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PubMed2000

Analytic validation of an infrared milk urea assay and effects of sample acquisition factors on milk urea results.

The objective of this study was to determine if milk samples, as they are routinely collected by Ontario Dairy Herd Improvement, would yield accurate milk urea results with an infrared assay. This investigation involved analytic validation of the infrared assay and assessment of the effect of DHI routine sample acquisition factors on milk urea results. Analytic validation of an automated milk urea assay was performed by assessing the relative accuracy and precision of milk urea results produced by the Fossomatic 4000 Milk Analyzer, an infrared method of analysis, compared with the Eurochem test, an accepted reference method. Results indicated that, when interpreted at the group level, milk urea results between the infrared method and the reference test were in good agreement. The two tests shared a similar and high level of precision. Milk urea concentrations obtained from composite (metered) milk samples, and not quarter stripping samples, were most representative of concurrent serum urea concentrations. The addition of bronopol preservative did not result in a numerically important change in milk urea concentrations. Storage of preserved metered milk samples for up to 4 d at either room temperature or by refrigeration, or for up to 3 d by freezing, did not result in changes in milk urea concentrations. We concluded that milk samples, as they are routinely collected and handled by DHI, are suitable for measurement of milk urea concentrations with the infrared method of analysis if data are interpreted at the group level.

Animals↗
PubMed2005

Regulated expression of renal and intestinal UT-B urea transporter in response to varying urea load.

Production, recycling, and elimination of urea are important to maintain nitrogen balance. Adaptation to varying loads of urea due to different protein intake or in renal failure may involve changes in urea transport and may possibly affect urea transporters. In this study, we examined the expression of the UT-B urea transporter in rats fed a low-protein diet (LPD), a high-protein diet (HPD), and a 20% urea-supplemented diet. In the kidney, UT-B protein abundance increased in the outer medulla of both LPD-fed rats and 20% urea-fed rats, without changes in the inner medulla of either group compared with controls. In HPD-fed rats, UT-B protein decreased significantly in both the outer and inner medulla. We identified expression of UT-B in the rat colon, as a 2-kb mRNA transcript and as an approximately 45-kDa protein, with apical localization in superficial colon epithelial cells. UT-B also is expressed in rat small intestine. In rat colon, UT-B protein abundance was mildly, but significantly, decreased in LPD-fed and 20% urea-fed rats. UT-B abundance also was examined in the colon of 7/8 nephrectomized, uremic rats and in HPD-fed rats and was not significantly different from that in control rats. These findings indicate that UT-B expression is regulated in response to different loads of urea, with a pattern that suggests involvement of tissue-specific regulatory mechanism in kidney and colon.

Animals↗
PubMedDate not supplied

Comparison of a modified urea kinetic model direct dialysis quantification and classic urea kinetic modeling.

In the classic urea kinetic model (UkM), the measurement of clearance (K) as a model input is onerous, and its result is higher than actual body clearance because of urea disequilibrium. Urea kinetics performed by direct dialysis quantification (DDQ), with an equilibrated post rebound sample, gives reliable results but is routinely impractical. The modified UKM (mUKM) method is based on the input of urea distribution volume (V), easily obtainable by several methods and more stable than clearance, and uses simple formulae derived from urea mass balance, avoiding iterative computation. Compared with DDQ, mUKM results are identical, provided that the V value obtained by DDQ is used as input. Compared with UKM, mUKM urea clearances are significantly lower (158.1 +/- 20.5 versus 180.7 +/- 26.8 ml/min), as are urea nitrogen generation rates (5.85 +/- 2.0 versus 6.41 +/- 2.14 mg/min), whereas V results are close (32,444 +/- 6301 versus 32,141 +/- 5293 ml): consequently, mUKM Kt/V is significantly lower than UKM Kt/V (1.07 +/- 0.17 versus 1.22 +/- 0.18). This is because both mUKM and DDQ take account of post dialysis urea rebound. Therefore, if UKM formulae are used with the DDQ body clearance and the equilibrated post rebound blood urea nitrogen value as input data, their results strictly approximate the reference DDQ (V = 32,457 +/- 6274; Kt/V = 1.07 +/- 0.17; G = 5.85 +/- 2.0), demonstrating the common mathematical basis of DDQ and UKM. Therefore, reliable results may be obtained by DDQ, by mUKM, and by "equilibrated" UKM; we suggest that the mUKM model, less cumbersome than DDQ, and more reliable than UKM because it avoids the clearance measurement and the need for iterative computation, could be useful for routine kinetics.

Blood Urea Nitrogen↗
PubMed2001

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia.

Urease and the cytotoxin VacA are two major virulence factors of the human pathogen Helicobacter pylori, which is responsible for severe gastroduodenal diseases. Diffusion of urea, the substrate of urease, into the stomach is critically required for the survival of infecting H. pylori. We now show that VacA increases the transepithelial flux of urea across model epithelia by inducing an unsaturable permeation pathway. This transcellular pathway is selective, as it conducts thiourea, but not glycerol and mannitol, demonstrating that it is not due to a loosening of intercellular junctions. Experiments performed with different cell lines, grown in a nonpolarized state, confirm that VacA permeabilizes the cell plasma membrane to urea. Inhibition studies indicate that transmembrane pores formed by VacA act as passive urea transporters. Thus, their inhibition by the anion channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid significantly decreases toxin-induced urea fluxes in both polarized and nonpolarized cells. Moreover, phloretin, a well-known inhibitor of eukaryotic urea transporters, blocks VacA-mediated urea and ion transport and the toxin's main biologic effects. These data show that VacA behaves as a low-pH activated, passive urea transporter potentially capable of permeabilizing the gastric epithelium to urea. This opens the novel possibility that in vivo VacA may favor H. pylori infectivity by optimizing urease activity.

Animals↗
PubMed1997

Effects of growth hormone and insulin-like growth factor-I singly and in combination on in vivo capacity of urea synthesis, gene expression of urea cycle enzymes, and organ nitrogen contents in rats.

Improvement of nitrogen balance is desirable in patients with acute or chronic illness. Both growth hormone (GH) and insulin-like growth factor-I (IGF-I) are promising anabolic agents, and their combined administration has been shown to reverse catabolism more efficiently than each of the peptides alone. This is believed to be mediated primarily through increased peripheral protein synthesis, whereas little attention has focused on a possible participation of amino acid metabolism in the liver. Four groups of rats were given: 1) placebo; 2) GH (200 micrograms/d); 3) IGF-I (300 micrograms/d); and 4) both GH and IGF-I. After 3 days, the maximum capacity of urea-nitrogen synthesis was determined by saturating infusion of alanine (n = 8 in each group), together with measurements of liver messenger RNA (mRNA) levels for urea cycle enzymes (n = 5 in each group) and N-contents of muscles, heart, and kidney. Basal plasma alpha-amino acid concentrations were similar in all groups. The capacity of urea-N synthesis [mumol/(min x 100 g body weight)] was reduced in a stepwise manner (placebo: 8.25 +/- 1.2; GH treatment: 6.52 +/- 0.8; IGF-I treatment: 5.5 +/- 0.6; and GH/IGF-I: 4.22 +/- 1.6 [P < .001 by ANOVA]), each step being lower than the former. Serum IGF-I increased stepwise from placebo (699 +/- 40 to 1,579 +/- 96 micrograms/L in the combined GH/IGF-I group), and was correlated negatively with the capacity of urea-nitrogen synthesis (P < .01). mRNA levels for urea cycle enzymes in the liver decreased after GH and IGF-I treatment, and the effect was more pronounced after the combined treatment in which the rate-limiting enzyme, argininosuccinate synthetase, was halved. Nitrogen contents of organs increased after both GH and IGF-I treatment, and even more so after the combination treatment, reaching an increase of 30% (P < .05). Data suggest that GH and IGF-I singly and, even more so in combination, additively inhibit urea synthesis. This is supposed to favor protein buildup in organs. We speculate that this inhibitory effect on the capacity of urea synthesis is caused by a decreased translation rate of the urea cycle enzymes caused by GH and IGF-I's down-regulatory effect on urea cycle enzyme gene transcription. The findings may indicate a novel mechanism of the protein anabolic action of GH and IGF-I.

Animals↗
PubMed2000

Raman spectroscopy of urea and urea-intercalated kaolinites at 77 K.

The Raman spectra of urea and urea-intercalated kaolinites have been recorded at 77 K using a Renishaw Raman microprobe equipped with liquid nitrogen cooled microscope stage. The NH2 stretching modes of urea were observed as four bands at 3250, 3321, 3355 and 3425 cm(-1) at 77 K. These four bands are attributed to a change in conformation upon cooling to liquid nitrogen temperature. Upon intercalation of urea into both low and high defect kaolinites, only two bands were observed near 3390 and 3410 cm(-1). This is explained by hydrogen bonding between the amine groups of urea and oxygen atoms of the siloxane layer of kaolinite with only one urea conformation. When the intercalated low defect kaolinite was cooled to 77 K, the bands near 3700 cm(-1) attributed to the stretching modes of the inner surface hydroxyls disappeared and a new band was observed at 3615 cm(-1). This is explained by the breaking of hydrogen bonds involving OH groups of the gibbsite-like layer and formation of new bonds to the C=O group of the intercalated urea. Thus it is suggested that at low temperatures two kinds of hydrogen bonds are formed by urea molecules in urea-intercalated kaolinite.

Kaolin↗
PubMed1999

Quest for postdialysis urea rebound-equilibrated Kt/V with only intradialytic urea samples.

BACKGROUND: Postdialysis urea rebound (PDUR) is a cause of Kt/V overestimation when it is calculated from predialysis and the immediate postdialysis blood urea collections. Measuring PDUR requires a 30- or 60-minute postdialysis sampling, which is inconvenient. Several methods had been devised for a reasonable approach to determine PDUR-equilibrated Kt/V in short dialysis without the need for a delayed sample. The aim of our study was to compare these different Kt/V methods during the longer eight-hour hemodialysis sessions, and to determine the optimum intradialytic urea sample time that fits best with PDUR. METHODS: The study included 21 patients (mean age 71.9 years) who were hemodialyzed for 60+/-60 months at three times eight hours weekly, using bicarbonate dialysate and cellulosic membranes. Blood urea samples were obtained at onset, and then at 17, 33, 50, 66, 75, 80, 85, and 100% of the dialysis session times, after 30 seconds of low flow, and then at 60-minutes postdialysis. All patients had a meal during dialysis. We compared four different formulas of Kt/V [(a) Kt/V-Smye with a 33% dialysis time urea sample, (b) two-pool equilibrated eKt/V, (c) Kt/V-std (Daugirdas-2) obtained with an immediate postdialytic sample, and (d) the different intradialytic urea samples for Kt/V (50, 66, 75, 80, and 85% of dialysis time)] with the equilibrated 60-minute PDUR Kt/V (Kt/V-r-60) formula as the reference method. RESULTS: The mean PDUR was 17.2+/-9%, leading to an overestimation of Kt/V-std by 12.2%. Kt/V-r-60 was 1.68+/-0.34. Kt/V-std was 1.88+/-0.36 (Delta = 12.2+/-4.8%, r = 0.8). eKt/V was 1.77+/-0.3 (Delta = 5+/-5%, r = 0.96), and Kt/V-Smye was 1.79+/-0.47 (Delta = 5.2+/-14%, r = 0.9). The best time for the intradialytic sampling was 80% (that is, at 6 hr and 24 min). The Kt/V-80 was 1.64+/-0.3 and was best fitted with Kt/V-r-60 (Delta = -1.8+/-8%, r = 0.91). The mean intradialytic urea evolution showed a three-exponential rate, in discrepancy with the two-exponential rate theoretical model. CONCLUSIONS: These results confirm that a significant postdialysis rebound exists in an eight-hour dialysis. An intradialytic urea sample taken at 80% of the total session time permits an estimation of the 60-minute Kt/V-rebound without the necessity of taking a delayed sample, with better accuracy than eKt/V or especially Kt/V-Smye. This may be related to a particular urea kinetics curve on the longer dialysis duration, which needs to be studied further.

Aged↗
PubMed1989

Changes in endogenous urea recycling and the handling of renal urea in pregnant and lactating Sardi sheep kept on a constant feeding level.

The kinetics of endogenous urea were compared during the last month of pregnancy, lactation, and a nonpregnant, nonlactating control period in Sardi sheep kept on a constant feed level. Urea entry rate estimated by injections of [14C]urea rose by 36% during pregnancy. Renal urea excretion was reduced by 40% during pregnancy and by 28% during lactation. Consequently, fractional urea recycling was greater during pregnancy and, to some extent, during lactation than during the control period. In a second series of experiments, glomerular filtration rate increased by 48% and urea filtration rate rose by 17% during pregnancy. During lactation, both glomerular filtration rate and urea filtration rate were close to control levels. It appears that the decreased renal urea excretion during pregnancy and lactation was due mainly to increased tubular reabsorption of urea. Rumination time increased by 15% during pregnancy. Rumen ammonia concentration was elevated in both pregnant and lactating ewes above the control period level. The results suggest that Sardi sheep possess a high potential for the conservation of nitrogen during pregnancy and lactation periods.

Animals↗
PubMed1995

Effect of colostomy on the occurrence of dietary [15N]urea in intestinal contents, blood, urine and tissues in chickens fed a low protein diet plus urea.

1. The occurrence of 15N was examined in excreta for 10 h, and in intestinal contents, blood and tissues at 10 h after [15N]urea was fed to conventional and colostomised cockerels. 2. Total-15N excretion and 15N-balance in control chickens were 18.88 and 44.79 mg/kg body weight/10 h), respectively. The former was increased and the latter was decreased by colostomy by 10.75 mg (P < 0.01). 3. Amounts of [15N]urea, [15N]ammonia and [15N]uric acid excreted by control birds were 13.78, 3.90 and 0.18 mg/kg body weight/10 h or 0.73, 0.21 and 0.01 of the total-15N excreted respectively. 4. The [15N]urea, [15N]uric acid and total-15N excreted were all increased after colostomy but [15N]ammonia was decreased (uric acid P < 0.05, others P < 0.01). The increase in total-15N was mostly accounted for by [15N]urea. 5. Colostomy resulted in significantly less total-15N in the contents of the whole intestine (P < 0.01), less total-15N, [15N]ammonia and [15N]urea in the contents of the colo-rectum (P < 0.01) and less total-15N and [15N]urea in the contents of the upper intestine (P < 0.05); it did not affect any in caecal contents. 6. [15N]Urea in blood, liver and kidney (blood P < 0.01, others P < 0.05), and [15N]glutamine amide (P < 0.05) and [15N]uric acid (P < 0.01) in blood were significantly decreased after colostomy. 7. The results support the hypothesis that most of the dietary urea is utilised as the result of a back-flow of ureteral urea into the caeca where it is rapidly converted into ammonia which is then metabolised to other compounds.

Animal Feed↗
PubMed1976

[Excretion of acetyl urea in milk following oral 14C-acetyl urea administration to dairy cows].

2 experimental cows were fed acetyl urea several weeks before the trial was started. The first cow received a daily amount of 200 g and the second cow 855 g. On the first day of experiment both cows were given 5 mCi of 14C acetyl urea intraruminally. Up to 6 hrs after the beginning of the experiment acetyl urea in blood plasma was shown to contain a higher proportion of 14C activity than urea. 0.21 g urea and 0.18 g acetyl urea were contained in 1 kg of milk from cow No 1 while 1 kg of milk from cow No 2 contained 0.18 g urea and 0.12 g acetyl urea. The feeding of acetyl urea to dairy cows is not recommended on the basis of the fact that any further contamination of human nutrition with foreign substances should be possibly avoided.

Animal Feed↗
PubMed2002

Five minute endoscopic urea breath test with 25 mg of (13)C-urea in the management of Helicobacter pylori infection.

OBJECTIVE: The endoscopic (13)C-urea breath test ((13)C-EUBT), which combines the urea breath test (UBT) with endoscopy, provides high accuracy for the detection of Helicobacter pylori. This study was conducted to determine whether the (13)C-EUBT using low doses of urea and short sampling times could preserve accuracy in the management of H. pylori infection. METHODS: Three hundred and twenty-five patients were randomized to receive the EUBT with 100, 50 or 25 mg of (13)C-urea by endoscopic spraying. The breath samples collected at 5, 10 and 20 min were analysed using an isotope selected non-dispersive infrared spectrometer. H. pylori infection was assessed by the rapid urease test and histology. In each sampling schedule and protocol, cut-off values were calculated by a receiver operating characteristic curve. We applied the EUBT with 25 mg of (13)C-urea at 5 min to the assessment of eradication in 135 patients who had received the antimicrobial treatment or to the detection of the organism in 61 patients with previous partial gastrectomy. RESULTS: Based on histology and the urease test, patients who had discordant results were excluded from the analysis. Using 100 mg of urea, the sensitivity and specificity of the test were both 100% at 10 and 20 min, and the sensitivity and specificity at 5 min were best with 98.6% and 100%, respectively. With 50 mg, they were both 100% at 20 min, and the best combination of sensitivity and specificity at 5 and 10 min was 97.3-96.6% and 97.3-100%, respectively. Even with 25 mg, the sensitivity and specificity were both 100.0% at 20 min, and at the 5 min and 10 min time point, the EUBT yielded a sensitivity of 98.7% and a specificity of 100%. There was a significant positive correlation between the test values of the 5 min (13)C-EUBT with 25 mg of test urea and those of the conventional UBT. The 5 min EUBT with (13)C-urea offered high accuracy in the assessment of H. pylori eradication, with the sensitivity and specificity being 100% and 96.4%, respectively. In patients with previous gastrectomy, the EUBT provided acceptable accuracy (a sensitivity of 96.4% and a specificity of 97.0%). CONCLUSIONS: Our results indicate that the (13)C-EUBT is an accurate method for detecting H. pylori infection. The EUBT using only 25 mg of (13)C-urea at the early (5 min) time point has satisfactory diagnostic efficacy in pre- and post-eradication treatment settings, providing a less expensive and more rapid way of performing the test. The EUBT may be a reliable method of assessing H. pylori status in the remnant stomach.

Adult↗
PubMed2002

Leaf urea metabolism in potato. Urease activity profile and patterns of recovery and distribution of (15)N after foliar urea application in wild-type and urease-antisense transgenics.

The influence of urease activity on N distribution and losses after foliar urea application was investigated using wild-type and transgenic potato (Solanum tuberosum cv Désirée) plants in which urease activity was down-regulated. A good correlation between urease activity and (15)N urea metabolism (NH(3) accumulation) was found. The general accumulation of ammonium in leaves treated with urea indicated that urease activity is not rate limiting, at least initially, for the assimilation of urea N by the plant. It is surprising that there was no effect of urease activity on either N losses or (15)N distribution in the plants after foliar urea application. Experiments with wild-type plants in the field using foliar-applied (15)N urea demonstrated an initial rapid export of N from urea-treated leaves to the tubers within 48 h, followed by a more gradual redistribution during the subsequent days. Only 10% to 18% of urea N applied was lost (presumably because of NH(3) volatilization) in contrast to far greater losses reported in several other studies. The pattern of urease activity in the canopy was investigated during plant development. The activity per unit protein increased up to 10-fold with leaf and plant age, suggesting a correlation with increased N recycling in senescing tissues. Whereas several reports have claimed that plant urease is inducible by urea, no evidence for urease induction could be found in potato.

Enzyme Induction↗
PubMed1991

Proteus mirabilis urease: use of a ureA-lacZ fusion demonstrates that induction is highly specific for urea.

Proteus mirabilis, a common agent of nosocomially acquired and catheter-associated urinary tract infection, is the most frequent cause of infection-induced bladder and kidney stones. Urease-catalyzed urea hydrolysis initiates stone formation in urine and can be inhibited by acetohydroxamic acid and other structural analogs of urea. Since P. mirabilis urease is inducible with urea, there has been some concern that urease inhibitors actually induce urease during an active infection, thus compounding the problem of elevated enzyme activity. Quantitating induction by compounds that simultaneously inhibit urease activity has been difficult. Therefore, to study these problems, we constructed a fusion of ureA (a urease subunit gene) and lacZ (the beta-galactosidase gene) within plasmid pMID1010, which encodes an inducible urease of P. mirabilis expressed in E. coli JM103 (Lac-). The fusion protein, predicted to be 117 kDa, was induced by urea and detected on Western blots (immunoblots) with anti-beta-galactosidase antiserum. Peak beta-galactosidase activity of 9.9 mumol of ONPG (o-nitrophenyl-beta-D-galactopyranoside) hydrolyzed per min per mg of protein, quantitated spectrophotometrically, was induced at 200 mM urea. The uninduced rate was 0.2 mumol of ONPG hydrolyzed per min per mg of protein. Induction was specific for urea, as no structural analog of urea (including acetohydroxamic acid, hydroxyurea, thiourea, hippuric acid, flurofamide, or hydroxylamine) induced fusion protein activity. These data suggest that induction by inactivation of UreR, the urease repressor protein that governs regulation of the urease operon, is specific for urea and does not respond to closely related structural analogs.

Cloning, Molecular↗
PubMed1992

Tracer studies of urea kinetics in growing pigs: II. The effect of starch infusion at the distal ileum on urea recycling and bacterial nitrogen excretion.

Six gilts, with an average BW of 70 kg, were fitted with a simple T-cannula at the distal ileum to study the effect of continuous starch infusion on urea kinetics by means of a radioisotope dilution technique. The pigs were fed twice daily 600 g of a cornstarch-based diet formulated to contain 16% CP by supplementation with isolated soy protein. Infusion of starch, compared with water, decreased (P < .05) plasma urea concentration, urea pool size, and entry, excretion, and degradation rates; urea turnover rate and urea space were not affected (P > .05). Expressed as a percentage of total entry rate, approximately 40% of urea was recycled into the digestive tract in both infusion treatments. The stimulation of microbial fermentation in the large intestine resulted in an increase (P < .05) in fecal N excretion, which was mainly due to an increased excretion of bacterial N. This increase could not be attributed to a greater secretion of urea into the large intestine and its subsequent utilization by the intestinal microflora. The increased bacterial N assimilation after starch infusion led to a reduction in ammonia absorption from the large intestine, which in turn was reflected by a reduced urinary N excretion. As a result, the overall N balance was not affected. In a second experiment, two barrows, with an average BW of 80 kg, were fed twice daily 1.4 kg of a cereal-based diet. The body urea pool of both pigs was labeled with a single injection of 1 g and 2 g of [15N]urea, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Effect of dialytic treatment and the relation between erythrocyte urea and plasma urea].

The existence of an intraerythrocytic binding between haemoglobin and urea is known; it determines, in normals, a higher erythrocyte than plasma urea concentration; this binding, in vitro, is progressive for an urea concentration range of 10-400 mg/dl. The only data found relating to dialysis patients, are reported by Nolph et al.; they indicate a decrease in the plasma-blood urea ratio during the blood transit through the dialyzer and a different ratio in comparison with normals, but in our opinion the method used to measure urea concentration was unsuitable. We determined urea distribution ratios by measuring, in blood and plasma, water and urea concentration in uremic inflow and outflow blood samples during dialysis. Our data indicate 1) an increase in outflow erythrocyte water (H2Oe inflow: 0.659, H2Oe outflow: 0.671 P less than 0.01) induced by a different erythrocyte osmotic gradient; 2) a not different ratio between urea of erythrocyte water and urea of plasma water in inflow and outflow samples of dialysed patients and in normals (respectively 1.06, 1.16, 1.13 p = n.s.). Our data from normal and uremic patients are like those found by Murdaugh & Doyle and by Colton & Lowrie in normals.

Body Water↗
PubMed1993

Accuracy of Kt/V estimations in high-flux haemodiafiltration using per cent reduction of urea: incorporation of urea rebound.

The estimation of Kt/V by utilization of the pre- and postdialysis urea concentrations (per cent reduction in urea and In(Upre/Upost)) provides a simple, quick technique that can be applied at the bedside. However, the accuracy of such techniques has been questioned. One possible reason for this inaccuracy may be the frequently observed postdialysis rebound in serum urea. We assessed the urea rebound at 30 min postdialysis in 34 haemodiafiltered patients and compared the calculation of Kt/V using this urea concentration with that using the immediate postdialysis concentration. These results were then compared to the Kt/V calculated by urea kinetic modelling (UKM), also utilizing the delayed serum urea concentration. The degree of urea rebound observed was large, 21.4%, being a reflection of the short-duration, rapid-flux dialysis. The formulae for calculation of Kt/V all significantly correlated with Kt/V by UKM but all gave results significantly different from Kt/V by UKM (P < 0.001 by paired t test). For assessment of Kt/V by these formulae or by UKM, the urea rebound is too large to ignore in the setting of short-duration, rapid-flux dialysis.

Blood Proteins↗