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E D Brewer

Publications and source records attributed to E D Brewer.

50 records · Page 3Linked to original sources
PubMed1986

Relationship of human milk pH during course of lactation to concentrations of citrate and fatty acids.

Human milk pH was measured in 309 samples obtained from 52 women who had delivered at term and lactated for as long as 10 months thereafter. The mean pH decreased from 7.45 for colostrum to a nadir of 7.04 during the second week of lactation. Thereafter, the pH of milk remained between 7.0 and 7.1 until 3 months postpartum and then increased gradually to 7.4 by 10 months. The change in hydrogen ion concentration in milk was associated with corresponding changes throughout lactation in the concentration of citrate but not with the concentration of lactose. Lactose concentration increased gradually for 3 weeks; the concentration of saturated medium-chain fatty acids increased more rapidly. One interpretation of these findings is that the hydrogen ions and citrate generated by mammary secretory cell metabolism are used after the second week of lactation for de novo synthesis of fatty acids more rapidly than they are synthesized. Milk samples from ruminants were found to have concentrations of hydrogen ions and citrate that are greater than and pH that is less than the respective measurements in human milk. The significance for the recipient infant of the predictable changes in human milk pH during lactation and of the higher pH of human milk throughout lactation relative to bovine milk is unknown. However, drug excretion into milk, milk enzyme activity, milk leukocyte function, and neonatal gastrointestinal function are affected by ambient pH and may be influenced by the pH of milk.

Animals↗
PubMed1983

Intermittent clean catheterization: an alternative to diversion in continent transplant recipients with lower urinary tract dysfunction.

A total of 3 renal transplant recipients who were candidates for urinary diversion underwent successful transplantation using a planned program of intermittent clean catheterization. The urinary tract dysfunction was caused by a lower motor neuron neurogenic bladder, prune belly syndrome and myelodysplasia. The patients remain dry between catheterizations and maintain serum creatinine levels of 1.1, 0.8 and 0.5 mg. per cent, respectively, with a followup of 6 to 25 months. There has been only 1 urinary tract infection during 42 patient-months at risk while on self-catheterization. Pre-transplant urologic evaluation and patient education are mandatory. The ideal candidate for intermittent clean catheterization is a patient with a low pressure bladder that fails to empty and who is continent between catheterizations. Intermittent clean catheterization is a safe and effective alternative to diversion in continent transplant recipients with lower urinary tract dysfunction.

Adult↗
PubMed1983

Maleic acid-induced reabsorptive dysfunction in the proximal and distal nephron.

Micropuncture and clearance studies were performed to assess reabsorptive function in the proximal and distal nephron of rats with experimental Fanconi's syndrome induced by maleic acid. Anesthetized rats were studied by free-flow micropuncture of the late proximal tubule 90-120 min after continuous intravenous administration of maleic acid, 100 mg X kg-1 X h-1. Compared with control rats, the reabsorption of sodium and phosphate was significantly reduced (P less than 0.001 and less than 0.02, respectively). Tubular fluid-to-ultrafiltrate (TF/UF) chloride concentration ratio was 1.00 +/- 0.02 compared with 1.16 +/- 0.03 (P less than 0.01) in controls, suggesting a nearly total inhibition of proximal bicarbonate reabsorption. Whole kidney fractional excretions of sodium and chloride were increased significantly (P less than 0.02) but could not be explained by enhanced delivery of these solutes out of the late proximal tubule. To assess whether distal nephron reabsorption of sodium and chloride were inhibited by maleic acid, clearance studies were performed during water diuresis in awake rats. During maleic acid administration, 200 mg X kg-1 X h-1, urine flow rate (P less than 0.02) and the fractional excretions of sodium and chloride (P less than 0.001) increased significantly, but fractional free water clearance decreased from 7.16 +/- 0.42 to 4.03 +/- 0.68% (P less than 0.001). In acetazolamide-treated control rats but not in maleic acid-treated rats with similar bicarbonaturia, the magnitude of fractional free water clearance closely approximated the simultaneously measured fractional distal delivery of chloride. These studies suggest that maleic acid inhibits reabsorption at a distal nephron site or sites as well as in the proximal tubule.

Absorption↗
PubMed1982

Proximal tubular necrosis associated with maleic acid administration to the rat.

Administration of maleic acid to the rat is used as an experimental model of Fanconi's syndrome. To determine the site and extent of morphologic injury within the kidney after maleic acid administration, we systematically examined renal tissue using light, transmission electron, and scanning electron microscopy. Tissue was studied either immediately or 24 hours after rats received maleic acid, 200 mg. or 400 mg. per kg. of body weight, and was compared with tissue from controls. In kidneys of maleic acid-treated rats, evidence of injury was observed only in cells of the late pars convoluta and the pars recta in the medullary rays of the cortex and in the outer stripe of the medulla. Injured cells were characterized by an increase in cytoplasmic density, accumulation of numerous small vesicles in the apical region of the cells, abnormal-appearing mitochondria with compressed cristal membranes and flocculent densities, and focal loss of microvilli. Injury was apparent immediately after maleic acid administration and progressed to extensive necrosis by 24 hours after either the 200- or 400-mg. per kg. dose. Except for the presence of granular and hyaline casts in the lumena, the loops of Henle and distal convoluted tubules were normal. Collecting ducts in the outer medulla, but not in the cortex, medullary rays, or inner medulla, had significantly increased numbers of dark cells per total cell population when compared with controls (p less than 0.005). This increase in dark cells may represent an adaptive response of the medullary collecting duct to the functional abnormalities of maleic acid-induced Fanconi's syndrome. Collecting ducts showed no evidence of cell injury or necrosis. These observations provide evidence that maleic acid, like many other renal toxins, produces tubular injury and necrosis only in the proximal tubules, primarily in the medullary rays, and outer stripe of the medulla, and not in the distal tubules.

Animals↗
PubMed1981

Hodgkin's disease complicated by nephrotic syndrome. New clinical observations on the response of both diseases to radiotherapy to the neck.

The clinical course of a 14-year-old boy who developed biopsy-proven minimal change nephrotic syndrome (MCNS) prior to institution of therapy for Hodgkin's disease (HD), mixed cellularity histologic subtype, is presented. In the first week of radiotherapy to the major site of disease in the neck, BUN and creatinine levels rose to 98 mg% and 8.4 mg%, respectively. During the second week of treatment, levels gradually decreased becoming normal in the third week. Body weight gradually decreased in the second week of radiotherapy, falling rapidly in the third and fourth week when diuresis was greatest. Although urine protein concentration fell initially, the concentration remained 1 + or more for 10 weeks following radiotherapy. Following radiotherapy to the neck, staging laparotomy demonstrated a single focus of Hodgkin's disease in the spleen. Radiotherapy was given to the splenic pedicle: six courses of multiagent chemotherapy (MOPP) followed. The boy remains free of any evidence of either HD or MCNS 33 + months from the time of the diagnosis. Circulating lymphocytes showed normal responses to stimulation by phytohemaglutinin, Concanavalin A, and pokeweed mitogens. The patient's monocyte-macrophage-mediated antibody-dependent cellular cytotoxicity (ADCC) was low both prior to and following radiotherapy. Lymphocyte-mediated ADCC was normal at both of these times.

Adolescent↗
PubMed1977

Maleic acid-induced impaired conversion of 25(OH)D3 to 1,25(OH)2D3: implications for Fanconi's syndrome.

Conversion of 25-hydroxyvitamin D3 [25(OH)D3] to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] occurs exclusively in the renal cortex. To determine whether a disorder of the renal cortical tubule capable of causing Fanconi's syndrome can also impair the synthesis of 1,25(OH)2D3, we investigated whether conversion of 25(OH)D3 to 1,25(OH)2D3 was reduced by maleic acid. In vitamin D-deficient rats, maleic acid was administered i.v. over two hours. Thirty minutes after its initiation, when the complex renal tubule dysfunction had occurred, 3H-25(OH)D3 was administered i.v. as a bolus. Five hours afterwards, the amount of 3H-1,25(OH)2D3 recovered in the kidney, small intestine mucosa, and blood was one-third to one-half that in tissues of control rats that received acetazolamide or only saline or were subjected only to the surgical procedure. The glomerular filtration rate, as measured by inulin clearance, did not decrease significantly with maleic acid. In intact vitamin D-deficient chicks, 24 and 22 hr after i.p. administration of maleic acid and 14C-vitamin D3, respectively, the amount of 14C-1,25(OH)2D3 recovered in small intestine mucosa was reduced by one-half when compared to saline-treated controls. In kidney homogenates and isolated renal tubules of vitamin D-deficient chicks, activity of 25-hydroxyvitamin D3-1-hydroxylase was diminished immediately after maleic acid was administered in vivo or added in vitro to the incubation medium, respectively. These data provide the first demonstration that the renal capacity to convert 25(OH)D3 to 1,25(OH)2D3 can be substantially impaired in vivo by a renal disorder in which the glomerular filtration rate is not reduced.

Acetazolamide↗
PubMedDate not supplied

Renal deposition of cytomegalovirus antigen in immunoglobulin-A nephropathy.

Renal biopsy specimens from patients with various glomerular disorders were examined by indirect immunofluorescence microscopy with three different heterologous antibodies directed against cytomegalovirus and two heterologous antibodies against herpes simplex virus (HSV) type 1. All 31 samples from patients with immunoglobulin-A (IgA) nephropathy, 1 of 12 with systemic lupus erythematosus (SLE), and 1 of 5 with Henoch-Schönlein purpura (HSP) showed mesangial staining with cytomegalovirus antiserum, whereas no sample from 37 patients with other forms of glomerulonephritis was positive. Antigens of herpes simplex virus I were demonstrated in samples from 4 of 31 patients with IgA nephropathy, 1 of 12 patients with SLE, 1 of 5 patients with HSP, and 1 of 37 patients with other glomerular diseases. The consistent finding of glomerular cytomegalovirus antigen in IgA nephropathy suggests but does not prove that the virus has a role in the aetiology of this disorder.

Adolescent↗