Biomedical subjects
Publications and source records attributed to E H Garin.
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Hypertension is a major medical problem with significant short- and long-term sequelae. Previous investigators have reported childhood hypertension to be secondary and when sexondary, renal. However, recent studies have shown primary (essential) hypertension to be more prevalent than secondary. Children with blood pressures at the 95th percentile for age deserve comprehensive evaluation and follow-up. Those with systemic evidence of side-effects will require therapy. Modern therapy should be based on pathophysiologic principles which include an understanding of volume-dependent and renin-dependent hypertension. The stepwise approach to therapy will produce the maximal therapeutic benefit.
One hundred forty-one children were selected from a clinic for children with recurrent bacteriuria to participate in a home culturing program. The parent was taught to employ a semiquantitative method to test the child's urine for bacteria. The degree and persistence of bacteriuria as detected by the parent strongly correlated with results obtained in the clinic, although there was a significant incidence of false-positive results as detected by the parent. Home culturing proved to be an inexpensive, reliable technique for following up children with recurrent urinary tract infections.
Twenty-five patients, aged six to 18 years, with lupus nephritis, followed for two to 103 months (median 22 months), have been classified according to renal histology into groups with diffuse proliferative glomerulonephritis (18), focal proliferative nephritis (2), and membranous nephropathy (5). Correlations have been made among specific histologic groups, clinical findings, renal function studies, urinary findings, and response to therapy. In sequential renal biopsies, lesions progressed in most patients with diffuse proliferative and membranous changes; however, chronic renal failure occurred in only one patient and the five-year survival rate (60.9%) is better than previously reported in pediatric patients.
This report evaluates the effectiveness of cephalexin in the treatment of bacteriuria in 93 children. Cephalexin therapy eradicated sensitive organisms in 97 per cent of the cases regardless of recurrence, structural abnormality, or status of renal function. Nevertheless, recurrences with a new, resistant organism occurred significantly in certain patients, expecially those with major anatomic abnormalities, during a six-week follow-up period. The incidence of drug reactions was low.
Membranous nephropathy and multiple sclerosis are believed to be mediated by immune mechanisms. A patient is reported with the first described association of membranous nephropathy and multiple sclerosis. Its significance and possible pathogenetic mechanisms are discussed.
Proteinuria in aminonucleoside of puromycin (PAN) nephrosis is due to an alteration of the glomerular charge- and size-selective barrier. Heparan sulfate seems to play a role in glomerular charge permeability to plasma proteins. We report a quantitative analysis and metabolism of glomerular basement membrane (GBM) heparan sulfate in PAN nephrosis. Studies were performed 5 and 10 days post-PAN administration (15 mg/100 g) to Sprague-Dawley rats. GBM heparan sulfate glycosaminoglycan was measured using the dimethylmethylene blue test after chromatographic separation of the digested GBM. Sulfate-35 uptake by GBM and catabolism of GBM-sulfated compounds were studied using glomerular cultures. The heparan sulfate glycosaminoglycans concentration on day 5 (1.42 micrograms/mg GBM protein) was within the normal range (1.17 +/- 0.25), but the concentration on day 10 was below the limit of detection (0.57 micrograms/mg). The sulfate-35 incorporated in the GBM glycosaminoglycan on day 5 (158 cpm/micrograms glycosaminoglycan) was lower than the uptake of control GBM (270 cpm/micrograms glycosaminoglycan), and markedly lower than the uptake on day 10 (1,590 cpm/micrograms glycosaminoglycan). The catabolism of the GBM sulfated compounds on day 5 and 10 was not different than the one seen in controls. These data suggest that PAN administration is associated with a decrease in synthesis of GBM-sulfated compounds on day 5 and a decrease in GBM heparan sulfate glycosaminoglycan on day 10. However, on day 10, an increased compensatory synthesis is observed. This may subsequently normalize the GBM heparan sulfate concentration and explain the resolution of the proteinuria.
We have previously shown a significant increase in 35sulfate uptake in rat glomerular basement membrane (GBM) when glomeruli were cocultured with peripheral blood mononuclear cells (PBMC) from idiopathic minimal lesion nephrotic syndrome (IMLNS) patients in relapse or with the supernatants of the same PBMC cultures. The purpose of this study was to determine the cell source of the supernatant factor. Rat glomeruli were cocultured with PBMC, with monocytes or with lymphocytes from 11 patients with IMLNS in relapse. Monocytes and lymphocytes were separated using adherence to plastic technique. Rat glomeruli cultured without PBMC served as controls. There was a significant increase in 35sulfate uptake in the GBM when glomeruli were cocultured with PBMC (geometric mean [GM]: 794 cpm/mg dry glomerular weight) as compared to glomeruli cultured with monocytes (GM: 316) (p less than 0.0005), glomeruli cultured with lymphocytes (GM: 309) (p less than 0.05), and glomeruli cultured alone (GM: 302) (p less than 0.00005). No significant differences in 35sulfate uptake were seen between monocytes, lymphocytes and glomeruli alone. These data showed that monocytes and lymphocytes are needed for the production of the supernatant factor that increases rat GBM 35SO4 uptake. Based on these and previous data (Concanavalin A stimulation of IMLNS PBMC results in an increased GBM uptake of 35sulfate, Pediatric Research 20: 321, 1986), we postulate that monocytes could trigger or amplify the production of the supernatant factor by lymphocytes.
Forty-seven biopsy specimens of renal allografts from pediatric transplant recipients were evaluated by light microscopy using a 117 item survey of histopathologic changes. The presence and distribution of immunofluorescent staining were also evaluated. Histopathologic findings associated with irreversible allograft rejection were determined using statistical methods and then correlated with one another. The effect on allograft survival when several of these features were present on the same specimen was assessed. Glomerular, arteriolar and small artery changes were associated with irreversible rejection. When several of these histologic findings occurred on the same biopsy specimen the allograft was always lost. Interstitial and tubular changes generally not predictive of rejection and immunofluorescent staining was not associated with graft loss.
The in vitro incorporation of 35sulfate into the glomerular basement membrane (GBM) of rats with puromycin aminonucleoside was compared with that of normal rats. 35Sulfate incorporation into the GBM of glomeruli from nephrotic rats did not differ significantly from that observed in normal rats. These data suggest that 35sulfate anionic charges in the GBM play no important role in the pathogenesis of the proteinuria in this experimental model.
We have studied the effect of peripheral blood mononuclear cells (PBMC) from nephrotic patients on the incorporation of 35Sulfate in rat glomerular basement membrane. 35Sulfate uptake increased when glomeruli were incubated with PBMC from 10 patients with idiopathic minimal lesion nephrotic syndrome (IMLNS) in relapse compared to simultaneous assays on 5 controls (2295 +/- 643 cpm/mg dry glomerular weight, mean +/- SEM, and 962 +/- 248 cpm/mg, respectively) (P less than 0.02). 35Sulfate incorporation did not increase when glomeruli were incubated with PBMC from seven nephrotic patients with other glomerulopathies (1283 +/- 642 cpm/mg) as compared to controls (1016 +/- 503 cpm/mg). No significant differences in 35Sulfate uptake were seen between glomerular cultures with and without control PBMC. These data show that PBMC from patients with IMLNS in relapse alter, at least in the rat GBM, the metabolism of sulfated compounds. Since these compounds have a role in glomerular permeability, this finding may have pathogenic significance.