Urinary Creatine Excretion Research Articles

INFLUENCE OF D-PINTOL ON WHOLE BODY CREATINE RETENTION

Creatine hyperaccumulation in muscle has been reported to be insulin dependent. The naturally occurring glycan D-pinitol has been reported to possess insulin-like effects. This study examined whether D-pinitol (InzitolTM) influences whole body creatine retention. 20 males with no history of creatine supplementation participated in this study. Subjects donated 24-h urine samples for 4-d. After an initial control day, subjects were matched and assigned to ingest in a single blind manner either a placebo (P = 4 × 5 g of dextrose), creatine monohydrate (CM = 4 × 5 g), creatine with low dose pinitol (LP = 4 × 5 g creatine + 2 × 0.5 g pinitol), for creatine with high dose pinitol (HP = 4 × 5 g creatine + 4 × 0.5 g pinitol) for 3-d. Additionally, another group ingested 2 × 0.5 g pinitol for 5-d followed by ingesting 4 × 5 g creatine + 2 × 0.5 g pinitol for 3-d (Pre P). Creatine retention was estimated by subtracting total urinary creatine excretion from total creatine intake over the 3-d period. Data were analyzed by ANOVA. Results revealed that cumulative creatine retention was significantly greater in the LP and Pre P groups (P = 0 ± 0; CM = 36.6 ± 9; LP = 49.7 ± 3; HP = 36.7 ± 13; Pre P = 46.7 ± 6 g, p = 0.001). This extrapolated to a significantly greater percentage of creatine retention in the LP and Pre P groups (P = 0 ± 0; CM = 61 ± 15; LP = 83 ± 5; HP = 61 ± 22; Pre P = 78 ± 9%, p = 0.001). These preliminary findings suggests that ingesting D- pinitol during creatine loading or prior to and during creatine loading may augment whole body creatine retention. Supported by Humanetics, Inc. (Minneapolis, MN)

The Effect of 7 Days of Creatine Supplementation on 24-Hour Urinary Creatine Excretion

Since the discovery that oral ingestion of creatine leads to an increase in intramuscular creatine, its supplementation has become widespread. However, the dosage necessary to maximize retention and create significant increases in intramuscular creatine is poorly understood. In this study, 24-hour urinary creatine and creatinine levels of 20 university men's football players and 20 university men's hockey players involved in a resistance-exercise program and supplementing with creatine were collected and analyzed. In a double-blind, randomized design, 10 football players and 10 hockey players were randomly assigned to either the supplement or placebo group. Subjects provided a 24-hour urine sample twice during the study: once prior to supplementation (baseline) and the second 7 days after daily supplementation and resistance exercise. Creatine dosage was 0.1 g·kg−1 lean body mass. The quantity of creatine ingested was compared with the amount excreted in the urine of those subjects supplementing with creatine and with placebo. Creatinine levels were compared between the first and second urine collection and between groups. Creatine and creatinine concentrations were determined using high-performance liquid chromatography. In 24-hours, 46% of the ingested creatine was excreted. There was no change in creatine levels for placebo subjects. Creatinine levels remained the same within groups at the first and second collection times (p < 0.05). Our findings indicate that when supplementing with dosages of 0.1 g·kg−1 lean body mass or between 6 and 8 g at a time, approximately half of the ingested creatine gets excreted. Because there was no change in urinary creatinine, it can be assumed that enhanced degradation of creatine did not occur.

The Effect of 7 Days of Creatine Supplementation on 24-Hour Urinary Creatine Excretion

Since the discovery that oral ingestion of creatine leads to an increase in intramuscular creatine, its supplementation has become widespread. However, the dosage necessary to maximize retention and create significant increases in intramuscular creatine is poorly understood. In this study, 24-hour urinary creatine and creatinine levels of 20 university men's football players and 20 university men's hockey players involved in a resistance-exercise program and supplementing with creatine were collected and analyzed. In a double-blind, randomized design, 10 football players and 10 hockey players were randomly assigned to either the supplement or placebo group. Subjects provided a 24-hour urine sample twice during the study: once prior to supplementation (baseline) and the second 7 days after daily supplementation and resistance exercise. Creatine dosage was 0.1 g x kg(-1) lean body mass. The quantity of creatine ingested was compared with the amount excreted in the urine of those subjects supplementing with creatine and with placebo. Creatinine levels were compared between the first and second urine collection and between groups. Creatine and creatinine concentrations were determined using high-performance liquid chromatography. In 24-hours, 46% of the ingested creatine was excreted. There was no change in creatine levels for placebo subjects. Creatinine levels remained the same within groups at the first and second collection times (p < 0.05). Our findings indicate that when supplementing with dosages of 0.1 g x kg(-1) lean body mass or between 6 and 8 g at a time, approximately half of the ingested creatine gets excreted. Because there was no change in urinary creatinine, it can be assumed that enhanced degradation of creatine did not occur.

Urinary Creatine Excretion - Early Indicator of Lean Body Mass Loss Following Thermal Injury

Urinary Creatine Excretion - Early Indicator of Lean Body Mass Loss Following Thermal Injury

Comparison of urinary creatine with other biomarkers for the detection of 2-methoxyethanol-induced testicular damage

Abstract This study has compared different biomarkers of testicular damage, in particular evaluating urinary creatine as a non-invasive marker. Male rats were exposed to various doses of 2-methoxyethanol, a known testicular toxicant. Pathological damage, testis weight, urinary creatine and creatinine, serum lactate dehydrogenase, isozyme C4 (LDH-C4), and serum testosterone were determined. 2-Methoxyethanol caused dose-dependent pathological damage to the testes which was detectable at the lowest dose (100 mg kg(-1)). Urinary creatine excretion was significantly raised at all doses but testis weight was only significantly decreased at the highest two doses (500, 750 mg kg(-1)). Serum testosterone was only significantly decreased at 500 mg kg(-1) and LDH-C4 was not significantly increased at any dose. Therefore urinary creatine was the most sensitive marker of 2-methoxethanol-induced testicular damage and dysfunction.

Study of muscular effects of short-term pyridostigmine treatment in resting and exercising rats.

1. Pyridostigmine (PYR) pretreatment is used by the military to obtain 20-30% whole blood acetylcholinesterase (AChE) inhibition in order to enhance the effectiveness of the standard therapeutic regimen for poisoning by an organophosphate anticholinesterase agent. The present study was undertaken to investigate in a rat model the potential muscle damage produced by this pretreatment when given alone or combined with physical exercise. 2. Grip strength and biochemical measurements, i.e. serum creatine phosphokinase (CPK) activity and creatine urinary excretion rate, together with histological studies, were performed in resting animals during a period of 14 days of PYR administration in a dose producing 20-30% whole blood acetylcholinesterase inhibition. No evidence was found of a deleterious effect of this treatment on the skeletal muscle. 3. In contrast, following physical exercise, the same treatment significantly exacerbated the biochemical changes reflecting a loss of integrity in skeletal muscles, namely, increased CPK and urinary creatine excretion rate. The significance of this observation remains to be clarified.

Biochemical Changes Associated with Muscle Fibre Necrosis after Experimental Organophosphate Poisoning

1. This study was initiated to ascertain the possibility of biochemically monitoring the rhabdomyonecrosis that occurs after organophosphate poisoning. The evolution of different parameters has been assessed in the rat 6, 16, 24 and 48 h following 0.67 x LD50 of soman. 2. Acetylcholinesterase (AChE) was inhibited to 60% of the control value in the diaphragm at 6 and 16 h and serum ChE levels inhibited to an average of 30% of the control value. At 24 h, total blood, brain and diaphragm AChE were inhibited by 40, 69 and 38%, respectively. 3. Rhabdomyonecrosis lesions occurred in the diaphragm after 24 h and were accompanied by a concurrent increase in urinary creatine excretion rate (300% of the control) and serum total creatine phosphokinase activity (280% of the control). Calcium-activated neutral protease and phosphorylase a activities were elevated in the muscle at the same time. 4. These biochemical markers will prove useful for investigating the possible relationships between the different neuromuscular syndromes occurring in the course of an OP poisoning and potential therapeutic or protective pharmacological measures.

An investigation of Urinary Creatine Excretion as a Potential Marker for Testicular Damage

1. This study assessed urinary creatine excretion as a marker for testicular atrophy. 2. Male rats received a single i.p. dose of 2-methoxyethanol at 0, 250 or 750 mg kg-1 and were sacrificed 2 d later. Urinary creatine and creatinine excretion were measured on days 0, 1 and 2. 3. Decreased testicular weights and histopathological assessment revealed dose-related testicular damage. 4. On day 1, at both doses of 2-methoxyethanol, urinary creatine levels increased and creatinine levels decreased, resulting in a dose-related increase in the creatine/creatinine ratio. On day 2, the creatine/creatinine ratio was elevated relative to controls, but was less marked than on day 1. 5. The study confirmed that creatine excretion is a potential marker for acute testicular damage.

Urinary creatine profiles after administration of cell-specific testicular toxicants to the rat.

Cell-specific testicular toxicants have been used to examine the distribution of creatine within the rat testis, and to examine the potential use of creatinuria as a non-invasive indicator of testicular damage. Groups of rats were administered single doses of various toxicants: a germ cell toxicant (methoxyacetic acid, MAA), one of two Sertoli cell toxicants (di-n-pentyl phthalate, DPP or 1,3-dinitrobenzene, 1,3-DNB), or a Leydig cell toxicant (ethane-1,2-dimethane sulphonate, EDS). Urinary creatine and creatinine levels were monitored in 24 h periods over the following 48 h, after which time the testes were removed, weighed and, after processing, sections were examined by light microscopy. All four treatments resulted in reductions in relative testis weight (RTW) and produced morphological changes similar to those which have been previously reported. In addition, MAA, DPP and 1,3-DNB all caused significant elevations in urinary creatine excretion and the urinary creatine:creatinine ratio (Cr/Crn) within 24 h. EDS had no such effect. We conclude that creatine is associated with the cells of the seminiferous epithelium, and that elevated urinary excretion of creatine may serve as a non-invasive marker for damage to these cells in vivo.

Biochemical markers of myositis in dermatomyositis.

Summary The relative value of 24-hour urinary creatine excretion and serum creatine kinase, as indicators of active myositis, was determined in a retrospective study of 26 patients with dermatomyositis. Initially, the 24-hour urinary creatine excretion was raised in 20 patients (77%) and the serum creatine kinase in 12 patients (46%). Simultaneous measurements on 45 occasions, during follow-up, showed that the 24-hour urinary creatine excretion was raised on 37 (82%) and the serum creatine kinase on 13 (29%) occasions. On presentation, elevation of the 24-hour urinary creatine excretion was the sole indicator of active myositis in 10 patients and the serum creatine kinase in two patients (P <005). During follow-up the 24-hour urinary creatine excretion was the only indicator of active myositis on 27 occasions and the serum creatine kinase on three occasions (P 0.001). Our findings indicate that 24-hour urinary creatine excretion is a more sensitive indicator of active myositis than serum creatine kinasc in patients with dermatomyositis. Ideally, both should be measured to provide optimum patient management.

Steroid myopathy: Incidence and detection in a population with asthma

Sixty steroid-treated patients with asthma were evaluated for the presence of muscle weakness by use of both manual muscle testing and the Cybex II isokinetic dynamometer. The patients were compared to age and sex-matched sedentary control subjects. Forty-eight percent of the patients ( 12 25 ) taking ⩾40 mg per day of prednisone had hip flexor strength ⩾2 SD below the mean of age and sex-matched control subjects by Cybex testing (CT). Sixty-four percent of the patients ( 16 25 ) taking ⩾40 mg per day of prednisone were found on manual muscle testing to have hip flexor weakness. Only one patient taking <30 mg per day of prednisone was found to have muscle weakness. Biochemical parameters, including CPK, aldolase, SGOT, LDH, and LDH isoenzymes were measured to assess the degree of steroid-induced muscle damage. They neither correlated with the degree of hip flexor weakness as measured by CT, nor did they discriminate between patients receiving small doses and large doses of steroids. Changes in urinary excretion of creatine did not help to confirm the diagnosis of steroid myopathy. Although CT provides an objective means of assessing muscle strength in these patients, at this time no definitive chemical test is available for the diagnosis of steroid myopathy.

Urinary creatine: biochemical indicator for evaluation of sickle cell crises.

In a patient with known sickle cell beta 0-thalassemia we measured serum lactate dehydrogenase (LD) activity and 24-h urinary creatine excretion rate as markers to evaluate sickle cell crises. We believe that a distinction based on biochemical findings can be made between hemolytic and painful vaso-occlusive sickle cell crises with muscular involvement. To assess hemolytic crises by objective biochemical measures, we have used assay of LD activity, and to assess painful crises with muscular involvement objectively, the 24-h urinary creatine excretion rate. We conclude that hemolytic crises are characterized by high serum LD activities. Furthermore, we conclude that--at least in this patient--painful crises are accompanied by high 24-h urinary creatine excretion rates. Our findings suggest that muscle involvement may play an important role in painful vaso-occlusive sickle cell crises.

A simple estimate of glomerular filtration rate in adolescent boys

We reexamined the relationship between creatinine clearance (Ccr) and body habitus in 212 girls and 356 boys, including 181 boys and 69 girls between 13 and 21 years of age. The use of formula Ccr = k L/Pcr, where k = 0.55 for the calculation of GFR, resulted in a significant underestimation of GFR in adolescent boys but was suitable for girls. In 51 adolescent boys the equation Ccr = 0.7 L/Pcr resulted in an accurate estimate of GFR. Regression analysis in 133 boys aged 3 to 21 years showed that the constant k increased gradually and linearly with age (r = 0.35, P less than 0.01). GFR could be better estimated for boys of any age by the linear bivariate equation Ccr = 1.5 (age) + 0.5 (L/Pcr), where age is given in years (r = 0.82, P less than 0.001). This equation yielded slightly better results than did 0.7 L/Pcr in 91 additional clearance studies performed in adolescent boys with native kidneys or functioning renal transplants. The larger value for the constant k (0.7) and the age correction for GFR reflect the greater rate of urinary creatine excretion (and thus muscle mass) per unit of body mass in adolescent boys.

Urinary excretion of creatine and creatinine in gamma irradiated rats.

Dose response relationships of creatine, creatinie excretions and their ratio in 24 hr urine samples have been studied on each individual day upto 4 days after 1-7 Gy whole body gamma irradiation to rats. Creatine excretion reaches the peak on the 2nd day while creatinine excretion reaches the peak on the first day and a plateau is maintained upto the 4th day in each case. Good dose response correlationship is maintained for creatine or creatinine levels upto the 4th day and for creatine creatinine ratio upto the 3rd day. Seperate dose response curves are needed on each individual day for using these parameters for biological dosimetry purpose. Administration of the radioprotectors viz., combination of 5-hydroxytryptophan (HT) and 2-amino-ethylisothiuronium bromide hydrobromide (AET), HT alone and optimum radioprotecting dose of AET before 5 Gy whole body γ-irradiation have not been of help for reducing creatinineurea.

Choline requirement of the preruminant lamb during the first two or three weeks of life

Preruminant male crossbred lambs, aged 1-2 days at the start of the experiment, were bottle-fed on milk replacers containing casein as the sole source of protein for an experimental period of 15-21 days. Choline-deficient diets were used in experiment 1 to determine the effect on the performance of the lambs of thc dictary protein concentration (10, 15 and 25% protein energy), and in experiment 2 of different sources of fat (butter oil, maize oil or lard), unsupplemented, or with supplements of choline chloride or L-cystine. Supplements of choline chloride decreased liver fat content and decreased urinary creatine excretion, irrespective of dietary protein concentration or source of dietary fat. Ira general, urinary ammonia excretion increased as the sulfur amino acid content of the diets increased, but there were interactions with the source of fat, so that although sulfur intake remained constant ammonia excretion was higher with diets containing lard than with those containing maize oil or butter oil. The effect of the supplements of 1,-cystine on liver fat content and urinary creatine excretion was not significantly different from that of the unsupplemented choline-deficient diets. In experiments 3 and 4 a choline-deficient diet with 25% protein energy and butter oil as the source of fat was supplemented with graded amounts of choline chloride. Energy intake was ad libitum, or restricted to 80% of ad libitum. When the lambs were fed ad libitum there was a significant decrease in liver fat content even with the smallest supplement of choline chloride (c. 9 mg MJ-1 gross energy), but no significant effect when energy intake was restricted. Since liveweight gains and nitrogen balances were unaffected by the presence or absence of the choline supplements it was concluded that in milk replacers containing 25% protein energy from casein, with butter oil as the source of fat, supplementation with choline chloride to provide 9 mg MJ-1 gross energy (233 mg kg-1 dry matter) would be sufficient to prevent the increased deposition of fat in the liver during the 6rst three weeks of life.

Sex-related normal intervals for an index of urinary creatine excretion.

Journal Article Sex-related normal intervals for an index of urinary creatine excretion. Get access C S Goodwin, C S Goodwin Search for other works by this author on: Oxford Academic Google Scholar J R Masarei J R Masarei Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 29, Issue 9, 1 September 1983, Page 1697, https://doi.org/10.1093/clinchem/29.9.1697 Published: 01 September 1983

Sotalol in hyperthyroidism.

Ten hyperthyroid patients were studied before and after 2 weeks' beta-adrenoceptor blockade with sotalol. The following variables were measured: resting pulse rate, blood pressure, weight, thyroid hormone levels, plasma lipids, alkaline phosphatase, plasma glucose and insulin responses to oral glucose, bromsulphthalein retention and the 24-h urinary excretion of calcium, hydroxyproline, creatine and creatinine. Sotalol produced a significant fall in pulse and blood pressure. Weight loss continued during treatment. No metabolic changes of any consequence were found. It is concluded that sotalol should not be used as the sole treatment of a patient with hyperthyroidism.

Effect of cimetidine on renal function in man.

1 Renal function was studied in nine patients with chronic peptic ulcer before and at repeated intervals during treatment with cimetidine (1.6g daily). 2 Plasma creatinine concentration was significantly increased on the first day after starting cimetidine, and at 3 weeks, but not at 12 weeks. Blood urea concentration was unchanged. 3. Clearances of creatinine 51Cr EDTA and 125I-hippuran were significantly reduced within 6 h of starting cimetidine. Clearances of 51Cr EDTA and 125I-hippuran returned to baseline within 3 weeks, and creatinine clearance within 12 weeks. 4 Urinary creatine excretion was significantly increased at 3 weeks, but there was no significant change in urinary creatinine excretion, or in serum creatine phosphokinase concentration. 5. These observations suggest that cimetidine causes an early but short-lived fall in glomerular filtration rate (GFR) and effective renal plasma flow. The later rise in plasma creatinine was unaccompanied by any change in GFR, and may have been due to competition by cimetidine for renal tubular handling. 6 Caution should be exercised when administering cimetidine to patients with pre-existing renal failure.

Urinary excretion of 3-methylhistidine and creatine in carriers of Duchenne muscular dystrophy

The mean molar ratio (0.0171) of 3-methylhistidine to creatinine in 24-h urine samples from carriers of Duchenne muscular dystrophy did not differ significantly from that of controls. The creatine/creatinine ratio was also normal.

Creatine metabolism in skeletal muscle of noradrenaline-treated rats.

Prolonged noradrenaline treatment did not affect the urinary creatine excretion, creatine radioactivity, and the creatine contents of all muscles studied. Radioactive creatine uptake by skeletal muscle was significantly lower in noradrenaline-treated rats than in controls, while those by heart and diaphragm were not affected by noradrenaline.