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PubMed1997

Urea rebound and delivered Kt/V determination with a continuous urea sensor.

BACKGROUND: The recent introduction of urea sensors for dialysis monitoring has made possible new approaches to urea kinetic modelling. In this study we show how the equilibrated postdialysis urea concentration (Ceq) and Kt/V corrected for double-pool urea kinetics (Kt/Vdp) can be accurately determined using an on-line sensor providing a continuous measure of blood water urea. A modification of the Smye constant volume double-pool theory led to the following equations for Ceq and Kt/Vdp [formula: see text] where Cpre is the blood concentration measured at the start of dialysis, t is the length of the dialysis session (in min) and S(ex) is the constant slope of the blood urea logarithm concentration decline following development of the intercompartmental urea concentration gradient in the first 30-60 min of dialysis. METHODS: These equations were tested in 11 patients undergoing 165-240 min of paired filtration dialysis with continuous monitoring of blood urea concentration. Cpre was determined as the plateau concentration during a preliminary period of 15-20 min of slow isolated ultrafiltration. S(ex) was accurately determined from linear regression applied to the urea sensor data from the 80-min point to the end of dialysis. RESULTS: Ceq and Kt/Vdp determined from the above equations compared closely to values determined from 25-40 min of urea rebound monitoring with the urea sensor: 10.6 +/- 3.0 versus 10.8 +/- 2.7 mmol/l (mean +/- SD) for Ceq and 1.21 +/- 0.24 versus 1.18 +/- 0.20 for Kt/Vdp, compared to single-pool values of Kt/V = 1.34 +/- 0.23. CONCLUSION: This technique may be readily programmed into on-line urea monitors to provide current and extrapolated values of Ceq and Kt/Vdp from about the first hour of dialysis.

Adult↗
PubMed1993

Diurnal variation of rumen ammonia, serum urea, and milk urea in dairy cows at high and low yields.

Milk urea content as an indicator of nutritional status may be a useful tool if major sources of variation are considered. Blood and milk samples were collected frequently during 16 to 19 h from four Holstein cows to study diurnal variation of urea content. Corn silage, alfalfa hay, and concentrates were fed. Rumen ammonia, VFA, and pH were measured in three of the cows. A clear serum urea peak, 70 to 85% higher than the lowest concentration, was observed in the higher yielding cows. The serum urea peak occurred 1.5 to 2.0 h after the rumen ammonia peak. Urea in milk equilibrated with serum with a time lag of 1 to 2 h when the rate of change in serum was .5 to 1.0 mM/h. At this rate, the average difference between serum and milk urea content was .8 mM. Urea in total milk tended to be more closely correlated to serum than samples from the gland cistern, but deviations were minor. Our results indicate a relatively rapid equilibration between blood serum and milk urea, also in the gland cistern. Equilibration may be explained by diffusion of urea along the mammary ducts and through the mucosa in the alveoli. If urea is to be used as an indicator of nutritional status, diurnal variations of serum and milk urea should be considered; time of sampling versus time of feeding is crucial. A small milk sample from a healthy quarter may give information on urea that is as good as that of a sample from regular milking.

Ammonia↗
PubMed1994

Urea peritoneal transfer evaluated using plasma water urea concentrations.

OBJECTIVE: To quantify differences in evaluation of urea peritoneal transport parameters according to the expression of urea concentration in whole plasma and plasma water. DESIGN: Prospective study in which the dialysate samples for urea determinations were taken at short dwell times (2.5-45 minutes) during three consecutive exchanges of intermittent peritoneal dialysis (IPD). Blood samples were drawn at the beginning and at the end of the study period. Urea peritoneal transport parameters were calculated using urea concentration in whole plasma and plasma water. The results were then compared. SETTING: Peritoneal dialysis unit of a nephrology department. PATIENTS: Ten stable patients on IPD. INTERVENTIONS: Dialysate and blood sample collections. MAIN OUTCOME MEASURES: Dialysate-to-plasma ratios (D/P), peritoneal clearances (Cp), and diffusive mass transport coefficients (KBD) of urea. RESULTS: At short dwell times, uncorrected (whole plasma) D/P and Cp of urea values were higher than the corrected (plasma water) values by 5.7%-5.9%. Uncorrected urea KBD, calculated using the simplified two-sample model of Garred et al., yielded an overestimation that significantly increased with prolongation of dwell (8.5 +/- 0.5% at 2.5 minutes vs 13.0 +/- 0.8% at 45 minutes). Urea KBD, assessed by the linear regression model of Garred and Spencer, was 9.4 +/- 0.3% higher for uncorrected values. CONCLUSIONS: The expression of urea concentration in whole plasma instead of plasma water overestimates urea peritoneal transfer parameters. The percent overestimation (y) of urea KBD, calculated using the simplified model of Garred et al., can be predicted with the equation y = 0.131x + 7.563, where x is the dwell time (in minutes.

Adult↗
PubMed2006

High urea and creatinine concentrations and urea transporter B in mammalian urinary tract tissues.

Although the mammalian urinary tract is generally held to be solely a transit and storage vehicle for urine made by the kidney, in vivo data suggest reabsorption of urea and other urine constituents across urinary tract epithelia. To determine whether urinary tract tissue concentrations are increased as a result of such reabsorption, we measured urea nitrogen and creatinine concentrations and determined whether urea transporter B (UT-B) was present in bladder, ureter, and other tissues from dogs and rats. Mean urea nitrogen and creatinine concentrations in dogs and rats were three- to sevenfold higher in urinary tract tissues than in serum and were comparable to those in renal cortex. In water-restricted or water-loaded rats, urea nitrogen concentrations in bladder tissues fell inversely with the state of hydration, were proportional to urine urea nitrogen concentrations, and were greater than the corresponding serum urea nitrogen concentration in every animal. Immunoblots of rat and dog urinary tract tissues demonstrated the presence of UT-B in homogenates of bladder and ureter, and immunocytochemical analysis localized UT-B to epithelial cell membranes. These findings are consistent with the notion that urea and creatinine are continuously reabsorbed from the urine across the urothelium, urea in part via UT-B, and that urine is thus altered in its passage through the urinary tract. Urea reabsorption across urinary tract epithelia may be important during conditions requiring nitrogen conservation and may contribute to pathophysiological states characterized by high blood urea nitrogen, such as prerenal azotemia and obstructive uropathy.

Animals↗
PubMed1989

Evidence that the adverse effect of urea fertilizer on seed germination in soil is due to ammonia formed through hydrolysis of urea by soil urease.

Studies using seeds of wheat (Triticum aestivum L.), rye (Secale cereale L.), barley (Hordeum vulgare L.), and corn (Zea mays L.) indicated that the adverse effect of urea fertilizer on seed germination in soil is due to ammonia formed through hydrolysis of urea by soil urease and is not due to urea itself, to urea fertilizer impurities such as biuret, or to nitrite formed by nitrification of urea nitrogen. Support for this conclusion was obtained from (i) comparison of the effects on seed germination in soil of purified urea, urea fertilizers, urea fertilizer impurities, and compounds formed by enzymatic and microbial transformations of urea in soil; (ii) studies showing that ammonia volatilized from soils treated with urea completely inhibited germination of seeds close to, but not in contact with, these soils; and (iii) experiments showing that the adverse effect of urea fertilizer on seed germination in soil was completely eliminated when the soil was autoclaved to destroy urease or was treated with phenylphosphorodiamidate to inhibit soil urease activity before treatment with urea fertilizer.

Journal Article↗
PubMed1997

Effects of urea on M4-lactate dehydrogenase from elasmobranchs and urea-accumulating Australian desert frogs.

We measured the effect of urea on M4-lactate dehydrogenase (M4-LDH) from elasmobranchs and Australian desert frogs (urea accumulators) and from two animals that do not accumulate urea, the axolotl and the rabbit. An analysis of the effect of urea on the Kd(NADH), V, V/K(m(prr)) and V/K(m(NADH)) shows that in all cases the major effect of urea was on the binding of pyruvate, which fits with data in the literature that show that urea acts as a competitive inhibitor of LDH. The characteristics of the elasmobranch enzymes are consistent with a proposed adaptation model, but the situation for the enzymes from the aestivating frogs is equivocal. Urea (400 mM) had less effect on the K(m(prr)) of M4-LDH from the urea accumulators than it did on the non-accumulators, suggesting a general adaptation and that the enzyme produced by the aestivating frogs (urea accumulators) is kinetically different from that of non-aestivating frogs (non-accumulators). A new approach is used to characterize the overall pattern of adaptation to urea. The pattern is similar in an enzyme from an elasmobranch and an aestivating frog despite the temporary presence of urea in the latter and the phylogenetic difference between these animals.

Ambystoma↗
PubMed2000

Effects of diet quality on urea fates in sheep as assessed by refined, non-invasive [15N15N]urea kinetics.

The effect of diet quality on urea production, entry into the gastrointestinal tract (GIT) and subsequent diversion to anabolic or catabolic fates was examined in four sheep (mean live weight 49.5 kg). The animals received, in a crossover design, each of two rations, hay-grass pellets (1:1 HG) and a mixed concentrate-forage (CF). Measurements were made of N balance and urea kinetics based on a 4 d continuous intravascular infusion of [15N15N]urea. Enrichments of [15N15N]- and [14N15N]urea in the urine, and faecal 15N content were determined each day. After 24 h of infusion, urinary [15N15N]urea enrichments reached constant enrichment but a further 24 h was required before [14N15N]urea enrichment was at plateau. The latter is derived from hydrolysis of urea to 15NH3 in the digestive tract with subsequent absorption and reconversion to urea. The diets were not isonitrogenous (14.3 v. 17.1 g N supplied daily for HG and CF respectively) but showed no difference in N balance. Urea-N production was much greater (16.3 v. 11.1 g/d; P = 0.011) for CF compared with HG and more urea-N entered the GIT (9.9 v. 7.7; P = 0.07). A larger proportion of GIT entry was returned to ureagenesis (51 v. 42%; P = 0.047) for the CF diet but a smaller fraction was lost in the faeces (3.3% v. 7.1%; P = 0.013). In consequence, most of the additional urea-N which entered the GIT on the CF diet was returned to the ornithine cycle (probably as NH3) and the absolute amount available for anabolic purposes was similar between the rations (3.9 v. 4.5 g N/d).

Animals↗
PubMedDate not supplied

Differential handling of urea and its analogues suggests carrier-mediated urea excretion in freshwater rainbow trout.

The possible presence of urea transport mechanisms in the gill and kidney of the freshwater rainbow trout (Oncorhynchus mykiss) was investigated in vivo by comparing the branchial and renal handling of analogues acetamide and thiourea with the handling of urea. Trout were fitted with indwelling dorsal aortic catheters and urinary catheters and injected with an isosmotic dose of [(14)C]-labeled urea analogue (acetamide or thiourea) calculated to bring plasma analogue concentrations close to plasma urea concentrations. Urea and analogue concentrations were significantly greater in the urine than in the plasma. Branchial clearance rate of acetamide was only 48% of urea clearance, whereas the clearance of thiourea was only 22%, a pattern that was also observed in branchial uptake of these substances and was similar to our previous observations in toadfish and midshipmen. The renal secretion clearance rates of urea and acetamide were similar, and on average, both substances were secreted on a net basis, although reabsorption did occur in some cases. In contrast, thiourea was neither reabsorbed nor secreted by the kidney tubule. The secretion clearance rates of both acetamide and urea were well correlated with the secretion clearance rates of Na(+), Cl(-), and water, whereas there was no relationship between thiourea and these substances. The pattern of acetamide, thiourea, and urea handling by the gill of the trout is similar to that found in the gills of the midshipman and the gulf toadfish and strongly suggests the presence of a UT-type facilitated diffusion urea transport mechanism. The pattern of differential handling in the kidney is unlike that in the gill and also unlike that in the kidney of the midshipman and the gulf toadfish, suggesting a different mechanism. In addition, renal urea secretion occurs against a concentration gradient, suggesting the involvement of an active transport mechanism.

Acetamides↗
PubMed1993

A noninvasive method for measuring urea kinetics with a single dose of [15N15N]urea in free-living humans.

A noninvasive method is described in which the endogenous rate of urea production can be determined in normal, free-living adults. A single dose of [15N15N]urea was given orally, and the amount of label excreted as [15N15N]urea and [15N14N]urea in urine over the subsequent 48 h was measured. From the rates of excretion of labeled and unlabeled urea the rate of urea production was derived. Using this single-dose protocol the rate of urea production was 207 +/- 56 (mean +/- SD) mg N/(kg.d) in six normal adult men consuming 74 g protein/d. These results were not different when compared with rates of urea production obtained with a prime/intermittent protocol in an earlier study in the same individuals [199 +/- 20 mg N/(kg.d)]. We conclude that urea kinetics can be measured noninvasively with a single dose of [15N15N]urea and that this method may be suitable for use in free-living individuals to determine urea production rates for habitual dietary intakes.

Administration, Oral↗
PubMed1996

Urea production in normal breast-fed infants measured with primed/intermittent oral doses of [15N, 15N]urea.

Urea kinetics were measured on 11 occasions in six normal, breast-fed infants aged 29-88 days. Prime and intermittent oral doses of [15N, 15N]urea with measurement of enrichment of urea in urine were used. The rate at which urea appeared in the urea pool was 265 mgN/kg per hour, 85% of which derived from endogenous production and 15% from the diet. Urinary excretion of urea was 87 mgN/kg per hour. Therefore, 60% of the urea entering the pool each day was hydrolysed by the metabolic activity of the colonic microflora and the nitrogen was made available for further metabolic interaction. The rate of urea appearance and the extent to which urea nitrogen was salvaged were greater in infants under 6 weeks than in those over 6 weeks, indicating that urea kinetics is a more active process at an early age, and slows with time. With respect to factors influencing urea kinetics, the apparently conflicting results which have appeared in the literature may be explained. The results may help explain the growth of breast-fed infants on low protein intakes.

Administration, Oral↗
PubMedDate not supplied

Blood urea levels 30 minutes before the end of dialysis are equivalent to equilibrated blood urea.

The steady decline in blood urea during high efficiency hemodialysis is followed by a rebound phase after dialysis in which the level of urea rises to an equilibrium value (Ct + 30) that may be up to 20% higher than the immediate post dialysis (Ct) concentration. The artificially low urea concentration immediately after dialysis leads to an overestimate of the efficiency of the dialysis calculated by Kt/V if the true equilibrium blood concentration of urea is not used in the calculation by the single-pool urea kinetic model. The measurement of equilibrium urea concentration requires a blood sample approximately 30 min after hemodialysis, which is an encumbrance on dialysis patients. This study was undertaken to determine whether an intradialytic sample taken 30 min before the end of dialysis (Ct - 30) may be representative of the equilibrium sample, and to compare the Kt/V using the Ct - 30 and Ct + 30 samples. Thirty-six patients were studied and blood urea concentrations were measured half an hour before the end of dialysis (Ct - 30), at the end of dialysis (Ct), and half an hour after the end of dialysis (Ct + 30). Kt/V (Daugirdas method) was calculated using urea concentration 30 min before the end of dialysis (Kt/Vt - 30) and was compared with Kt/V calculated using equilibrium urea concentration (Kt/Vt + 30). There were no significant differences between the Kt/Vt - 30 and the KtVt + 30 (1.25 versus 1.22, p = 0.65). The correlation between Kt/Vt - 30 and Kt/Vt + 30 was excellent with r2 = 0.93, regression y = 1.05 x -0.033. Kt/Vt - 30 also compared favorably with the Kt/V double pool method (Kt/Vdp) described by Daugirdas (1.25 versus 1.19, p = 0.23). Using the Ct - 30 to calculate Kt/V by the percent urea reduction methods of jindal (Kt/Vpru) decreases the Kt/V value by 0.14 on average, but it remains significantly higher than the Daugirdas method. The authors conclude that calculations using urea concentration 30 min before the end of dialysis improves the accuracy of dose estimation in high efficiency dialysis, without inconveniencing the patient.

Female↗
PubMed2005

Association between blood plasma urea nitrogen levels and reproductive fluid urea nitrogen and ammonia concentrations in early lactation dairy cows.

Two experiments were conducted to study the relationship of blood plasma urea nitrogen (PUN) concentrations with NH3, urea nitrogen, K, Mg, P, Ca, and Na concentrations in fluid of preovulatory follicles (experiment 1) and the relationships of PUN concentration and stage of estrus cycle with ammonia and urea nitrogen concentrations in uterine fluids (experiment 2) in early lactation dairy cows. Mean PUN levels were used to distribute cows into two groups: cows with PUN>or=20 mg/dl (HPUN), and cows with PUN<20 mg/dl (LPUN). In experiment 1, blood and follicular fluids from preovulatory follicles of 38 early lactation dairy cows were collected on the day of estrus (day 0) 4h after feed was offered. Follicular fluid NH3 was higher (P<0.01) in HPUN cows (339.0 micromol/L+/-72.2) compared to LPUN cows (93.9 micromol/L+/-13.1). Follicular fluid urea N was higher (P<0.001) in HPUN cows (22.4 mg/dl+/-0.4) compared to LPUN cows (17.0 mg/dl+/-0.3). PUN and follicular fluid urea N were correlated (r2=0.86) within cows. In experiment 2, blood and uterine fluids were collected from 30 cows on day 0 and on day 7. Uterine fluid NH3 was higher (P=0.05) in HPUN cows (1562 micromol/L+/-202) than in LPUN cows (1082 micromol/L+/-202) on day 7, but not on day 0. Uterine fluid urea N was higher (P<0.001) in HPUN cows than in LPUN cows on day 0 (26.9 mg/dl+/-1.3 and 20.4 mg/dl+/-0.7) and day 7 (26.5 mg/dl+/-1.1 and 21.4 mg/dl+/-1.1). There was a correlation (r2=0.17) between PUN and uterine fluid urea N within cows. The results of this study indicate that high PUN concentrations were associated with elevated NH3 and urea N concentrations in the preovulatory follicular fluids on the day of estrus and in the uterine fluid during the luteal phase of the estrous cycle in early lactation dairy cows. Elevated NH3 or urea N concentrations in the reproductive fluids may contribute to reproductive inefficiency in dairy cows with elevated plasma urea nitrogen due to embryo toxicity.

Ammonia↗
PubMed1984

Renal control of plasma urea level in sheep: the diuretic effect of urea, potassium and sodium chloride.

Two merino ewes were fed 800 and then 1000 g of lucerne chaff per day and renal responses and extracellular fluid volume (E.C.F.) were determined. Urine urea nitrogen, glomerular filtration rate (G.F.R.), urine volume, effective renal plasma flow (E.R.P.F.) and E.C.F. increased in both animals with the greater nitrogen intake. In a second experiment, five merino wethers and four merino ewes were infused intraruminally with increasing quantities of urea, whilst being fed a mainly roughage ration, and the above parameters were determined. No significant changes in G.F.R., E.R.P.F. or E.C.F. were noted. Urinary excretion maintained a linear response to nitrogen input until 20.6 g of urea nitrogen per day were infused. At this level of infusion, an increased fractional reabsorption of urea resulted in a large increase in plasma urea concentration, but when 500 mmol of NaCl or KCl were added to the infusate, urine urea nitrogen excretion increased from 10.4 to 11.4 and 11.9 g/d respectively and plasma urea concentration decreased from 68.0 to 35.2 and 37.3 mg nitrogen/100 ml. Urea clearance virtually trebled with both electrolyte infusions and E.C.F. and G.F.R. increased by approximately 10 and 25% respectively. It is concluded that urea alone has limited diuretic ability and that the increased electrolyte content of higher protein dry roughage diets aids urine urea excretion by increasing G.F.R., and the urine flow rate by an osmotic diuretic effect.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Determination of protein catabolic rate in patients on chronic intermittent hemodialysis: urea output measurements compared with dietary protein intake and with calculation of urea generation rate.

We assessed the agreement between different methods of determining protein catabolic rate (PCR) in hemodialysis patients and the possible influence of postdialysis urea rebound and the length of the interdialytic interval on the PCR determination. Protein catabolic rate derived from measured total urea output was compared with recorded daily protein intake (DPI) and calculated urea generation rate (G), calculated by the interdialytic increase in serum urea and an estimated urea distribution volume using either the Watson equation or 58% of postdialysis body weight, and by single-pool urea kinetic modelling. In 16 patients PCR derived from calculated G by fixed urea distribution volume showed a significant decrease with blood samples obtained 10 minutes after dialysis onward as compared with immediately after dialysis, leading to an approximately 6% decrease at 60 minutes. Protein catabolic rate values derived from blood samples taken 15 to 60 minutes after dialysis were not significantly different. Urea kinetic modelling led to a significant increase in calculated PCR with samples from 5 minutes after dialysis onward and a total increase by 11.5% at 60 minutes. Different methods for determining PCR were compared in 13 clinically stable outpatients treated with conventional hemodialysis on cellulose acetate membrane dialyzers during 1 week. The mean PCR calculated from measured total urea output was 61.3 g/24 hr (range, 43.7 to 83.2 g/24 hr). Assessment of DPI as compared with PCR calculated from measured total urea output was lower by 7.5% (95% confidence intervale [CI], 1.4 to 17.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗
PubMed2003

Branchial and renal handling of urea in the gulf toadfish, Opsanus beta: the effect of exogenous urea loading.

The objective of this study was to determine whether the pulsatile facilitated diffusion transport mechanism (tUT) found in the gills of the gulf toadfish (Opsanus beta) and the active secretion transporter thought to be present in its kidney could be saturated when faced with elevated plasma urea concentrations. Toadfish were infused with four consecutive exogenous urea loads at a rate of 0, 150, 300 and 600 micromol kg(-1) h(-1). Initial plasma and urine urea concentrations were 8.1+/-0.9 and 12.4+/-1.5 mmol l(-1), respectively, and steadily increased with increasing infused loads of urea to a maximum of 36.8+/-2.8 mmol l(-1) in the plasma and 39.8+/-6.5 mmol l(-1) in the urine. There was only a very weak relationship (r=0.17) between pulse size (measured as branchial excretion during pulsatile excretion of urea) and plasma urea concentration (slope=9.79 micromol-N kg(-1) per mmol-N l(-1); P<0.05) suggesting that the branchial excretion mechanism was already saturated at normal plasma urea concentrations. Urine flow rate (0.15+/-0.03 ml kg(-1) h(-1)) and glomerular filtration rate (0.025+/-0.004 ml kg(-1) h(-1)) remained constant throughout the experiment despite the increased volume load. Renal urea secretion rate maintained a strong linear relationship (r=0.84) to plasma urea levels (slope=0.391 micromol-N kg(-1) h(-1) per mmol-N l(-1); P<0.001) with no observable transport maximum, suggesting that the renal secretory transport mechanism was not saturated even at plasma urea levels well above normal, in contrast to the branchial excretion mechanism.

Animals↗
PubMed1981

Influences of dietary sucrose and urea on transfer of endogenous urea to the rumen of sheep and numbers of epithelial bacteria.

1. The rates of transfer of plasma urea to the rumen of six sheep given brome grass (Bromus inermis) pellets alone or with supplements of sucrose or urea were determined using [14C] urea and 14C-labelled sodium bicarbonate infusions during three periods. 2. The sheep were slaughtered after the third period and samples of rumen epithelium were taken for assessment of numbers of adherent bacteria. 3. Maximum transfer (0.31 g nitrogen/h) of urea ot the rumen was observed for sheep given supplements of 150 g sucrose/d plus 20 g urea/d. Maximum clearance of plasma urea to the rumen (rate of urea transfer to the rumen per unit plasma urea concentration, 5.8 1/h) was observed for sheep given 300 g sucrose/d. 4. Urea clearance to the rumen was negatively related to rumen ammonia concentration; the slope of the relationship was increased with each addition of sucrose to the diet. 5. Numbers of facultative bacteria adherent to the rumen epithelium were increased by urea and sucrose supplements. 6. The results are discussed in relation to a hypothesis which relates the ureolytic capability of the bacteria adherent to the rumen epithelium to the control of the rate of transfer of urea into the rumen.

Ammonia↗
PubMedDate not supplied

Plasma urea, creatinine, and urea: creatinine ratio in reindeer (Rangifer tarandus tarandus) and in Svalbard reindeer (Rangifer tarandus platyrhynchus) during defined feeding conditions and in the field.

Variation in plasma urea and creatinine concentration and plasma urea:creatinine ratio (U:C) were studied in semidomestic free-ranging reindeer (Rangifer tarandus tarandus) on the Norwegian mainland, in wild Svalbard reindeer (Rangifer tarandus platyrhynchus), and in captive reindeer maintained either on a lichen-based diet or a protein-rich concentrate to investigate whether these parameters could be used as indicators of the nutritional status of reindeer. In the mainland animals, plasma creatinine concentration was high in winter and early spring and decreased by two-thirds toward the summer. The overall range in mean plasma creatinine concentration (+/-SE) was from 90+/-1.26 to 280+/-2.88 micromol/L. Mean plasma urea concentration (+/-SE) varied from 2.46+/-0.10 in winter up to 17.44+/-0.29 mmol/L in summer and autumn. Month of sampling explained 65% and 90% of the variation in plasma urea and creatinine concentrations, respectively, indicating that seasonality in the diet had the greatest influence on these parameters. Reindeer given lichens as the only feed showed an increase in plasma creatinine and a decrease in plasma urea concentration. Food restriction caused a temporary elevation in urea level but had no significant effect on plasma creatinine concentration. The slight effect of energy intake on urea and creatinine levels was supported by the fact that severe undernutrition in the Svalbard reindeer population had only a small effect on plasma urea and creatinine levels. Protein-rich pellet feed increased plasma urea from around 3 mmol/L to above 10 mmol/L and reduced creatinine concentrations to less than 100 micromol/L, suggesting that the protein content of forage is an important determinant of these blood parameters. Mean U:C ratio (+/-SE) in plasma varied from 8.9+/-0.28 to 120.8+/-1.88. Ratios above 20 appeared when protein intake was low and energy intake was restricted or when protein intake was high. Low ratios occurred when protein intake was low but energy intake adequate. Plasma urea and creatinine concentrations and the U:C ratio showed complex dynamics that were affected by both season and the protein and feed intake. We conclude that they appear to be difficult to interpret as single measures of nutritional status of reindeer.

Animals↗
PubMed1989

Inhibition of urea transport in inner medullary collecting duct by phloretin and urea analogues.

Arginine vasopressin (AVP) increases the urea permeability of the rat terminal inner medullary collecting duct (IMCD) to levels much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of an AVP-stimulated facilitated transport pathway. We tested whether inhibitors of facilitated urea transport in erythrocytes and toad bladder also inhibit urea transport in the isolated perfused IMCD. Apparent urea permeability (Purea) was determined by measuring the flux due to an imposed 5 mM concentration gradient. Phloretin (0.25 mM in lumen or bath) reversibly inhibited Purea. Phloretin, however, did not alter the osmotic water permeability. Urea analogues (200 mM) in the bath inhibited Purea (thiourea, 74% inhibition; methylurea 65%; acetamide 35%). Urea analogues in the lumen decreased Purea with the same order of potency. The inhibitory K1/2 for thiourea in the lumen was 27 +/- 2 mM and did not change with 10(-10) M AVP (28 +/- 3), despite a fourfold increase in Purea. We conclude the following. 1) Inhibitor actions on urea transport in the IMCD are similar to those in red blood cells and toad bladder, suggesting that the urea transporter could be a membrane protein similar to that in the other tissues. 2) Inhibition of Purea by phloretin without an effect on vasopressin-stimulated water permeability supports the view that the urea pathway is not the vasopressin-stimulated water channel. 3) The ability of AVP to increase Purea without an effect on the inhibitory K1/2 for thiourea indicates that AVP probably does not act by altering the binding affinity of individual transporters for urea.

Amiloride↗