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Biomedical subjects

B L Warshaw

Publications and source records attributed to B L Warshaw.

28 records · Page 2Linked to original sources
PubMed1983

Captopril. Long-term treatment of hypertension in a preterm infant and in older children.

Five children with high-renin hypertension unresponsive to conventional medications were effectively treated with the angiotensin I-converting enzyme inhibitor, captopril, for six to 26 months. Age groups included children 6 to 13 years old and a 33-week gestation preterm infant with hypertension related to umbilical artery catheterization. Significant adverse reactions were limited to transient renal insufficiency in the preterm infant and increased azotemia in an older child with chronic renal failure.

Adolescent↗
PubMed1983

Renal tubular acidosis in a patient with recurrent metabolic alkalosis.

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine PCO2-blood PCO2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Acidosis, Renal Tubular↗
PubMed1982

Progression to end-stage renal disease in children with obstructive uropathy.

The course of 54 patients (35 boys and 19 girls) with end-stage renal disease resulting from obstructive uropathy was reviewed. The mean age at the initial sign of obstructive uropathy was 3.5 years. Twenty-two patients (41%) manifested evidence of obstructive uropathy during the first year of life. The mean age at the time of onset of ESRD (dialysis) was 12.2 years and was similar in boys and girls. The mean time interval between the first sign of obstructive uropathy and the initiation of dialysis was nine years. Fourteen patients operated upon at less than one year of age developed ESRD one to 20 years (mean ten years) following their initial surgery. Progression to ESRD occurred despite appropriate surgical management, including corrective as well as diversionary urologic procedures. However, because the patients were selectively referred for care of ESRD, no assessment of the incidence of ESRD caused by obstructive uropathy was possible. The data indicate that prolonged follow-up periods are necessary to assess the ultimate outcome of renal function in young patients with obstructive uropathy. Despite early intervention and intact renal function for many years during childhood, progression to ESRD may occur.

Adolescent↗
PubMed1980

Renal transplantation in children with obstructive uropathy.

The outcome of renal transplantation was examined in 52 pediatric patients (mean age 13 years) whose primary renal disease was obstructive uropathy. The bladder was used at transplantation in 45 allograft recipients, 39 of whom had had a previous lower urinary tract operation or bladder defunctionalization. An ileal loop was used in 7 recipients. The 52 patients received 73 renal allografts from 58 cadaver and 15 live-related donors. Presently, 40 patients (77 per cent) have functioning allografts, 4 have returned to dialysis and 8 (15 per cent) have died. The results indicate that the outcome of renal transplantation in patients with obstructive uropathy is similar to that of other transplant recipients. Damaged and defunctionalized bladders may be used successfully in most cases. If necessary an ileal conduit is an effective alternative. Post-transplant urologic complications occur with increased frequency but with appropriate management allograft salvage and patient survival are excellent.

Adolescent↗
PubMed1980

The effect of chronic furosemide administration on urinary calcium excretion and calcium balance in growing rats.

The study was designed to determine the calciuretic effect of furosemide and its impact upon calcium balance during chronic (25 days) furosemide administration to growing rats. Experiments were performed on 18 six-wk-old rats. Nine animals received furosemide, and 9 served as controls. The administration of furosemide in a dose of 40 mg resulted in a significant increase in calcium excretion in the treated group; urinary calcium excretion almost doubled that of the controls during the first 24-hr collection (3.74 +/- 0.44 mg in the treated animals compared with 1.90 +/- 0.15 mg in the controls; P less than 0.05). The average daily urinary calcium excretion during each of four subsequent 6-day periods remained approximately three-fold higher in animals which received furosemide compared with controls (P less than 0.001 for each 6-day period). The furosemide-induced increase in urinary calcium excretion did not diminish with time. Sodium excretion did not significantly increase either acutely or chronically in response to furosemide. Daily urinary volume increased approximately 40 to 60% in the furosemide-treated group compared with that of the controls (P less than 0.001). The cumulative calcium balance in the control group exceeded by 7% that of the furosemide-treated animals [2696.3 +/- 20.8 mg versus 2518.6 +/- 20.1 mg (P less than .001]. The findings indicate that distal nephron compensatory mechanisms effecting sodium conservation following furosemide do not result in similar conservation of calcium. Calcium balance may be deleteriously affected.

Administration, Oral↗
PubMed1979

Focal glomerulosclerosis and renal transplantation.

Eighteen patients with corticosteroid-resistant nephrotic syndrome developed end-stage renal disease and received one or more renal allografts. The lesion of focal segmental glomerulosclerosis and/or of focal glomerular obsolescence was demonstrable in the native kidneys of each patient. Following transplantation, nephrosis developed in three recipients. Two recipients developed nephrosis at two weeks and nine months posttransplant in association with rejection; the lesion of FGS was present in association with chronic rejection. Only one recipient developed recurrence of nephrosis and FGS unrelated to rejection. This was manifested by immediate onset of nephrosis in two successive allografts and histologic evidence of the lesion of FGS. The immediate recurrence in successive allografts suggests a circulating factor responsible for the renal lesion in this patient and indicates a separate etiology for a small number of patients with corticosteroid-resistant nephrosis and FGS.

Cadaver↗