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      Effects of Ionizing Radiation on Progressive Experimental Renal Disease: A Hemodynamic Approach

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          In order to evaluate the progression of renal disease, Munich-Wistar rats were submitted to 5/6 nephrectomy and given whole-body x- or γ-irradiation with or without remnant kidney protection or were submitted only to remnant kidney irradiation. All groups received a single 6-Gy dose immediately after surgery. Whole-kidney function, glomerular hemodynamics, 24-hour proteinuria and histopathology were assessed 60 days after surgery and irradiation. The irradiated nephrectomized animals presented whole-kidney function parameters comparable to those of normal rats. In addition, they were less hypertensive and had higher hematocrit. They showed glomerular hyperfiltration and hypertension even greater than their respective nephrectomized controls. However, the interrelations among the glomerular filtration determinants were somewhat different in irradiated animals. Their 24-hour proteinuria was significantly lower and the sclerosis index and tubulointerstitial injury score were markedly smaller. Among irradiated animals, the worst sclerosis index was observed in those with a shielded remnant kidney and the best in those without protection of the remnant kidney. This led us to speculate about a possible influence of resident mesangial cells on the early events following renal mass ablation and on the maintenance of subsequent physiopathologic changes. Therefore, radiation undoubtedly provoked a beneficial change in the course of renal disease when the renal mass ablation model was employed. Many factors could have contributed to this favorable feature including lower levels of systemic arterial pressure, less increment in ΔP, diminished proteinuria, and maintenance of tubulointerstitial space integrity. Our data also suggest that development of glomerulosclerosis seems to be determined by events occurring immediately after injury.

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          Recent advances in radiation oncology.

          Radiotherapy remains an important component of the management of malignant disease. Especially when combined with cytotoxic chemotherapy, limited surgical excision, or both, irradiation has been shown to control disease in the primary site and regional nodes without the need for surgical extirpation as frequently as in past years. New developments in three-dimensional treatment planning and the precise delivery of high-dose radiation promise to increase the benefit of radiation treatment. Finally, molecular studies of the cell's response to radiation and the phenomena of DNA damage and repair are providing explanations for heretofore unexplained radiobiologic observations. Such research is laying the groundwork for targeted manipulation of the cell's response to radiation, which will be tested in the near future.
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            A comparative study of total body irradiation as a method of inducing granulocyte depletion in mice.

            Since conventional methods of inducing depletion of polymorphonuclear granulocytes (PMNs) in mice, such as treatment with cytostatic drugs and anti-PMN sera, proved to be insufficient to induce a stable PMN depletion for several days, and were accompanied by considerable toxic side effects, we induced neutrophil depletion in mice by total body irradiation (TBI) in a single dose of 6.0 Gy (600 rads.) at a dose rate of 0.20 Gy/min. This treatment reduced the number of PMNs in the peripheral circulation to values below 150/microliter from day 3-10 after irradiation. The number of lymphocytes fell simultaneously. Platelet counts remained above 60% of normal values during the first 7 days after irradiation. Complement levels were not significantly affected by TBI. The results show that TBI of 6.0 Gy induces pronounced and stable PMN depletion in mice for at least 7 days. Furthermore, under an aseptic regimen the mice can be kept in good condition and losses are less than 5%.

              Author and article information

              S. Karger AG
              22 January 2001
              : 87
              : 1
              : 58-65
              Escola Paulista de Medicina, Universidade Federal de São Paulo, SP, Brazil
              45885 Nephron 2001;87:58–65
              © 2001 S. Karger AG, Basel

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              Figures: 1, Tables: 4, References: 37, Pages: 8
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/45885
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