Comparative study of 24-hour urinary excretion of glycosaminoglycans by renal stone formers and healthy adults

In order to find out the possible aetiological factors for urolithiasis in North-Western India, an endemic region for urinary calculi, we studied the 24-hour urinary excretion of glycosaminoglycans (GAGs), inhibitors of calcium oxalate crystallisation and/or crystal aggregation, in 58 healthy adults and in 100 stone formers. GAGs were colorimetrically estimated in urine in terms of glucuronic acid content after precipitation of GAGs by cetyl pyridinium chloride. The 24-hour urinary excretion of GAGs was significantly less in stone formers as compared to healthy adults (15.32 +/- 6.94 vs. 22.44 +/- 5.54 mumol/day; p less than 0.001). There was no significant difference in the 24-hour urinary excretion of GAGs between male and female stone formers, or between male and female healthy adults. There was no correlation between age and 24-hour urinary excretion of GAGs in any of the groups. In conclusion, 24-hour urinary excretion of GAGs is significantly less both in male and in female stone formers. The 24-hour urinary excretion of GAGs is not related to age or sex in both healthy adults as well as in stone formers.     

Low urine citrate excretion as main risk factor for recurrent calcium oxalate nephrolithiasis in males.

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.     

Urinary pyrophosphate in patients with recurrent calcium urolithiasis and in healthy controls: a re-evaluation

The excretion of inorganic pyrophosphate was studied in daily, fasting and postprandial urine specimens of normocalciuric and hypercalciuric patients with recurrent renal calcium stone disease (40 men and 40 women), and healthy controls (20 men and 20 women). Both populations were subdivided into younger (20 to 40 years old) and older (more than 40 years old) individuals. In general, there was a tendency towards higher urinary pyrophosphate excretion with increasing age (both sexes and all groups studied), and lower excretion in women than in men. The urinary pyrophosphate excretion rate was unchanged in daily and fasting urine specimens of the younger male normocalciuric and idiopathic hypercalciuric stone patients, whereas in the daily and postprandial urine of younger women the median excretion rate was reduced (controls versus normocalciuric plus idiopathic hypercalciuric subjects, 3 versus 1 mumol., p less than 0.05). In contrast, in older men urinary pyrophosphate was reduced in daily specimens (controls versus normocalciuric plus idiopathic hypercalciuric subjects, 55 versus 33 mumol., p less than 0.05) but it was unchanged in fasting urine specimens. In older women no change was detectable in any of the 3 urine portions. Factorization of urinary pyrophosphate for the associated urinary creatinine did not alter these results substantially, and the presence of renal stones did not modify pyrophosphate excretion significantly. Urinary pyrophosphate was correlated significantly with urinary volume, citrate and phosphorus. We conclude that only subclassification of stone patients with respect to sex, age and type of calciuria, and consideration of additional urine portions besides the daily urine may help to uncover states of urinary pyrophosphate deficit. On the basis of the data, we recommend that clinically relevant studies on inhibitory effects of urinary pyrophosphate on the nucleation and growth of crystals and stones should be done preferentially in urine portions with a proved pyrophosphate deficit.     

Increase in urinary kallikrein excretion following hemodialysis

Urinary kallikrein excretion (UKE) was measured in 20 patients before and after hemodialysis (HD). When compared to the values of normal subjects (136 +/- 56 micrograms/24 h, n = 100), UKE was decreased in all patients before HD (6.6 +/- 5.8 micrograms/24 h, p less than 0.001, n = 20). After HD a significant increase in 24-hour UKE was observed in all patients (18.6 +/- 7.2 micrograms/24 h, p less than 0.05, n = 20). Expressed as the individual percent increase, the UKE enhancement ranged from 16 to 670%. It was due to an enhancement in the excretion of the active form which represented 52 +/- 6.8% before HD and reached 76.3 +/- 7.5% of the total form after HD (p less than 0.01). The excretion of the inactive form remained unchanged. The increase in UKE was found to be significantly correlated with reductions in urinary sodium, potassium, and osmolality (r = -0.826, r = -0.568, r = -0.847, respectively, p less than 0.01, n = 20). The increase in UKE following HD could not be explain by an increase in aldosterone as urinary aldosterone decreased. A transient improvement in intracellular homeostasis (removal of inhibitory toxins and normalization of osmotic pressure) could be evoked. The increase in UKE 24 h after HD points out a new situation confirming the relations of UKE with changes in osmolality and extracellular volume.     

The urinary response to an oral oxalate load in recurrent calcium stone formers

PURPOSE: Dietary oxalate may contribute up to 50% to 80% of the oxalate excreted in urine. We studied the urinary response to an oral oxalate load in male and female idiopathic recurrent calcium oxalate stone formers with and without mild hyperoxaluria to evaluate the potential pathophysiological significance of dietary oxalate. MATERIALS AND METHODS: A total of 60 recurrent calcium stone formers underwent an oral oxalate load test. Urine samples were obtained after an overnight fast. Each patient then received an oral oxalate load (5 mM. sodium oxalate dissolved in 250 ml. distilled water) and 3, 2-hour urine samples were obtained 2, 4 and 6 hours after the oxalate load. We compared the response to the oxalate load in patients with and without mild hyperoxaluria, and in male and female patients without hyperoxaluria. RESULTS: The peak urinary response occurred 4 hours after the oral oxalate load in all patients. Those with mild hyperoxaluria had a mean fasting urinary oxalate-to-creatinine ratio +/- SE of 0.027 +/- 0.003 and a mean peak urinary oxalate-to-creatinine ratio of 0.071 +/- 0.006. In comparison, patients with normal oxalate excretion had a fasting and peak urinary oxalate-to-creatinine ratio of 0.018 +/- 0.001 and 0.056 +/- 0.004, respectively (p <0.05). The mean 6-hour increment for urinary oxalate excretion after the oxalate load for patients with hyperoxaluria versus those with normal urinary oxalate excretion was 17.2 +/- 1.9 versus 12.1 +/- 0.98 mg. (p <0.05). In the subset of patients with normal urinary oxalate excretion mean 6-hour cumulative urinary oxalate excretion was 16.8 +/- 1.3 and 13.3 +/- 1.4 mg. in males and females, respectively (p not significant). CONCLUSIONS: Recurrent calcium stone formers with mild hyperoxaluria have higher fasting urinary oxalate and an exaggerated urinary response to an oral oxalate load compared with recurrent calcium stone formers with normal urinary oxalate excretion. Men and women stone formers without hyperoxaluria excrete similar fractions of an oral oxalate load. Increased gastrointestinal absorption and renal excretion of dietary oxalate may be a significant pathophysiological mechanism of stone formation in patients with mild hyperoxaluria.     

Whole-body protein breakdown and 3-methylhistidine excretion during brief fasting, starvation, and intravenous repletion in man.

Simultaneous whole-body protein breakdown (using 15N-glycine) and urinary 3-methylhistidine (3MH) excretion rates were determined in six hospitalized normal volunteers after 10 days of starvation and a subsequent 10-day period of total parental nutrition (TPN). These data were contrasted to whole-body protein breakdown and urinary 3MH excretion in ten depleted (14.8% body weight loss) patients with benign intraabdominal disease studied in the basal (48 hours without nutrient intake) and intravenously refed states. The rates of whole-body protein breakdown were significantly reduced from basal (brief fasting or starvation) conditions in both normal volunteers (p less than 0.01) and depleted patients (p less than 0.01) during TPN. The rate of protein catabolism normalized for creatinine excretion in patients was higher than that observed in normal subjects during both basal (p less than 0.05) and intravenous feeding conditions. Daily urinary 3MH excretion was reduced during intravenous feeding in both starved normal volunteer (235 +/- 13 mumol/d to 197 +/- 9 mumol/d p less than 0.05) and in depleted patients (209 +/- 31 mumol/d to 140 +/- 35 mumol/d), and an apparent linear relationship between protein breakdown and urinary 3MH, normalized for creatinine excretion, was obtained in both volunteer and patient (r = 0.85) populations during fasting-refeeding. However, separate regression analysis of the protein breakdown and 3MH responses of both volunteer and patient groups under conditions of fasting, starvation, and refeeding revealed significant differences between volunteer and patient populations during intravenous refeeding (p less than 0.01). Further analysis of 3MH excretion in relationship to nitrogen balance during refeeding suggests a complex relationship between urinary 3MH excretion and whole-body protein metabolism that may be partly related to the degree of antecedent malnutrition.     

Intestinal oxalate and calcium absorption in recurrent renal stone formers and healthy subjects

The fractional intestinal absorption of oxalate and calcium was investigated by isotope techniques in 20 normal subjects and in 12 idiopathic calcium oxalate stone formers. The greatest amount of 14C-oxalate was excreted during the first six hour period in controls as well as in stone formers. The stone formers had a greater intestinal uptake of oxalate (11 +/- 5.1%) than the controls (6.2 +/- 3.7%; p less than 0.01). There was no significant relationship between the fractional absorption of oxalate and the total urinary oxalate excretion. The stone formers also had a higher fractional uptake of calcium compared to the controls (55 +/- 11% vs. 47 +/- 9.1%; p less than 0.05). There was a positive relationship (r = 0.47) between the urinary excretions of calcium and oxalate in the stone formers. During these conditions no correlation could be demonstrated between the fractional absorptions of oxalate and calcium, neither in the stone formers nor in the controls. In conclusion, patients with recurrent formation of calcium oxalate containing stones appear to have an enhanced intestinal uptake of both oxalate and calcium. This disturbance could be of primary pathogenic importance for their stone forming propensity.     

Effect of dietary control of urinary uric acid excretion in calcium oxalate stone formers and non-stone-forming controls

BACKGROUND AND PURPOSE: Hyperuricosuria is a well-recognized risk factor for calcium oxalate urolithiasis. Some studies have demonstrated elevated urinary uric acid excretion in stone formers compared with non-stone-forming controls; nevertheless, these studies were limited by patient consumption of self-selected diets. With the recognition that dietary differences may induce variations in urinary uric acid excretion, we evaluated excretion of this compound in stone formers and controls consuming a standardized diet. SUBJECTS AND METHODS: A standardized formula diet was administered to 65 calcium oxalate stone formers and 61 age-matched non-stone-forming controls. During the 3 days of dietary intervention, 24-hour urine collections were obtained. Mean urinary uric acid excretion indexed to urinary creatinine was calculated for each subject, and the results in the two groups were compared. RESULTS: Stone-forming subjects did not have an elevation in urinary uric excretion compared with control subjects, with mean indexed urinary uric acid excretions of 337 +/- 64 mg/g of creatinine and 379 +/- 76 mg/g of creatinine, respectively. CONCLUSIONS: With dietary standardization, there was no observed increase in urinary uric acid excretion in our sampled populations. These findings emphasize the role of dietary factors in urinary uric acid excretion and highlight the potential value of dietary interventions.     

Urinary glycosaminoglycans in normal subjects and patients with stones

Urinary glycosaminoglycans are thought to be macromolecular inhibitors of calcium stone formation. The 24-hour excretion of urinary glycosaminoglycans was measured quantitatively in 24 normal subjects and 206 patients with different etiologies of stone disease. In both groups a positive correlation was found between urinary glycosaminoglycans and total urinary volume and urinary sulfate. In normal subjects total urinary volume was r equals 0.716, p less than 0.001 and urinary sulfate was r equals 0.813, p less than 0.001, while in patients with stones these values were r equals 0.338, p less than 0.001 and r equals 0.326, p less than 0.001, respectively. The only significant difference in excretion of urinary glycosaminoglycans between the groups was found in the subgroup of patients with type I absorptive hypercalciuria. The type I absorptive hypercalciuria value of 33.4 +/- 14.9 mg. per day in patients with stones was significantly higher than the 25.8 +/- 8.3 mg. per day detected in normal subjects (p less than 0.05). Urinary glycosaminoglycan excretion in all other subgroups of nephrolithiasis as well as in a combined group of all patients with stones showed no significant difference when compared to that of normal subjects. Thus, no major quantitative relationship could be demonstrated between urinary glycosaminoglycan excretion and calcium stone formation in this study.     

Calcium oxalate retention in subjects with crystalluria

Calcium oxalate retention was studied in non-stone-forming volunteers. All subjects were placed on a constant diet for 5 days. After the oral administration of 10 microCi of [14C]-oxalic acid, the pattern of urinary oxalate excretion was followed for 48 h. Each subject was then given 10 microCi of [14C]-oxalic acid mixed with sufficient sodium oxalate (7.5 mg/kg body weight) to induce calcium oxalate crystalluria. Urinary oxalate excretion was then recorded for 48 h. After the administration of labeled oxalic acid (without additional sodium oxalate), 76.6 +/- 5.9% of the total recovered dose was excreted by 4 h. When the labeled oxalic acid was mixed with a sodium oxalate load, 62.4 +/- 8.8% was excreted by 4 h (p less than 0.01). Induction of calcium oxalate crystalluria results in the retention of oxalate in the kidney. The degree of retention varies among individuals. Differences in particle retention may help explain the differences between stone formers and non-stone formers.     

Renal excretion of hydrogen ions in stone formers.

Urinary hydrogen ion excretion has been studied in 68 adult stone formers and in 50 controls. Under basal state, the stone formers showed statistically significant higher urinary pH, and lower 24-hour urinary titrable acid, ammonium and total hydrogen. On the 3rd day of ammonium chloride loading test, the stone formers showed statistically significant higher urinary pH and lower 24-hour urinary titrable acid, ammonium, total hydrogen and plasma bicarbonate. 'Clearance' indices of hydrogen ion excretion were also depressed in a great majority of the stone formers. The results indicate the frequent co-existence of defective urinary acidification with nephrolithiasis.     

Urinary excretion of endothelin-1 in normal subjects and patients with renal disease

To elucidate the pathophysiological significance of urinary endothelin-1 (ET-1), we measured urinary excretion of ET-1-like immunoreactivity (L1) in 17 patients with renal disease and 9 normal subjects. Twenty-four hour urinary ET-1-L1 excretion in patients with renal disease (358 +/- 68 ng, mean +/- SE) was significantly (P less than 0.005) greater than that of normal subjects (77 +/- 5 ng). In patients with renal disease. ET-1-L1 clearance (CET) exceeded creatinine clearance (CCR); CET/CCR (305 +/- 81%) was significantly (P less than 0.005) greater than that of normal subjects (43 +/- 13%). The 24-hour urinary excretion of ET-1-L1 in patients with renal disease showed significant correlation with that of N-acetyl-beta-D-glucosaminidase (r = 0.587, P less than 0.05), beta 2-microglobulin (r = 0.614, P less than 0.01) and albumin (r = 0.484, P less than 0.05). Intravenous infusion of saline (500 ml) in seven normal subjects did not affect urinary ET-1 excretion rate. These data suggest that urinary excretion of ET-1 derives mainly from renal tubular secretion at least in patients with renal disease, and that degradation and/or reabsorption of ET-1 at the tubular site may also contribute to the renal handling of ET-1. Therefore, urinary excretion of ET-1 should serve as a potential marker for renal injury.     

Urine calcium excretion, nephrogenous cyclic-adenosine monophosphate and serum parathyroid hormone levels in patients with essential hypertension.

To evaluate the role of calcium and the parathyroid gland in the pathophysiology of essential hypertension, creatinine clearance, urinary excretion of sodium, calcium and nephrogenous cyclic adenosine monophosphate (NcAMP) and serum parathyroid hormone (PTH) levels were measured in 25 newly diagnosed essentially hypertensive patients before institution of any treatment and in 25 age- and sex-matched normal volunteers. While no significant differences in creatinine clearance, serum total calcium levels or 24-hour sodium excretion existed between the two groups, hypertensives had a higher mean (+/- SD) 24-hour calcium excretion rate (199.0 +/- 44.7 vs. 152.8 +/- 33.6 mg, p less than 0.001), a higher mean NcAMP excretion rate (2.54 +/- 0.8 vs. 1.87 +/- 0.5 nmol/100 ml glomerular filtrate, p less than 0.001) and a higher mean serum PTH concentration (1.87 +/- 0.6 vs. 1.53 +/- 0.4 ng/ml, p less than 0.001) than the normotensives. A significant positive correlation existed between calcium and sodium excretion in both hypertensives (r = 0.66, p less than 0.001)) and normotensives (r = 0.67, p less than 0.001), but given the same levels of creatinine clearance and sodium excretion, hypertensives excreted more calcium than normotensives (p less than 0.001)). In both hypertensives and normotensives, serum PTH levels were positively correlated with NcAMP excretion (r = 0.42, p less than 0.05, and r = 0.41, p less than 0.05, respectively) and the ratio of urinary sodium to urinary calcium excretion (r = 0.59, p less than 0.001, and r = 0.75, p less than 0.001), respectively). The above results suggest that in essential hypertension, increased activity of parathyroid glands may occur as a consequence of increased urinary calcium losses which are presumably due to an intrinsic defect in renal calcium handling.     

Comparative study of the circadian rhythmicity in the urinary concentration of glycosaminoglycans in patients of calcium oxalate nephrolithiasis and in healthy adults

Glycosaminoglycans (GAGs) are potent inhibitors of calcium oxalate crystallisation and/or crystal aggregation. Urinary concentration of GAGs has been shown to vary during 24 h; therefore, circadian rhythmicity in urinary concentration of GAGs was investigated in 33 healthy male adults in the age group of 20-40 years and in 27 male patients of a similar age group with calcium nephrolithiasis. Three-hourly urine samples were collected for 24 h beginning from 00.00 h for estimation of urinary concentration of GAGs. The data of each patient was analysed by single cosinor rhythmometry and population mean-cosinor rhythmometry was then applied to each group. Twenty-four-hour urinary excretion of GAGs was significantly less in renal calculus patients (16.867 +/- 5.89 mumol) than in healthy subjects (22.588 +/- 5.32 mumol; p less than 0.001). A statistically validated circadian rhythm in urinary concentration of GAGs was demonstrated in both the groups. However, the amplitude-acrophase test revealed a significant difference between the two groups (F2,57 = 8.305; p less than 0.001); the amplitude was 2.354 mumol/l in patients with nephrolithiasis, whereas the amplitude was 7.028 mumol/l in healthy adults. The mesor test also revealed a significant difference in the 3-hour urinary concentration of GAGs between the two groups (18.536 mumol/l in healthy adults vs. 9.728 mumol/l in patients with nephrolithiasis). Thus in patients with nephrolithiasis, not only is the 24-hour urinary excretion of GAGs significantly low but the 3-hourly urinary concentration of GAGs is also significantly decreased as compared to healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Low urinary calcium excretion in Bartter's syndrome

The urinary calcium excretion has been determined in 19 patients with Bartter's syndrome and found to be significantly lower than the calcium excretion in 92 healthy subjects (1.16 +/- 0.82 vs. 4.36 +/- 2.71 mmol/24 h, p less than 0.001). There were no differences in height, weight, glomerular filtration rate, urinary sodium excretion or serum calcium concentration between the patients and the control subjects to account for the disparity in calcium excretion. In the patients, the concentrations for ionized calcium, PTH, 25-OH vitamin D and 1,25-(OH)2 vitamin D were normal. A low urinary calcium excretion appears to be a characteristic feature of Bartter's syndrome. The cause remains unexplained.     

Silicon metabolism. I. Some aspects of renal silicon handling in normal man

Renal silicon handling was investigated in 23 healthy adults using electrothermal atomic absorption techniques. The mean urinary silicon excretion was 33.1 +/- 3.85 mg/day; the mean renal silicon clearance was 88.6 +/- 7.94 ml/min; the mean fractional excretion of silicon was 86.35 +/- 8.1%, and the mean urine silicon concentration was 0.265 micrograms/ml. Using multiple correlation analysis, the urinary silicon was found to be highly significantly correlated with the urine magnesium concentration (p less than 0.001) and also with urinary sodium and urinary osmolality (p less than 0.01). 24-hour urinary silicon excretion was highly significantly correlated with fractional excretion of silicon (p less than 0.001), sodium (p less than 0.001), phosphorus (p less than 0.001), magnesium (p less than 0.001), and osmolar load. In split urine studies in 7 subjects urinary silicon was correlated highly significantly with urinary magnesium in all 7 and with urinary osmolality, urine calcium, and urine creatine concentration in 6 of 7. There was a highly significant correlation between renal silicon clearance and fractional excretion of silicon (p less than 0.0005), with magnesium excretion (p less than 0.01), and with sodium excretion. It is suggested that ion pairing of orthosilicate and magnesium may explain some of these urinary findings.     

正常人和尿路结石病人的尿液GAGs分析

分析４０例尿路结石病人和１６名正常人的２４小时尿液ＧＡＧｓ水平。结果表明：结石患者２４小时尿ＧＡＧｓ总量和浓度分别为２７．９３±１０．９２ｍｇ和１９．００±７．５μｇ／ｍｌ，较正常人３４．３７±７．９０ｍｇ和２３．３０±６．４μｇ／ｍｌ为低，两组具有显著性差异（Ｐ＜０．０５）。对尿ＧＡＧｓ抑制尿路结石形成的机理及其应用前景进行讨论。     

Urinary albumin excretion in patients with non-insulin-dependent diabetes mellitus in an early microalbuminuric stage.

We investigated the urinary albumin excretion and renal hemodynamics of normotensive nonobese patients with impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) in an early microalbuminuric stage (defined by albuminuria less than 30 mg/day). In comparison with normal subjects, a significant increase in urinary albumin excretion was observed already in the IGT stage [U-albumin/U-creatinine: NL (20 subjects), 5.3 +/- 1.7 mg/g Cr; IGT (23 subjects), 11.9 +/- 6.7 mg/g Cr; DM (20 subjects), 12.8 +/- 5.7 mg/g Cr]. A 3-week diet therapy combined with physical exercise prescribed for 53 normotensive non-obese mild NIDDM patients resulted in improvement in glucose tolerance, concomitant with lowered systemic blood pressure and a decrease in urinary albumin excretion (SBP: 128.4 +/- 13.0 to 106.4 +/- 10.2 mm Hg, p less than 0.01; DBP: 78.2 +/- 10.8 to 66.0 +/- 8.0 mm Hg, p less than 0.01; U-albumin: 19.4 +/- 10.3 to 10.1 +/- 9.1 mg/day, p less than 0.01). However, glomerular filtration rate, renal plasma flow, filtration fraction and urinary beta 2-microglobulin excretion remained unchanged. From these results, we hypothesized that focal glomerular hyperperfusion increases urinary albumin excretion in patients with early NIDDM.     

Value of routine citrate analysis and calcium/citrate ratio in calcium urolithiasis

24-hour urinary citrate excretion was measured in 176 calcium oxalate stone formers and 100 normal controls. A statistically significant difference (p less than 0.03) could be found between the two groups. When stone formers were divided into a group of 69 patients with recurrent calcium urolithiasis (RCU) and a group of 106 patients with a single stone episode, the latter did not differ from the control group, while in RCU a significantly lower citrate excretion compared with controls (p less than 0.005) could be found. Thus, patients with RCU could benefit from alkali citrate prophylaxis. A female-male difference in citrate excretion could not be found in either the control group or stone formers. Recurrent stone formers presented a significantly higher calcium/citrate ratio compared with controls, which would indicate an increased risk for stone formation. The value of routine citrate analysis is limited, however, by the great, variability of citrate levels in stone formers and controls.     

Barbiturate therapy reduces nitrogen excretion in acute head injury

The effect of pentobarbital on nitrogen and energy metabolism was evaluated in seven severely head-injured patients (Glasgow Coma Scale 4.7 +/- 1.7) within the first week postinjury. Measured energy expenditure (% of predicted) was significantly lower in the pentobarbital group (n = 4) versus control (n = 3) (76 +/- 23% versus 132 +/- 28%, respectively, p less than 0.01). Similarly, 24-hour urinary nitrogen excretion was lower for the barbiturate group compared to control (11.2 +/- 4.0 gm versus 19.5 +/- 3.3 gm, respectively, p less than 0.01). No statistical difference was noted for urinary 3-methylhistidine excretion between the barbiturate and control groups (43 +/- 12 mcg/day versus 47 +/- 14 mcg/day, respectively, p = N.S.). Barbiturate therapy decreases measured energy expenditure and reduces nitrogen excretion without significantly altering 3-methylhistidine excretion in head-injured patients. The metabolic effects of pentobarbital may enable the ability to achieve energy and nitrogen equilibrium during metabolic support of acutely head-injured patients.