Renal hemodynamic changes in humans: Response to protein loading in normal and diseased kidneys

This study was undertaken to define the renal hemodynamic changes that mediate the acute response to an oral protein load. Three groups of subjects were studied: (1) disease-free subjects; (2) patients with chronic renal disease of various causes, except for diabetes mellitus, documented by history...

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Veröffentlicht in:The American journal of medicine 1986-11, Vol.81 (5), p.809-815
Hauptverfasser: Bosch, Juan P., Lew, Susie, Glabman, Sheldon, Lauer, Allan
Format: Artikel
Sprache:eng
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Zusammenfassung:This study was undertaken to define the renal hemodynamic changes that mediate the acute response to an oral protein load. Three groups of subjects were studied: (1) disease-free subjects; (2) patients with chronic renal disease of various causes, except for diabetes mellitus, documented by history and/or renal biopsy; and (3) patients with diabetes mellitus, that is, a history of hyperglycemia requiring antihyperglycemic therapy. All subjects were studied before (baseline) and after (test) ingestion of a protein load. Glomerular filtration rate and effective renal plasma flow were evaluated by inulin and para-aminohippurate, respectively. In the disease-free subjects, the mean baseline glomerular filtration rate and renal plasma flow were 122 ± 10 ml/minute/1.73 m 2 and 644 ± 64 ml/minute/1.73 m 2, whereas test glomerular filtration rate and renal plasma flow were 151 ± 15 ml/ minute/1.73 m 2 and 791 ± 111 ml/minute/1.73 m 2, respectively. In patients with chronic renal disease, the test glomerular filtration rate and renal plasma flow were related to the severity of the disease. The more severe the disease, the lower the absolute test values and the smaller the increment from baseline to test values. Patients with diabetes mellitus had a paradoxic response to ingestion of a protein load. Glomerular filtration rate fell while renal plasma flow remained unchanged. This response was observed in all diabetic patients regardless of the type of diabetes or whether clinical evidence of diabetic nephropathy was absent, minimal, or severe.
ISSN:0002-9343
1555-7162
DOI:10.1016/0002-9343(86)90350-5