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Biomedical subjects

B H Brouhard

Publications and source records attributed to B H Brouhard.

At least 55 records · Page 3Linked to original sources
PubMed1990

Spinal bone mineral density in children aged 5.00 through 11.99 years.

Lumbar spine (L-2, L-3, L-4) bone mineral density was measured in 184 healthy boys and girls aged 5.00 through 11.99 years by dual photon absorptiometry. Weight, height, age, triceps skinfold thickness, and midarm circumference were also measured. Weight, height, and age were highly correlated with bone mineral density. In the population studied, a quadratic regression equation using body weight as the independent variable best described bone mineral density: bone mineral density = 0.3209 + [0.0168 (weight)] - [0.0001 (weight2)].

Body Height↗
PubMed1990

Effect of dietary protein restriction on functional renal reserve in diabetic nephropathy.

PURPOSE, PATIENTS, AND METHODS: Functional renal reserve in patients with insulin-dependent diabetes mellitus, as determined by the glomerular filtration rate (GFR) response test, is a measure of the capacity of the kidney to increase glomerular filtration in response to the stimulus of a protein meal or amino acid infusion. This 12-month study evaluated the changes in functional renal reserve in eight patients with insulin-dependent diabetes mellitus with nephropathy (micro-albuminuria [greater than or equal to 30 micrograms/minute]) who chronically decreased their dietary protein intake to a mean of 0.6 g/kg/day (Group 1) compared with a group of similar patients (n = 7) who maintained their unusual dietary protein intake (1.0 g/kg/day, Group 2). Patients were evaluated and measurements taken at 3-, 6-, and 12-month intervals. Absolute and percent increases in GFR were calculated from three averaged 1-hour measurements after an 80-g protein test meal. RESULTS: Although the initial absolute mean rise (14 +/- 12 versus 18 +/- 13 mL/minute/1.73 m2) in GFR and maximal percent rise (16% +/- 16% versus 32% +/- 27%) after the meal did not differ significantly between the two groups, at 12 months, values in the lower protein group increased (27.8 +/- 9.5 mL/minute/1.73 m2 and 54.7% +/- 48.8%), whereas those in the normal protein intake group declined significantly (3.7 +/- 3.6 mL/min-ute/1.73 m2 and 6.5% +/- 6.5%) (p less than 0.05). Both urine urea and microalbuminuria decreased significantly (p less than 0.05) in the low protein group. Unstimulated GFR at the end of 12 months was significantly less (p less than 0.05) in Group 2 (47 +/- 2 mL/minute/1.73 m2) than in Group 1 (71 +/- 21 mL/minute/1.73 m2). The rate of decline in GFR was significantly greater (p less than 0.05) in the normal protein intake group than in the low protein intake group (0.68 +/- 0.4 versus 0.28 +/- 0.15 mL/minute/1.73 m2/month). CONCLUSIONS: This study indicates that sustained dietary protein restriction can help to preserve renal function, decrease albuminuria, and lower the baseline GFR while maintaining functional renal reserve in patients with insulin-dependent diabetes mellitus.

Adult↗
PubMed1990

Hyperphosphaturia and hypermagnesuria in children with IDDM.

Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.

Adolescent↗
PubMed1990

Lipoprotein abnormalities in the progression of renal disease.

Chronic renal disease is a progressive process. Implicated factors include abnormalities of the clotting cascade, altered prostaglandin metabolism, increased dietary protein intake, and abnormalities of lipoprotein metabolism. Several animal models have associated increased serum concentrations of cholesterol and triglycerides with progressive decline in renal function. The mechanism(s) of lipid-associated renal injury are unknown but may relate to lipid uptake by glomerular mesangial cells, hyperviscosity secondary to the hyperlipidemia, and a direct effect of the lipids on the glomerular basement membrane. Patients with chronic renal disease have well recognized increases in serum lipid concentrations. Whether lowering these concentrations will delay or prevent progressive renal failure or renal histologic abnormalities is unknown, but studies are underway to evaluate the effect of lipid-lowering agents in patients at risk for chronic progressive renal disease.

Animals↗
PubMed1989

Effect of indomethacin on the glomerular filtration rate after a protein meal in humans.

The renal response to a protein meal has been characterized by increases in glomerular filtration rate (GFR) and renal plasma flow and decrease in renal vascular resistance. Several hormonal mediators of this response have been proposed, including renal prostaglandins (PGs). We studied ten normal subjects before and after ingestion of indomethacin. All subjects had three 30-minute baseline creatinine and iothalamate clearances measured before and three one-hour clearances measured after an 80-g protein meal. The night before the second test, the subjects took 25 mg indomethacin and 150 mg one hour before the test meal. Urine PG excretion decreased significantly during the second test, from 0.60 +/- 0.23 to 0.30 +/- 0.14 ng/min (P less than 0.01). Initial iothalamate clearance increased from 110 +/- 10 to a mean of 122 +/- 15 mL/min/1.73 m2 (average increase of 12 mL/min/1.73 m2) during the second hour after the test meal. After ingestion of indomethacin, the GFR remained unchanged from a baseline of 101 +/- 9 to 101 +/- 7 mL/min/1.73 m2 (average change of -1 mL/min/1.73 m2). Because the time of peak increase after the meal varied from subject to subject, the maximal increase in GFR after the meal was calculated and found to be significantly less during the second test, 13 +/- 3 v 22 +/- 4 mL/min/1.73 m2 (P less than 0.05). Because PGs can stimulate glucagon secretion and because glucagon has been suggested to mediate the protein-stimulate GFR response, we measured plasma glucagon during both tests; these levels were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of growth hormone on the glomerular filtration response to a protein meal.

The role of dietary protein intake in the pathogenesis of progressive renal disease has been recently reexamined. Studies of both animal and humans with chronic renal disease have shown that restriction of dietary protein may slow the progression of the decline in renal function. This occurs because of a decrease in intraglomerular blood flow and pressure. The mechanism of this phenomenon is not known. The effect of protein intake on renal function is thought to be hormonally mediated. Since growth hormone can increase renal blood flow as well as GFR, we tested the hypothesis that the presence of growth hormone is necessary for the increase in glomerular filtration rate (GFR) seen after the ingestion of a protein meal. We evaluated the change in GFR after a standardized mixed protein meal in 13 patients with growth hormone deficiency. Neither basal creatinine clearance after an overnight fast (76 +/- 17 ml/min/m2; mean +/- SD) nor maximum increment after a 50 g/m2 protein meal (33 +/- 11 ml/min/m2) differed in these growth hormone-deficient patients from 16 normals controls (76 +/- 18 and 30 +/- 15 ml/min/m2, respectively). Twelve hours after an injection of exogenous growth hormone, 0.06 mg/kg up to a maximum of 5 mg, the GFR response to a protein meal did not differ from the pretreatment response (77 +/- 19 and 32 +/- 17 ml/min/m2, respectively). We conclude that the presence of physiologic amounts of growth hormone is not necessary for the GFR response to a standard protein meal.

Adolescent↗
PubMed1988

Renal transplantation in the infant and young child.

Fourteen renal transplantations were performed in 13 children, aged 5 years or younger, including three infants. The mean duration of follow-up was 68 months, with a range of 14 to 203 months. Eleven children are alive; of these, nine had prolonged graft function. Graft survival rate was 92% at one year and 73% at two and five years following surgery. Sustained catch-up growth occurred in all growth-retarded children who underwent successful transplantation. At this writing, the oldest patient is 20 years of age and a junior in college; all school-age children are functioning at the appropriate grade level, except one, who is one year behind. The youngest child is 3 years old and is developing normally. Infants and young children appear to be good candidates for renal transplantation.

Child Development↗
PubMed1988

Sex of the parental donor and cellular rejection of renal allografts in children.

The survival of renal allografts of maternal and paternal origin has been assumed to be identical, and in reports concerning graft survival the outcome of parental transplants is not analyzed by sex of the donor. Fifty-five children received a parental kidney between January 1973 and March 1987 at one institution. There were 6 technical failures. Analysis of renal graft survival in the remaining 49 children indicates a disparity between maternal and paternal graft survival, with an increased propensity for loss of paternal grafts from cellular rejection. Nine of 22 parental grafts are no longer functioning; 7 were lost from cellular rejection. In comparison, cellular rejection resulted in the loss of only 2 of 27 maternal grafts. This disadvantage of paternal grafts is most conspicuous in patients followed for 2 or more years; 7 of 15 paternal but only 1 of 20 maternal grafts were lost because of cellular rejection (P = 0.01). With causes of graft loss other than cellular rejection treated as withdrawal, actuarial survival of the 27 maternal grafts at 1 and 5 years is 96% and 91%, respectively, while that of the 22 paternal grafts is 83% and 58% (P = 0.017). Analysis of data from other centers will help determine whether our observation is of clinical significance.

Child↗
PubMed1987

Somatostatin limits rise in glomerular filtration rate after a protein meal.

To evaluate the glomerular filtration rate (GFR) response to a protein meal in patients with diabetes and to study the role of glucagon and growth hormone, we studied inulin clearance for three 30-minute periods before and 3 hours after an 80 g protein meal in seven healthy volunteers and 10 patients with diabetes. Patients with diabetes were chosen because their renal response to such a meal has been reported to be abnormal. All had an increase in GFR and plasma glucagon levels after the protein meal. The peak rise in GFR occurred from 1 to 2 1/2 hours after the meal (mean +/- SEM, delta 26 +/- 5 mL/min/m2, controls; delta 22 +/- 7 mL/min/m2, patients with diabetes), with the mean time to normal rise in GFR occurring at 2 hours after the meal. Similarly, plasma glucagon values peaked at different times in individual patients (delta 769 +/- 532 pg/mL, controls; delta 267 +/- 69 pg/mL, patients with diabetes), with the mean plasma glucagon rise occurring 1 hours after the meal. Premeal growth hormone levels tended to be higher in the patients with diabetes (7.6 +/- 1.4 vs 2.1 +/- 0.4 ng/mL), and did not change after the meal. To allow study of the contribution of the increased plasma glucagon to the rise in GFR, eight of these patients (five with diabetes) volunteered to undergo a second GFR response test with a simultaneous infusion of somatostatin. The glucagon response was significantly lowered at all time periods during the infusion (P less than 0.05); no significant change in growth hormone occurred. Without somatostatin in these eight patients, peak increase in postmeal GFR average 20.6 +/- 1.5 mL/min/m2; with the somatostatin, peak increase in GFR was 6.0 +/- 1.8 mL/min/m2 (P less than 0.01). Neither metabolic control nor degree of albuminuria was significantly different at the time of the two studies. Thus, as has been shown in animals, somatostatin infusion limits the rise in GFR after a protein meal in humans.

Adolescent↗