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      Perfusion of the Residual Renal Cortex in Patients with Chronic Renal Disease

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          In 32 patients with chronic renal disease due to glomerulonephritis, pyelonephritis, advanced nephrosclerosis or renal allograft rejection, xenon washout from the diseased kidney was analyzed by the method of maximum likelihood, which provides an excellent fit to the data even when the rapid component of xenon washout represents only 10% of total blood flow. A reduction in mean renal blood flow and the fraction of flow entering the most rapid, or cortical, component of renal blood flow are already established in chronic renal disease. This study was designed to assess the flow rate in the residual, most normal renal cortex. A significant correlation was established between the serum creatinine concentration (x) and the rapid component flow rate over a range of serum creatinine concentrations from 1.0 to 8.0 mg/dl (y = 3.65 – 2.87 logio x, r = 0.59; F = 34.2; p < < 0.0l). Intrarenal perfusion rates did not vary with diagnosis but the rapid component flow rate was significantly higher when hypertension was minimal or absent (3.05 ± 0.30 vs. 2.27 ± 0.20 ml/g/min; p < 0.02) than in patients in whom hypertension represented a major clinical problem. According to the intact and adaptive nephron hypotheses, a normal or even increased rapid component flow rate was anticipated. The results of this study do not deny these hypotheses, which rest on a substantial body of data, but suggest that additional factors are operative in patients with chronic renal disease and make the ability of the chronically diseased kidney to maintain a semblance of order even more remarkable. The possibility that prolonged hypertension contributes to the abnormality of kidney and its ultimate destruction has therapeutic implications.

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          Author and article information

          S. Karger AG
          02 December 2008
          : 22
          : 1-3
          : 81-90
          Departments of Radiology and Medicine, Harvard Medical School and Peter Bent Brigham Hospital, Boston, Mass.
          181426 Nephron 1978;22:81–90
          © 1978 S. Karger AG, Basel

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          Pages: 10
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