PubMed Health⌕ Search

Biomedical subjects

B H Brouhard

Publications and source records attributed to B H Brouhard.

At least 91 records · Page 5Linked to original sources
PubMed1982

Idiopathic membranous nephropathy in children.

To determine the prognosis in children with membranous nephropathy, we reviewed the clinicopathologic features and outcome of 22 patients, 11 male and 11 female, age 11 months to 19.9 years (mean 12.0 years). Patients had biopsies within six months of onset of symptoms and were divided into two groups according to the biopsy findings: group 1 (Stages I and II) and group 2 (Stages III and IV). Follow-up time was identical in both groups (mean 4.8 years). The nephrotic syndrome was present in 13 of 16 patients in group 1 and in all six patients in group 2. In group 1, eight of the 16 patients had repeat biopsies one to 11 years (mean three years) after onset. Of these, two progressed to Stages III and IV, whereas progression to renal insufficiency occurred in only one. In group 2, two of the six patients had repeat biopsies two years after onset and remained in the same group; progression to renal insufficiency occurred in five of the six patients. The difference in progression to renal insufficiency between the two groups is significant (P = 0.001). The stage of glomerular lesion at the time of onset seems to be a factor in predicting the prognosis of membranous nephropathy in pediatric patients.

Adolescent↗
PubMed1982

Immune deposits and mesangial hypercellularity in minimal change nephrotic syndrome: clinical relevance.

Occasional patients with nephrotic syndrome and minimal histologic change demonstrate glomerular deposition of small amounts of immunoglobulin and complement. Some consider this a disease distinct from MCNS. To investigate the clinical importance of immune deposits and mesangial hypercellularity in the initial biopsy, the clinical records, follow-up data, and renal biopsies of 68 patients (ages 6 months to 16 years) with MCNS by light microscopy were reviewed. Among 68 patients followed a mean of 6.2 years, eight of 25 patients with immune deposits on initial renal biopsy were steroid nonresponsive. Only one of 43 patients without immune deposits was steroid nonresponsive (P = 0.00005). Of 44 patients with normal mesangial cellularity, 31 experienced fewer than three relapses a year, whereas of 15 patients with mesangial hypercellularity, only six experienced fewer than three relapses a year (P = 0.035). The data suggest that immune deposits and increased mesangial cellularity in children with NS and minimal light microscopic change may predict the clinical course.

Adolescent↗
PubMed1982

Effects of hemodialysis and dimercaprol in acute dichromate poisoning.

A 22-month-old infant died after ingesting sodium dichromate his father had brought from work. Treatment included folic acid and dimercaprol administration, hemodialysis, and exchange transfusion. To evaluate this treatment, four dogs were hemodialyzed after receiving intravenous sodium dichromate: their dialyzer chromate clearance was similar to their renal chromate clearance and their dialyzer chromate clearance was not significantly different before or after dimercaprol administration. This and other cases in the literature indicate that although chromate poisoning is often fatal, supportive care, forced diuresis, and chelating agents may be helpful. Hemodialysis may be required if renal failure occurs. Awareness of toxicity and prevention remain the most important approaches.

Acute Disease↗
PubMed1982

Urinary kallikrein excretion in renal transplant patients.

Urinary kallikrein, as a reflection of the intrarenal kallikrein, is distinct from plasma kallikrein. The kallikrein-kinin system, activated via antigen-antibody complexes, has been implicated in the pathophysiology of acute transplant rejection. We studied urinary excretion of sodium, potassium, protein, and kallikrein following renal transplantation in nine patients, In four patients who took steroids daily and were followed from the time of transplantation (without rejection episodes), urinary kallikrein remained stable (3.7 +/- 0.5 EU/24 hr, x +/- SEM). Since sodium-retaining steroids influence urinary kallikrein excretion, two patients were studied 2 and 3 months post-transplantation while receiving alternate-day prednisone. Values from urinary kallikrein in these patients did not differ from those in patients taking steroids daily (3.7 +/- 0.5 versus 2.7 +/- 0.3 EU/24 hr). In three patients experiencing acute rejection episodes, urinary kallikrein excretion rose markedly (24 to 260 EU/24 hr) and remained elevated until the patients became oliguric. Furthermore, this rise occurred 1-3 days before the clinical diagnosis of rejection was made. For the group as a whole there was no significant correlation between urinary kallikrein excretion, the excretion of sodium or potassium, or urine volume. Although the number of patients studied is small, the increases observed in urinary kallikrein suggest that activation of the intrarenal kallikrein-kinin system is associated with acute transplant rejection.

Adolescent↗
PubMed1982

Focal segmental glomerulosclerosis, crescent, and rapidly progressive renal failure.

The usual clinical course of focal segmental glomerulosclerosis is marked by progressive decrease in renal functional and sclerosis on biopsy over a period of months to years. We report a variant exemplified by 2 children who developed chronic renal failure within 12 weeks of the onset of nephrotic syndrome; repeat renal biopsies demonstrated extensive extracapillary glomerular proliferation and crescent formation. Both were males, less than 5 years of age, presenting with nephrotic syndrome resistant to steroid therapy and normal renal function. Renal biopsies done after 8 weeks of therapy, demonstrated findings compatible with focal segmental glomerulosclerosis. Within 12 weeks of onset of nephrotic syndrome, both patients experienced a decrease in renal function requiring dialysis. Repeat renal biopsies revealed extensive extracapillary glomerular proliferation with crescent formation. These patients represent a variant of focal segmental glomerulosclerosis characterized by rapid progression to renal failure with extensive extracapillary glomerular proliferation and crescent formation.

Biopsy↗
PubMed1981

The association of idiopathic hypercalciuria and asymptomatic gross hematuria in children.

Seven children with asymptomatic gross hematuria are described. Six had recurrent hematuria; one had a single episode. Occasional global glomerulosclerosis and/or mesangial electron dense deposits were present in the three patients in whom renal biopsy was performed; the changes were felt to be insufficient to account for the hematuria. None of the patients had urolithiasis or any significant urinary tract abnormality. One was an adopted child; a family history of urolithiasis was obtained in the other six. Idiopathic hypercalciuria was documented in six patients; the seventh subsequently passed a calcium oxalate calculus. One patient is 10 weeks of age at the time of this submission. Of the remainder, three patients received no specific therapy; renal calculi developed six months, six years, and eight years later. Three patients were treated with a thiazide diuretic soon after onset of hematuria and confirmation of idiopathic hypercalciuria; there was complete cessation of hematuria within five days with no recurrence as long as therapy was continued. We suggested that measurement of urinary calcium excretion as part of the initial evaluation of a child with gross hematuria may, in some cases, obviate invasive investigations and allow for effective therapy.

Calcium↗
PubMed1981

Adverse reactions to parenteral lincomycin.

Lincomycin use has not been reported exclusively in children and inasmuch as it has been extensively used at our institution, a chart review of 265 patients who received parenteral lincomycin at a dose of 100 mg/kg/day in four divided doses for five days or longer was undertaken. The following conditions were diagnosed: cellulitis, 39%; septic arthritis, 21%; osteomyelitis, 16%; abscess, 13%; lymphadenitis, 9%; and pneumonia, 1%. Cures were achieved in all. The majority of organisms cultured were Staphylococcus aureus and Streptococcus pyogenes. Duration of therapy ranged from five to 63 days, with a mean of 15 days. The lincomycin dose ranged from 75 to 2,400 mg every six hours. The majority of patients received the drug intravenously, but 25.7% received it only intramuscularly. There were no adverse reactions at the administration sites. Only 3% of the patients developed diarrhea, which was not felt to be secondary to the drug. There were no cases of pseudomembranous colitis. Therefore parenteral lincomycin in children appears to be a safe and effective antibiotic when used for infections due to Gram-positive cocci.

Abscess↗
PubMed1980

Observations on prostaglandins in normal and leukemic human lymphocytes.

Prostaglandins E (PGE) and F2 alpha (PGF2 alpha) were measured in lymphocytes of normal subjects, children with acute lymphocytic leukemia (ALL), and adults with chronic lymphocytic leukemia (CLL). In ALL lymphocytes PGE increased from a normal value of 25 pgrams to 270 pgrams/10(6) cells, and PGF 2 alpha increased from a normal value of 31 pgrams to 482 pgrams/10(6) cells. In CLL lymphocytes, levels of PGE and PGF2 alpha were normal or low. When normal lymphocytes were stimulated with phytohemagglutinin (PHA), the level of PGE and PGF2 alpha fluctuated, followed by corresponding changes in the level of cyclic nucleotides. In cultured ALL lymphocytes, the level of PGE remained high, while cyclic 3':5'-adenosine monophosphate (c-AMP) level was constantly low, and the initial level of PGF2 alpha fluctuated in relation to similar oscillations of cyclic 3':5'-guanosine monophosphate (c-GMP). These values were lower, although not significantly, when ALL lymphocytes were stimulated with PHA. When CLL lymphocytes were stimulated with PHA, the level of PGE remained low (20 pgrams), as did that of c-AMP. The level of PGF2 alpha, after a brief initial increase (130 pgrams), returned to and remained at a lower level (60 pgrams) while the level of c-GMP was persistently high. These results suggest: (1) prostaglandins may indirectly influence the cell cycle, possibly through modulation of cyclase activity and levels of cyclic nucleotides; and (2) some derangement of this regulatory mechanism may be present in leukemic lymphocytes.

Adult↗
PubMed1980

Rapidly progressive glomerulonephritis in children: a report of thirteen cases and a review of the literature.

The clinical course and outcome of rapidly progressive glomerulonephritis (RPGN) of variable etiology are not well defined in children. The present investigation reports on the clinical characteristics, the course and outcome, as well as the results of treatment of 13 children with apparent postinfectious RPGN. Three of 7 patients with documented streptococcal RPGN and 3 of 6 patients with RPGN of nonstreptococcal etiology progressed to chronic renal failure. In some patients, anticoagulant and antiplatelet therapy appear to have improved survival. The severity of crescent formation, not the presumable etiology, appears to be a reliable prognosticator.

Adolescent↗
PubMed1979

Phototherapy and plasma immunoreactive prostaglandin A values. Its effect in premature infants.

Plasma immunoreactive prostaglandin A (iPGA) values were determined for 14 premature infants before and after 48 hours of phototherapy and in a control group of six age-matched premature infants. At 4 to 8 days of life, the infants who had received phototherapy for 48 hours had significantly lower iPGA values compared with controls. At 2 to 3 days of life, four infants with a clinically apparent patent ductus arteriosus were found to have significantly elevated iPGA values compared with controls. After 48 hours of phototherapy, these infants likewise had a significant decrease in iPGA values compared with controls; in all four infants, the ductus closed spontaneously. Phototherapy is an effective method for decreasing plasma iPGA values in premature infants.

Ductus Arteriosus, Patent↗
PubMed1979

Effect of inhibiting prostaglandin synthesis on edema formation and albumin leakage during thermal trauma in the rat.

Prostaglandins (PGs) participate in the inflammatory response, but the contribution of endogenously synthesized PGs to edema formation and increased vascular permeability is not known. Using a 10% scald burn in the rat, we measured water content (as percent, wet minus dry/wet weight) and 131I-RISA leakage (counts/g dry tissue) in scalded and normal skin at 30 minutes and 3 hr post injury. Four groups (10 rats/group) in each time period studied: control; scald; scald, 5 mg/kg indomethacin; scald, 10 mg/kg indomethacin. Indomethacin was administered intravenously 30 minutes before the scald; RISA was injected intravenously 30 min before termination of the study. In all indomethacin-treated groups immunoreactive plasma PGA was significantly lower (p less than 0.05) than in scalded, untreated groups. All scalded groups showed significantly higher RISA counts and water content than did the control group (p less than 0.01). At 30 min post-injury the indomethacin -treated groups did not differ from the untreated scald group (p greater than 0.20). In the 3 hour study all scalded groups had significantly higher content and RISA counts than control (p less than 0.01). Thus PGs produced during thermal trauma do not greatly contribute to the edema formation and increase in vascular permeability.

Albumins↗
PubMed1979

Urinary kallikrein excretion in idiopathic nephrotic syndrome.

The plasma kallikrein-kinin system, a potent vasodilator, has been implicated in causing the protein loss of the idiopathic nephrotic syndrome. However, the kidney possesses a kallikrein-kinin system separate from the plasma system. Thus, urinary kallikrein may reflect more accurately intrarenal events. Using a radiochemical esterolytic assay we measured the urinary kallikrein excretion in a patient with a minimal lesion nephrotic syndrome during relapse. Protein excretion was initially elevated (8.1 plus or minus 2.0 gm. per 24 hours) as was urinary kallikrein excretion (96.4 plus or minus 46.6 EU per 24 hours). After initiation of steroid therapy protein and kallikrein excretion decreased significantly (p less than 0.05). During the entire study kallikrein excretion was significantly correlated with protein excretion (r equals 0.89, p less than 0.01). It is tempting to speculate that activation of the intrarenal kallikrein-kinin system participates in the protein loss characteristic of the nephrotic syndrome.

Amylases↗