Advertisement
Research Article Free access | 10.1172/JCI109784
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Ichikawa, I. in: JCI | PubMed | Google Scholar
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Purkerson, M. in: JCI | PubMed | Google Scholar
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Klahr, S. in: JCI | PubMed | Google Scholar
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Troy, J. in: JCI | PubMed | Google Scholar
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Martinez-Maldonado, M. in: JCI | PubMed | Google Scholar
Laboratory of Kidney and Electrolyte Physiology, Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts 02115
Renal Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Brenner, B. in: JCI | PubMed | Google Scholar
Published May 1, 1980 - More info
To determine the physiological basis for the low glomerular filtration rate in chronic malnutrition, micropuncture studies were performed in Munich-Wistar rats chronically pair-fed isocaloric diets of either low (group 1, nine rats) or high protein content (group 2, nine rats). Despite the absence of hypoalbuminemia, average values for single nephron and total kidney glomerular filtration rate were nearly 35% lower in group 1 than in group 2. Mean values for glomerular capillary and Bowman's space hydraulic pressures were essentially identical in the two groups, thereby excluding glomerular transcapillary hydraulic pressure difference as the cause for the low filtration rates in group 1 animals. On the other hand, average glomerular capillary plasma flow rate and glomerular capillary ultrafiltration coefficient were significantly lower (by ∼25 and ∼50%, respectively) in group 1 than in group 2. The fall in glomerular capillary plasma flow rate was the consequence of increased afferent and efferent arteriolar resistances. Plasma and erythrocyte volumes were found to be equal in five additional pairs of group 1 and group 2 rats. Thus, the substantial alterations in the ultrafiltration coefficient, glomerular capillary plasma flow rate, and renal arteriolar resistances responsible for the low filtration rate in group 1 animals were not merely a consequence of decreased circulating blood or plasma volumes. Mean values for glomerular cross sectional area were significantly lower in group 1 than in group 2 despite similar values for kidney weight in the two groups. This reduction in glomerular cross sectional area in group 1 rats is presumed to reflect a decrease in effective filtration surface area and therefore likely accounts, at least in part, for the decline in ultrafiltration coefficient observed in this group.
Finally, since the daily caloric intake of group 2 animals was restricted because of pair feeding requirements tied to the group 1 rats, we studied a third group of seven rats (group 3) allowed an ad lib. intake of the same high protein diet as given to group 2 rats. Average values for single nephron glomerular filtration rate and its determinants were found to be indistinguishable between groups 2 and 3. These results suggest that low protein intake, rather than calorie deficiency per se, is primarily responsible for the reduction in filtration rate seen in this experimental model of chronic malnutrition.
Images.