citrulline in the presence of ammonia. A considerable accelerating effect of N-acetylglutamate on the synthetic rate was observed, but a rather high concentration of N-acetylglutamate was required in order to obtain the maximum effect possibly, because its permeability into liver cells may be limited. A marked additive effect on the rate of urea formation was observed with the combined addition of ornithine and N-acetylglutamate. The metabolic conversion of glutamine nitrogen to urea in the perfused rat liver and the effect of several compounds which stimulated urea synthesis with ammonia were further examined. The process of conversion of glutamine nitrogen to urea might be composed of the following three steps. In the first lag phase, a small amount of glutamine was removed from the medium. In the second stage, the glutamine level decreased rapidly and ammonia was accumulated in the perfusate. The third stage was a period in which glutamine concentration remained at a constant low level, and the accumulated ammonia was rapidly conversed to urea. The rate of urea formation in this third stage was found to be much higher than that with ammonia as the substrate. The maximum rate of glutamine removal was obtained at pH 7.7 of the perfusate and at a concentration of 10mM glutamine. Urea formation with glutamine was also stimulated by the addition of ornithine, malate, or N-acetylglutamate, which had accelerating effects on the urea synthesis with ammonia. This stimulation was due to an effective conversion of ammonia to urea, but no change in the rate of removal glutamine was obtained.

Ammonium Chloride↗

Measurement of urea kinetics in vivo by means of a constant tracer infusion of di-15N-urea.

We have assessed the feasibility of studying urea metabolism in vivo in both steady state and nonsteady state situations by means of the primed constant infusion of di-15N-urea and the analysis of the resulting enrichment in plasma urea. Both hepatectomized dogs with known rates of urea infusion and intact dogs were studied. The enrichment of the bistrimethylsilyl derivative of urea was determined on a gas chromatograph-mass spectrometer. Selected ion monitoring was set for m/e 189 (M - 15), m/e 190 (A + 1), and m/e 191 (A + 2), thus enabling the calculation of the rate of urea production from nonrecycled NH3 (from A + 2 data) (Ra N), the rate of recycling of NH3 into urea (Ra R) (from A + 1 data), and thus the total rate of urea production (Ra N + Ra R). When urine collections were made, the incorporation of urea-N into protein was estimated from the difference between Ra N and urea excretion. We found that, in the steady state in a hepatectomized dog, the rate of appearance of urea can be determined accurately. In the nonsteady state in both hepatectomized and intact dogs, urea appearance could be estimated within +/- 20% in most situations. The only situation in which this was not the case was when we attempted to measure rapid changes in Ra R. Thus, within limits, this can be a useful technique enabling the quantitation of various aspects of urea metabolism.

Animals↗

Urea gradient-associated fluid absorption with sigma urea = 1 in rat terminal collecting duct.

It has been proposed that inner medullary collecting ducts (IMCDs) can absorb fluid in the absence of a transepithelial osmolality gradient if a perfusate-to-bath urea gradient is present. Such a process has been suggested to be caused by a nonunity reflection coefficient for urea (sigma urea less than 1). However, our recent measurements of sigma urea yielded values not significantly different from 1.0. The present study was done to readdress the possibility of direct coupling of water and urea transport in the rat IMCD. Isolated rat terminal IMCD segments were studied in the presence of 10(-10) M vasopressin with the osmolality of the perfusate equal to that of the peritubular bath but with a perfusate-to-bath urea gradient (bath osmolality balanced with NaCl). We measured both fluid absorption rate and urea concentration in collected fluid and calculated the osmolality of the collected fluid. We observed rapid fluid absorption associated with substantial urea absorption. The urea absorption caused a large fall in the osmolality of the collected fluid with respect to the bath. Simulations with a mathematical model of an isolated perfused tubule revealed that the transepithelial osmolality gradient generated along the length of tubule (caused by urea absorption) was large enough to account for the fluid absorption. Measurement of sigma urea with the "zero-flux" (or null point) method revealed a value of 1.00 +/- 0.02. Thus we conclude that the observed fluid absorption is the result of a transepithelial osmolality gradient generated by rapid urea absorption and does not require sigma urea less than one.

Absorption↗

Urea and urea nitrate decomposition pathways: a quantum chemistry study.

Electronic structure calculations have been performed to investigate the initial steps in the gas-phase decomposition of urea and urea nitrate. The most favorable decomposition pathway for an isolated urea molecule leads to HNCO and NH3. Gaseous urea nitrate formed by the association of urea and HNO3 has two isomeric forms, both of which are acid-base complexes stabilized by the hydrogen-bonding interactions involving the acidic proton of HNO3 and either the O or N atoms of urea, with binding energies (D0(o), calculated at the G2M level with BSSE correction) of 13.7 and 8.3 kcal/mol, respectively, and with estimated standard enthalpies of formation (delta(f)H298(o) of -102.3 and -97.1 kcal/mol, respectively. Both isomers can undergo relatively facile double proton transfer within cyclic hydrogen-bonded structures. In both cases, HNO3 plays a catalytic role for the (1,3) H-shifts in urea by acting as a donor of the first and an acceptor of the second protons transferred in a relay fashion. The double proton transfer in the carbonyl/hydrogen bond complex mediates the keto-enol tautomerization of urea, and in the other complex the result is the breakdown of the urea part to the HNCO and NH3 fragments. The enolic form of urea is not expected to accumulate in significant quantities due to its very fast conversion back to H2NC(O)NH2 which is barrierless in the presence of HNO3. The HNO3-catalyzed breakdown of urea to HNCO and NH3 is predicted to be the most favorable decomposition pathway for gaseous urea nitrate. Thus, HNCO + NH3 + HNO3 and their association products (e.g., ammonium nitrate and isocyanate) are expected to be the major initial products of the urea nitrate decomposition. This prediction is consistent with the experimental T-jump/FTIR data [Hiyoshi et al. 12th Int. Detonation Symp., Aug 11-16, San Diego, CA, 2002].

Journal Article↗

Urea reduction ratio considering urea rebound.

An American National Study shows that survival benefits from higher dialysis doses appear to be present up to a Kt/V level of 1.3 or a urea reduction ratio (URR) of 70%. The effect of increasing dialysis efficiency magnified urea rebound and the error in URR determinations. Several formulas have been developed to calculate URR considering the urea rebound (URRr). Smye and coworkers have proposed a method whereby the equilibrated blood urea nitrogen is predicted by additional intradialytic urea sample. Maduell and colleagues, based on analysis of postdialysis urea rebound, have proposed a method whereby the urea rebound is predicted. To compare measured URRr to estimated by Smye and Maduell formulas, 384 patients were studied, 211 males and 173 females, who received a dialysis session with their habitual parameters. Measurements of plasma urea concentration were obtained at the beginning, 90-100 min following the start of dialysis, at the end, and 45 min after dialysis. The postdialysis urea rebound was 22.4+/-9.7%. The urea kinetic model Kt/V was 1.365+/-0.26, and Kt/Vr was 1.14+/-0.23. URR was 68.7+/-6.6%, and when it was calculated with urea rebound, it decreased to 61.9+/-7.4%. The URRr correlated with calculations by Smye and Maduell formulas: 60.7+/-8.4 (r = 0.722, p < 0.001) and 61.8+/-6.6 (r = 0.933, p < 0.001), respectively. The precision of estimated limits of agreement and percentage of error by Bland and Altman analysis show that URRr estimated Maduell formula could be used in place of the URRr. Otherwise, the degree of agreement of the Smye method was not clinically acceptable. In conclusion, our results led us to suggest that in actual dialysis, the use of URR is not adequate for delivered hemodialysis dose, and URRr should be used. URRr estimated by Maduell formula could be a simple and accurate method for use in clinical practice. The recommended dialysis dose by the American National Study of URR of 70% could correspond, considering urea rebound, to Kt/Vr 1.18 or URRr of 64%.

Adult↗

Quantitative assessment of urea, glucose and ammonia changes in human dental plaque and saliva following rinsing with urea and glucose.

The rates of three processes associated with the rise and fall in plaque pH, that normally occur following a urea rinse, were determined: (i) disappearance of urea from plaque, (ii) disappearance of urea from saliva and (iii) formation and disappearance from plaque of the ammonia produced by the plaque bacteria from the urea. Also examined were two processes associated with the fall and rise in pH following a glucose rinse: the disappearance of glucose from plaque and from saliva. Entry into plaque of either urea or glucose during rinsing was immediate; the subsequent disappearance of both from the plaque was slow and followed first-order kinetics. The ammonia formation and urea-disappearance results suggested that clearance of urea from the plaque occurred mainly by bacterial degradation and not by diffusion out of the plaque. The rate constants for ammonia formation and for its subsequent disappearance from the plaque made it clear why a rapid rise and a slow subsequent fall in the pH occurs after urea rinsing. The rate constants enabled calculation of the ammonia produced as a percentage of the urea utilized. Only 16-26 per cent of the urea was recovered as ammonia and the remainder of the urea-N was stored probably as NH2 moieties of certain amino acids. Such storage may enable the plaque bacteria to maintain the pH at an elevated level for an extended period of time by bacterial production of ammonia from these stored compounds after the urea ceases to be available as a source of substrate.

Ammonia↗

Evaluation of urea kinetics utilizing stable isotope urea and pharmacokinetic modeling.

The determination of urea kinetics plays a central role in clinical dialysis prescription. There persist, however, significant limitations to current approaches, particularly as they pertain to rigorous explorations of urea metabolism, distribution, and removal. This report describes methodologies designed to address these limitations by coupling a stable nitrogen isotope method with strict compartmental pharmacokinetic modeling. The findings of the present study can be summarized as follows. First, the use of stable isotope labeled exogenous urea is a reliable clinically applicable method for determination of urea kinetics. Second, this method offers significant advantages in that it allows for an accurate measurement of urea distribution space, endogenous urea production, and non-renal clearance of urea. Third, this method is significantly more rigorous than urea kinetic models that utilize only endogenous urea and do not carefully fit data points. Finally, pharmacokinetic modeling suggests that a two-compartment model satisfies all aspects of urea distribution and removal, but these compartments should not be equated with specific physiologic spaces. The combination of stable isotope urea compartmental modeling is a rigorous methodology for the assessment and validation of urea kinetics.

Adult↗