Urea Appearance Research Articles

Assessment of magnesium sulphate usage in pre-eclamptic and eclamptic women in Omdurman Maternity Hospital, 2017: A cross-sectional study

Background: Eclampsia, the end phenomena of the preeclampsia spectrum, appears as new onset grand mal seizures in women with preeclampsia. Recently, the World Health Organization has recommended magnesium sulphate (MgSo4) as the main drug of choice to treat/prevent eclampsia. However, in Sudan no real assessment data about MgSo4 efficacy, benefits and risks in preeclamptic and eclamptic women has been reported. Methods: A cross-sectional hospital-based study was conducted between January and April 2017 at Omdurman Maternity Hospital using a checklist. Data was collected from the medical records of 130 preeclamptic/eclamptic pregnant women, including: age, blood pressure, protein urea appearance, admission diagnosis, reason for using MgSo4, policy of MgSo4 administration, outcomes after using MgSo4, side effects of using MgSo4, and MgSo4 toxicity recording. After data collection, IBM SPSS (version 21) was used to analyze the data. Results: Out of 130 recruited women, 78% were diagnosed with preeclampsia and 22% were diagnosed with eclampsia. Magnesium sulphate was indicated as a prophylactic in 88 patients and as treatment in 42 patients. Interestingly, only 9 patients had uncontrolled- recurrent seizures after using magnesium sulphate and only one patient developed drug related toxicity. Conclusion: After MgSO4 administration, the majority of patients (121; 93.1%) had controlled seizures and only one patient developed MgSO4 toxicity (respiratory paralysis). Therefore, MgSo4represents an effective and safe drug of choice used to treat/prevent eclampsia in Sudan.

Controlled Release of Agrochemicals Intercalated into Montmorillonite Interlayer Space

Periodic application of agrochemicals has led to high cost of production and serious environmental pollution. In this study, the ability of montmorillonite (MMT) clay to act as a controlled release carrier for model agrochemical molecules has been investigated. Urea was loaded into MMT by a simple immersion technique while loading of metalaxyl was achieved by a rotary evaporation method. The successful incorporation of the agrochemicals into the interlayer space of MMT was confirmed by several techniques, such as, significant expansion of the interlayer space, reduction of Barrett-Joyner-Halenda (BJH) pore volumes and Brunauer-Emmett-Teller (BET) surface areas, and appearance of urea and metalaxyl characteristic bands on the Fourier-transform infrared spectra of the urea loaded montmorillonite (UMMT) and metalaxyl loaded montmorillonite (RMMT) complexes. Controlled release of the trapped molecules from the matrix was done in water and in the soil. The results reveal slow and sustained release behaviour for UMMT for a period of 10 days in soil. For a period of 30 days, MMT delayed the release of metalaxyl in soil by more than 6 times. It is evident that MMT could be used to improve the efficiency of urea and metalaxyl delivery in the soil.

Isotope-labelled urea to test colon drug delivery devices in vivo: principles, calculations and interpretations

This paper describes various methodological aspects that were encountered during the development of a system to monitor the in vivo behaviour of a newly developed colon delivery device that enables oral drug treatment of inflammatory bowel diseases. [13C]urea was chosen as the marker substance. Release of [13C]urea in the ileocolonic region is proven by the exhalation of 13CO2 in breath due to bacterial fermentation of [13C]urea. The 13CO2 exhalation kinetics allows the calculation of a lag time as marker for delay of release, a pulse time as marker for the speed of drug release and the fraction of the dose that is fermented. To determine the total bioavailability, also the fraction of the dose absorbed from the intestine must be quantified. Initially, this was done by calculating the time-dependent [13C]urea appearance in the body urea pool via measurement of 13C abundance and concentration of plasma urea. Thereafter, a new methodology was successfully developed to obtain the bioavailability data by measurement of the urinary excretion rate of [13C]urea. These techniques required two experimental days, one to test the coated device, another to test the uncoated device to obtain reference values for the situation that 100 % of [13C]urea is absorbed. This is hampered by large day-to-day variations in urea metabolism. Finally, a completely non-invasive, one-day test was worked out based on a dual isotope approach applying a simultaneous administration of [13C]urea in a coated device and [15N2]urea in an uncoated device. All aspects of isotope-related analytical methodologies and required calculation and correction systems are described.

Safety and Efficacy of Early Parenteral Lipid and High-Dose Amino Acid Administration to Very Low Birth Weight Infants

To assess the efficacy and safety of early parenteral lipid and high-dose amino acid (AA) administration from birth onwards in very low birth weight (VLBW, birth weight <1500 g) infants. VLBW infants (n = 144; birth weight 862 ± 218 g; gestational age 27.4 ± 2.2 weeks) were randomized to receive 2.4 g of AA kg(-1) · d(-1) (control group), or 2.4 g AA kg(-1) · d(-1) plus 2-3 g lipids kg(-1) · d(-1) (AA + lipid group), or 3.6 g AA kg(-1) · d(-1) plus 2-3 g lipids kg(-1) · d(-1) (high AA + lipid group) from birth onwards. The primary outcome was nitrogen balance. The secondary outcomes were biochemical variables, urea rate of appearance, growth rates, and clinical outcome. The nitrogen balance on day 2 was significantly greater in both intervention groups compared with the control group. Greater amounts of AA administration did not further improve nitrogen balance compared with standard AA dose plus lipids and was associated with high plasma urea concentrations and high rates of urea appearance. No differences in other biochemical variables, growth, or clinical outcomes were observed. In VLBW infants, the administration of parenteral AA combined with lipids from birth onwards improved conditions for anabolism and growth, as shown by improved nitrogen balance. Greater levels of AA administration did not further improve the nitrogen balance but led to increased AA oxidation. Early lipid initiation and high-dose AA were well tolerated.

Effec Of Low Protein Diet On Chronic Renal Failure Due To Autosomal Dominant Polycystic Kidney Disease

There are few reports about therapeutic effects of low protein diet on the progression of chronic renal failure due to autosomal dominant polycystic kidney disease (ADPKD), although the disease is common.The annual incidence rate for end-stage renal disease caused by ADPKD is around 6 per million.In this retrospective study in one center, ten chronic renal failure patients due to ADPKD with creatinine clearnce of 17.0±3.3 mL/min /1.73 m 2 and serum creatinine (Cr) level of 4.4±0.7 mg/dL were studied for 40 months after the introduction of severe low protein diet (SLPD) (0.48±0.03 g/kgBW/day) without supplementation of essential amino acids or keto-analogues. Dietary protein intake was estimated by urea appearance rate from 24hr urine sample according to Mitch-Maroni's formula. The results clearly showed that ▵1/Cr/month(×10 −3 ) was significantly suppressed from 5.8±0.9 to 2.0±0.6 following the introduction of SLPD ( p p

High-carbohydrate/low-protein–induced hyperinsulinemia does not improve protein balance in children after cardiac surgery

ObjectiveIn pediatric cardiac surgery, fluid-restricted low-protein (LoProt) diets account for cumulative protein deficits with increased morbidity. In this setting, we aimed to inhibit proteolysis by a high-carbohydrate (HiCarb)-intake–induced hyperinsulinemia and improve protein balance. MethodsThe effect of a HiCarb/LoProt (glucose 10 mg · kg−1 · min−1/protein 0.7 g · kg−1 · d−1) versus a normal-carbohydrate (NormCarb)/LoProt (glucose 7.5 mg · kg−1 · min−1/protein 0.3 g · kg−1 · d−1) enteral diet on whole-body protein breakdown and balance was compared in a prospective, randomized, single-blinded trial in 24 children after cardiac surgery. On the second postoperative day, plasma insulin and amino acid concentrations, protein breakdown (endogenous rate of appearance of valine), protein synthesis (non-oxidative disposal of valine), protein balance, and the rate of appearance of urea were measured by using an isotopic infusion of [1-13C]valine and [15N2]urea. ResultsThe HiCarb/LoProt diet led to a serum insulin concentration that was three times higher than the NormCarb/LoProt diet (596 pmol/L, 80–1833, and 198 pmol/L, 76–1292, respectively, P = 0.02), without differences in plasma glucose concentrations. There were no differences in plasma amino acid concentrations, non-oxidative disposal of valine, and endogenous rate of appearance of valine between the groups, with a negative valine balance in the two groups (−0.65 μmol · kg−1 · min−1, −1.91 to 0.01, and −0.58 μmol · kg−1 · min−1, −2.32 to −0.07, respectively, P = 0.71). The serum cortisol concentration in the HiCarb/LoProt group was lower compared with the NormCarb/LoProt group (204 nmol/L, 50–544, and 532 nmol/L, 108–930, respectively, P = 0.02). ConclusionIn children with fluid restriction after cardiac surgery, a HiCarb/LoProt diet compared with a NormCarb/LoProt diet stimulates insulin secretion but does not inhibit proteolysis further and therefore cannot be advocated for this purpose.

Corticosteroids Increase Protein Breakdown and Loss in Newly Diagnosed Pediatric Crohn Disease

Children with Crohn disease have altered growth and body composition. Previous studies have demonstrated decreased protein breakdown after either corticosteroid or anti-TNF-α therapy. The aim of this study was to evaluate whole body protein metabolism during corticosteroid therapy in children with newly diagnosed Crohn disease. Children with suspected Crohn disease and children with abdominal symptoms not consistent with Crohn disease underwent outpatient metabolic assessment. Patients diagnosed with Crohn disease and prescribed corticosteroid therapy returned in 2 wk for repeat metabolic assessment. Using the stable isotopes [d5] phenylalanine, [1-(13)C] leucine, and [(15)N(2)] urea, protein kinetics were determined in the fasting state. Thirty-one children (18 controls and 13 newly diagnosed with Crohn disease) completed the study. There were no significant differences in protein breakdown or loss between patients with Crohn disease at diagnosis and controls. After corticosteroid therapy in patients with Crohn disease, the rates of appearance of phenylalanine (32%) and leucine (26%) increased significantly, reflecting increased protein breakdown, and the rate of appearance of urea also increased significantly (273%), reflecting increased protein loss. Whole body protein breakdown and loss increased significantly after 2 wk of corticosteroid therapy in children with newly diagnosed Crohn disease, which may have profound effects on body composition.

No effect of CYP450 and P‐glycoprotein on hydroxyurea in vitro metabolism

Our objectives were (1) to study the HU metabolism via human cytochromes and (2) to test if HU is a substrate of P-gp. HU metabolism was investigated by determining the appearance of urea and HU decreasing upon incubation with human liver microsomes. Quantification was determined using HPLC coupled with UV-detection at 449 nm. Our method was linear between 5 and 1000 microm, precise (coefficients of variation ranging from 1.7 to 9.9%), accurate (97.7-103.9%). The limit of quantification was 7 microm. The ATPase activity of human P-gp membranes was determined by measuring inorganic phosphate liberation. HU and urea measurements in microsomes were not different between 0 and 60 min whatever HU concentration used from 30 to 300 microm. The presence of NADPH in the medium has no effect on HU and urea measurements. In the absence of verapamil, the ATPase activity was unaffected by HU at concentrations of 10, 30, 100 and 300 microm. HU is unlikely to cause clinically relevant drug interactions with the substrates of these enzymes/transporters. However, it will be necessary to validate these in vitro data in patients with sickle cell anemia to evaluate the impact of genetic polymorphisms of these enzymes in a black population.

Indicators of lean body mass catabolism: emphasis on the creatinine excretion rate

The major stress response to critical illness leads to a catabolic state and loss of lean body mass. To test whether an increased rate of creatinine excretion might provide unique and timely information to monitor cell catabolism; to relate this information to balances of cell constituents (nitrogen, potassium, phosphate and magnesium); to evaluate the effectiveness of nutritional therapy to reverse this catabolic process. Prospective observational study. Children with severe traumatic brain injury admitted to the paediatric critical care units of The Hospital for Sick Children, Toronto, Canada and Hospital das Clínicas, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Brazil were studied. Complete 24 h urine collections were obtained for measurement of creatinine excretion rate and daily balances of nitrogen, potassium, phosphate and magnesium. Seventeen patients were studied for 3-10 days. On Day 1, all had negative balances for protein and phosphate. Balances for these intracellular constituents became positive when protein intake was >/=1 g/kg/day and energy intake was >/=50% of estimated energy expenditure (P < 0.0001). Creatinine excretion rate was positively correlated with the urea appearance rate (r = 0.60; P < 0.0001), and negatively with protein balance (r = -0.45; P < 0.0001). Sepsis developed in four patients; before its clinical detection, there were negative balances for all intracellular markers and an abrupt rise in the excretion of creatinine. Negative balances of intracellular components and an increase in rate of creatinine excretion heralded the onset of catabolism.

Pre-operative nutritional status does not alter the metabolic response to major gastrointestinal surgery in patients with oesophageal cancer

Malnutrition is associated with an increased incidence of perioperative morbidity and mortality. To evaluate the effect of malnutrition on the metabolic and inflammatory response to surgery in patients with oesophageal cancer, we studied the effects of oesophagectomy in six patients with major (13.9 (se 1.3) %) weight loss and five patients with minor (0.7 (se 0.6) %) weight loss in the 6 months before to surgery. Rates of appearance (Ra) of glucose, glycerol, leucine and urea were determined by stable isotopically labelled tracer infusion before and after surgery. C-reactive protein was measured as an inflammation marker. BMI was lower in the patients with major weight loss than those with minor weight loss (20.3 (se 0.7) and 24.9 (se 1.5) kg/m2, P = 0.02). With the exception of greater glucose Ra in the major weight loss than minor weight loss subjects (11.1 (se 0.3) v. 9.5 (se 0.3) mumol/kg per min, P = 0.01), there were no differences in substrate kinetics before surgery between groups. Surgery increased glucose Ra, leucine Ra and urea Ra by 41, 24 and 58 %, respectively, in the total group. Changes in substrate kinetics in response to surgery were not different between patients with major and minor weight loss. Surgery increased C-reactive protein concentrations to a comparable extent in both groups. In conclusion, major upper gastrointestinal tract surgery in patients with oesophageal cancer elicits a catabolic response, characterized by increased inflammation, glucose production and protein breakdown. However, this catabolic response does not seem to be influenced by pre-operative nutritional status.

Purine and pyrimidine metabolism by estuarine bacteria

AME Aquatic Microbial Ecology Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsSpecials AME 42:215-226 (2006) - doi:10.3354/ame042215 Purine and pyrimidine metabolism by estuarine bacteria Gry Mine Berg1,*, Niels O. G. Jørgensen2 1Department of Geophysics, Stanford University, Stanford, California 94305, USA 2Department of Ecology, Royal Veterinary and Agricultural University, Thorvaldsensvej 40, 1871 Frederiksberg, Denmark *Email: mineberg@stanford.edu ABSTRACT: Nucleotide bases are ubiquitous in living organisms, but the fate of these compounds in natural environments is poorly understood. Here we studied the metabolism of selected purines and pyrimidines in estuarine bacterial assemblages from the Øresund, Denmark. Depletion of nucleotide bases in the incubations was followed by the appearance of urea. The purine guanine and the catabolic intermediates hypoxanthine and xanthine were depleted 2 times faster from seawater incubations than the purine adenine, and 8 to 35 times faster than the pyrimidines thymine, cytosine, and uracil over the course of 141 h. After 48 h, 45 to 60% of guanine-N, hypoxanthine-N and xanthine-N was converted to urea-N while the conversion of adenine and pyrimidines to urea was slower, corresponding to 34% and 19 to 23%, respectively. After 96 h, urea concentrations declined in most of the incubations, indicating hydrolysis of urea by the bacterial populations. Bacterial metabolism of adenine in Øresund water was estimated to contribute up to 10% of the urea pool, but due to the efficient conversion of adenine, the ecosystem importance of adenine degradation to urea production was most likely greater. Growth of bacterial microcolonies on 0.2 µm pore-sized polycarbonate filters floating on natural seawater enriched with individual nucleotide bases varied significantly with substrate enrichment. Despite growth of only a small fraction of bacteria present in the natural assemblage on the filters, variation in bacterial microcolony biomass explained most of the variation in substrate utilization and urea production among the treatments. Our results suggest that bacterial catabolism of particularly purines and their intermediates, and to lesser extent pyrimidines, is a major process by which the N moiety of natural, heterocyclic bases are converted into urea which is easily assimilated. KEY WORDS:Purines · Pyrimidines · Urea production · Estuarine bacteria · Microcolony approach Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in AME Vol. 42, No. 3. Online publication date: March 29, 2006 Print ISSN: 0948-3055; Online ISSN: 1616-1564 Copyright © 2006 Inter-Research.

Amino Acids, Glutamine, and Protein Metabolism in Very Low Birth Weight Infants

Glutamine has been proposed to be conditionally essential for premature infants, and the currently used parenteral nutrient mixtures do not contain glutamine. De novo glutamine synthesis (DGln) is linked to inflow of carbon into and out of the tricarboxylic acid (TCA) cycle. We hypothesized that a higher supply of parenteral amino acids by increasing the influx of amino acid carbon into the TCA cycle will enhance the rate of DGln. Very low birth weight infants were randomized to receive parenteral amino acids either 1.5 g/kg/d for 20 h followed by 3.0 g/kg/d for 5 h (AA1.5) or 3.0 g/kg/d for 20 h followed by 1.5 g/kg/d for 5 h (AA3.0). A third group of babies received amino acids 1.5 g/kg/d for 20 h followed by 3.0 g/kg/d for 20 h (AA-Ext). Glutamine and protein/nitrogen kinetics were examined using [5-(15)N]glutamine, [2H5]phenylalanine, [1-(13)C,15N]leucine, and [15N2]urea tracers. An acute increase in parenteral amino acid infusion for 5 h (AA1.5) resulted in decrease in rate of appearance (Ra) of phenylalanine and urea, but had no effect on glutamine Ra. Infusion of amino acids at 3.0 g/kg/d for 20 h resulted in increase in DGln, leucine transamination, and urea synthesis, but had no effect on Ra phenylalanine (AA-Ext). These data show an acute increase in parenteral amino acid-suppressed proteolysis, however, such an effect was not seen when amino acids were infused for 20 h and resulted in an increase in glutamine synthesis.

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

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. 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. 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). 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.

Oral carbonaceous absorbent modifies renal function of renal ablation model without affecting plasma renin-angiotensin system or protein intake.

Although it has been repeatedly shown that the oral carbonaceous absorbent AST-120 ameliorates the progression of chronic renal failure, the mechanisms remain unknown. Male Sprague-Dawley rats (6 weeks old), weighing 180-210 g, were 4/5 nephrectomized, and were divided into two groups: one given AST-120 (0.4 g/100 g body weight BW; n= 9) and the other not given AST-120 ( n = 9). Body weight, blood pressure, and serum and urine chemistry, as well as the plasma components of the renin-angiotensin system, were measured for 22 weeks. Proteinuria was significantly greater in the controls than in the AST-120 group (102 +/- 22 vs 51 +/- 7 mg/day at 22 weeks). Urea clearance was lower in the former (3.7 +/- 0.4 vs 3.9 +/- 0.4 ml/min). There were no differences in plasma renin activity (1.4 +/- 0.3 vs 1.9 +/- 0.4 mg/ml per h), or in angiotensin I (756 +/- 119 vs 1042 +/- 168 pg/ml) and II (35.1 +/- 7.4 vs 46.6 +/- 7.6 pg/ml) or angiotensin-converting enzyme activity (39.0 +/- 2.4 vs 37.9 +/- 2.2 IU/l) between the two groups. Protein intake, estimated from urinary urea appearance, was not different. Serum phosphate concentration (6.6 +/- 0.3 vs 5.9 +/- 0.3 mg/dl) was higher in the control than in AST-120, while the urinary phosphate excretion rate (31.5 +/- 0.8 vs 28.1 +/- 1.8 mg/day) tended to be lower in the latter. Conclusions. AST-120 retarded the progression of renal failure in the 4/5 renal ablation model without affecting the plasma renin-angiotensin system or protein intake, both of which were the most important risk factors for the progression of renal failure. We hypothesize that the renal protective effects of the oral absorbent AST-120 may be, at least in part, due to its lowering phosphate absorption from the diet as a phosphorus binder.

The precision of estimating protein intake of patients with chronic renal failure

Biochemical methods for estimating protein intake are based on the concept that nitrogen-containing products of protein in diet plus the products arising from endogenous protein are excreted as either urea or non-urea nitrogen (NUN). This formulation is based on the fact that the urea is the principal end product of amino acid degradation and, hence, the urea appearance rate (or net urea production) is parallel to protein intake. The urea nitrogen appearance (UNA) rate is measured as the amount of urea excreted in urine plus the net amount accumulated in body water. A more difficult problem is how to estimate NUN, the sum of fecal nitrogen, and all forms of non-urea urinary nitrogen. Maroni, Steinman, and Mitch (Kidney Int 27:58-65, 1985) proposed estimating nitrogen intake (IN MARONI) from UNA plus NUN excretion rate of 0.031 g nitrogen/kg body weight/day, as they found NUN correlated with body weight but not with dietary nitrogen. Kopple, Gao, and Qing (Kidney Int 27:486-494, 1997) proposed a different equation for estimating nitrogen intake (IN KOPPLE) = 1.20 UNA + 1.74, concluding that dietary nitrogen directly correlates with fecal nitrogen and that NUN is constant for all patients. Their report prompted us to review all nitrogen balance measurements we had conducted in order to address the following questions. Does dietary protein increase fecal nitrogen excretion? Does NUN vary with weight or is it constant? How do the two methods (IN MARONI and IN KOPPLE) compare in estimating dietary protein from UNA? We examined nitrogen balance and its components measured in 33 patients with chronic renal failure (CRF) who were eating diets varying from 4.1 to 10.1 g nitrogen/day. We evaluated relationships between dietary nitrogen [intake nitrogen (IN)], NUN, fecal nitrogen, body weight, and the predictability of the two methods. Neither fecal nitrogen nor NUN were significantly correlated with IN (r = 0.04 and r = -0.07, respectively). NUN significantly correlated with body weight (P = 0.008). Measured IN averaged 5.75 +/- 0.41 g nitrogen/day; the estimated IN MARONI value was 5.61 +/- 0.27 g nitrogen/day; the estimated IN KOPPLE was 6.04 +/- 0.44 g nitrogen/day. The prediction errors associated with the IN KOPPLE equation were slightly but not statistically higher than that associated with IN MARONI. Fecal nitrogen is not correlated with IN. NUN is not constant but varies with weight, and the traditional method of estimating IN in stable chronic renal insufficiency (CRI) patients from UNA and weight as proposed by Maroni, Steinman, and Mitch is valid.

Mechanisms of urea tolerance in urea-adapted populations of Drosophila melanogaster.

When behavioral avoidance cannot prevent an animal from being exposed to novel environmental toxins, physiological mechanisms must cope with the toxin and its effects. We are investigating the basis of urea tolerance in populations of Drosophila melanogaster that have been selected to survive and develop in food containing 300 mmol l(-1) urea. Previous research has demonstrated that the urea-selected larvae have lower levels of urea in their body than control larvae reared under the same conditions. The current series of experiments focuses on three possible ways of reducing urea levels in the body: urea metabolism, increased urea excretion and decreased urea uptake from the environment. We tested for urea metabolism directly, by assaying for activity of two urea-metabolizing enzymes, and indirectly, by looking for reduced urea content of their medium. To measure urea excretion rates in whole animals, we reared control and urea-selected larvae on urea-containing food (urea food), switched them to normal food and monitored the loss of urea from their hemolymph. We measured urea uptake by rearing control and selected larvae on normal food, switching them to urea food and monitoring the rate of urea appearance in the hemolymph. We found no evidence for urea metabolism by either direct or indirect methods. Control larvae excreted urea at a higher rate than selected, probably because they contained more urea than the selected larvae and thus had a greater gradient for urea loss. The rate of urea uptake in selected larvae was 2 mmol l(-1) h(-1) slower than the rate in control larvae, a difference that could account for the measured differences in body urea levels. Thus the selected larvae appear to have adapted to urea exposure primarily by decreasing the ability of urea to enter their body in the first place. The mechanism responsible for this reduction in uptake is uncertain.

Urea and nitrogen excretion in pediatric peritoneal dialysis patients

Adequate nutrition is critical to the care of children with end-stage renal disease, and failure to reach the target dietary intake is associated with growth failure. Prospective studies of urea and nitrogen output in adults have led to the derivation of quantitative relationships, which allow assessment of dietary protein intake when only urea appearance is known. Such a clinically useful relationship has not been defined in children receiving chronic peritoneal dialysis (PD). We studied 18 pediatric PD patients (ages 0.8 to 14.3 years) on 132 occasions and determined norms of urea nitrogen appearance (UNA), total nitrogen appearance (TNA), and nonurea nitrogen appearance (NUNA). We stratified data on UNA, TNA, NUNA, nonprotein nitrogen appearance, and the protein equivalent of nitrogen appearance by age groups (0 to 5, 6 to 10, and 11 to 15 years of age) and demonstrated significant differences. In addition, dietary protein and energy intake were measured in the outpatient setting with food scales and dietitian interviews, and the results were stratified by age, presence of residual renal function, and recombinant human growth hormone (rhGH) therapy. UNA (3.05 +/- 1.38 g/day, 103 +/- 42 mg/kg/day) and TNA (4.67 +/- 1.86 g/day, 159 +/- 52 mg/kg/day) varied significantly between different age groups. NUNA in pediatric subjects (56 +/- 24 mg/kg/day) was significantly greater than previously published adult norms. A linear relationship was defined between UNA and TNA that was specific to pediatric PD patients [TNA (g/day) = 1.26(UNA) + 0.83]. When the relationship was scaled to body mass, the y intercept was significantly different in the youngest subjects [TNA = 1.03 (UNA) + 0.02 (weight in kg) + 0.56 (for subjects age 0 to 5) or 0.98 (for subjects age 11 to 15 or 6 to 10), r2 = 0.91]. Dietary protein intake was significantly greater in subjects receiving rhGH therapy, although nitrogen excretion was unchanged. Markers of protein metabolism in pediatric PD patients are age dependent and differ from adult values. An age-specific relationship between TNA and UNA is defined for pediatric subjects; it does not vary with rhGH or the presence of residual renal function.

Plasma Urea Appearance Rate Is Lower When Children with Kwashiorkor and Infection Are Fed Egg White-Tryptophan Rather than Milk Protein

In kwashiorkor, there is less endogenous proteolysis in response to acute infection than in a well-nourished state. Thus the amino acid composition of dietary protein may be more important in facilitating the acute phase response in kwashiorkor. This study tested the hypothesis that during the treatment of kwashiorkor with infection, there is a lower rate of urea appearance when the dietary intake of amino acids more closely resembles the amino acid composition of acute phase proteins. Thirty children in Malawi with kwashiorkor and acute infection were fed isoenergetic, isonitrogenous meals containing either egg white-tryptophan or milk as a protein source. After 24 h, the rates of urea appearance and whole-body protein breakdown and synthesis were measured with the use of 1-13C-leucine and 15N2-urea tracers. Plasma concentrations of seven acute phase proteins, interleukin 6 and tumor necrosis factor-alpha were measured on admission, and at 24 and 48 h. The 16 children who received egg white-tryptophan had lower rates of urea appearance than those who received milk [57+/-30 vs. 87+/-36 micromol/(kg x h), mean +/- SD, P<0.02]. No significant differences were found in the rates of whole-body protein turnover or in the concentration of any of the acute phase proteins or cytokines. The concentration of interleukin 6 was consistent with an appropriate proinflammatory response and correlated directly with the concentrations of C-reactive protein (r = 0.67, P<0.01) and alpha1-antitrypsin (r = 0.40, P<0.05). The findings suggest that egg white-tryptophan is associated with less amino acid oxidation in kwashiorkor and acute infection than is milk.

Calculation of the Protein Equivalent of Total Nitrogen Appearance from Urea Appearance. Which Formulas Should be Used?

Calculation of the Protein Equivalent of Total Nitrogen Appearance from Urea Appearance. Which Formulas Should be Used?

Whole-body protein kinetics in marasmus and kwashiorkor during acute infection

Marasmus and kwashiorkor are clinically distinct manifestations of severe malnutrition. This study tested the hypothesis that rates of whole-body protein synthesis and breakdown are higher in marasmus than in kwashiorkor during acute infection. We measured whole-body protein kinetics using stable isotope tracers in eight children with marasmus and acute infection (pneumonia or malaria) to determine the rate of appearance of urea and leucine in plasma. Serum concentrations of total protein, albumin, and C-reactive protein were also measured. These findings were compared with those reported previously for 13 children with kwashiorkor (including marasmic kwashiorkor) and acute infection who were studied with the same methods. HIV infection was present in 10 of 21 children. Rates of protein breakdown and synthesis were higher in marasmus than in kwashiorkor (227 +/- 59 compared with 103 +/- 30 micromol leucine x kg(-1) x h(-1) and 216 +/- 60 compared with 97 +/- 30 micromol leucine x kg(-1) x h(-1), P < 0.001). The concentration of globulin (total protein minus albumin) was higher in marasmus than kwashiorkor (40 +/- 17 compared with 25 +/- 7 g/L, P < or = 0.01), but C-reactive protein was not different (73 +/- 79 compared with 83 +/- 89 mg/L). HIV infection and body composition did not explain the differences between marasmus and kwashiorkor. The accelerated rate of protein turnover in children with marasmus and acute infection requires further investigation.