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Biomedical subjects

I Greifer

Publications and source records attributed to I Greifer.

50 records · Page 3Linked to original sources

Late nonresponsiveness to steroids in children with the nephrotic syndrome.

Among 195 nephrotic children, ten developed resistance to prednisone therapy after responding to this drug on one or more occasions (late nonresponders). All were found to have "minimal lesions" on renal biopsy. Nine of these patients went into remission: one responded to further prednisone therapy, one went into remission while receiving azathioprine, and the remaining seven children responded to cyclophosphamide. Five of these seven patients subsequently relapsed; three of them have continued to respond to prednisone. The other two eventually became steroid resistant a second time, but in both instances a second course of cyclophosphamide again induced a remission. These nine patients have been followed for periods ranging from 6 months to 9.5 years (median = 53 months); all are doing well and have normal renal function. The tenth patient died from sepsis four months after the onset of steroid resistance.

Azathioprine↗

Recurrent hemolytic-uremic syndrome: a case report.

A girl who developed HUS at 2 years of age had four further episodes of the disease during the next 2 1/2 years. No renal or hematologic abnormalities were detected during or between the attacks. Reduced levels of serum complement were found during three of the episodes.

Child, Preschool↗

Hemodialysis at a summer camp.

A successful pediatric hemodialysis program was established at a summer camp. The dialysis campers had an opportunity to develop peer relationships and improve their self image by mastery of new skills and by increasing their sense of independence. Families were able to gain perspective on their child's development. The program will be continued and expanded. Further efforts will be made to determine how a vaction dialysis program aids in the rehabilitation of a dialysis patient,

Adolescent↗

Clinical manifestations of herpesvirus infections in pediatric renal transplant recipients.

We report our experience with 29 symptomatic herpesvirus infections occurring during the course of 87 pediatric transplant procedures performed over the 10-year period, 1973 to 1982. The yearly attack rate ranged from 0.05 to 0.40 case per cumulative patient years at risk. A greater proportion (9 of 14) of children who received more than 10 units of whole blood or packed red blood cells prior to transplantation developed a viral infection compared with those given 10 transfusions or fewer (8 of 25) (P = 0.10). Fever occurred in 22 (76%) children, pulmonary disease in 8 (28%), hepatitis in 11 (35%), leukopenia in 7 (24%), thrombocytopenia in 9 (31%) and central nervous system disease in 3 (10%). Herpesvirus infections were responsible for allograft loss in 7 (24%) patients. However, no differences in the actuarial graft survival curves were noted for transplants performed since 1979 in children with and without viral infection. The etiologic viral agents were cytomegalovirus in 19 (65%) episodes, herpes simplex virus in 8 (28%), Epstein-Barr virus in 2 (7%) and varicella-zoster virus in 2 (7%). Cytomegalovirus-infected patients were younger and more commonly developed primary infection compared with children with herpes simplex virus disease who were more likely to have secondary infection and to manifest a mucocutaneous vesicular rash. We conclude that the etiologic agents and clinical features of herpesvirus infections are similar in pediatric and adult renal allograft recipients. Moreover except for distinctive syndromes such as mucocutaneous vesicular eruption or a central nervous system lymphoma, the various herpes-viruses cause clinically indistinguishable illnesses in pediatric transplant patients with similar end organ involvement and untoward renal consequences.

Adolescent↗

Analysis of adhesion molecule expression by tubular epithelial cells using urine immunocytology.

On their surface, renal tubular cells present intercellular adhesion molecule-1 (ICAM-1) during acute renal allograft rejection. We propose that the extent of ICAM-1 expression by renal tubular cells can be estimated from urine immunocytology. To test this hypothesis, we obtained 52 samples of urine from 31 renal transplant recipients with either acute tubular necrosis, rejection or stable renal function. Cytocentrifuged aliquots of urinary sediment were incubated with monoclonal antibodies to ICAM-1 in an avidin-biotin-peroxidase technique. To corroborate our findings, biopsy specimens were obtained for conventional and immunohistology one hour following vascular anastomosis and during rejection episodes. The proportion of renal tubular cells that expressed ICAM-1 was low in patients with acute tubular necrosis (23.8 +/- 3.6%) and high in patients with rejection (53.1 +/- 4.4% [SEM]) (P < .001). In 11 patients who recovered from rejection, the proportion of ICAM-1-positive renal tubular cells decreased from 55.9 +/- 5.6% to 25.5 +/- 4.3% (P < .05). In two patients who initially had acute tubular necrosis and then rejected their transplants, the expression of ICAM-1 on renal tubular cells tended to increase (from 27.5 +/- 2.5% to 60.0 +/- 20.0%, P = .12). In eight patients with acute tubular necrosis who never rejected their transplants, ICAM-1 expression remained low (23.1 +/- 3.8%). Immunocytology correlated well with immunohistology and the clinical diagnosis. Our findings suggest that urine immunocytology may be useful in monitoring adhesion molecule expression by renal tubular cells.

Adult↗