Why the study?
Does intravenous infusion of 2.5% sodium chloride solution alter tubular sodium handling differently in normotensive patients with chronic glomerulonephritis compared to controls?
Does intravenous infusion of 2.5% sodium chloride solution alter tubular sodium handling differently in normotensive patients with chronic glomerulonephritis compared to controls?
Normotensive patients with early-stage chronic glomerulonephritis demonstrate exaggerated natriuresis in response to sodium loading due to decreased proximal tubular sodium reabsorption.
Supports differential tubular sodium handling in glomerulonephritis; hypothesis-generating and requires prospective validation before clinical consideration.
In 11 normotensive patients with biopsy verified chronic glomerulonephritis and 14 controls, glomerular filtration rate (GFR), proximal and distal tubular handling of sodium determined by the lithium clearance technique, and overall tubular sodium handling determined by absolute and fractional sodium excretion were measured before, during and after intravenous infusion of a 2.5% sodium chloride solution. Patients and controls were comparable by means of GFR in that no significant differences were found between the two groups either before, during or after sodium chloride infusion. During infusion both groups responded by a decrease in GFR (p less than 0.01 in both groups). Patients exhibited an increased natriuretic response during infusion both when measured as absolute and fractional sodium excretion (p less than 0.05 both). During the infusion the increase in absolute proximal output and decrease in fractional proximal and distal tubular sodium reabsorption were more pronounced in patients than in controls (p less than 0.05). It is concluded that patients with chronic glomerulonephritis at a very early stage of the disease where blood pressure and GFR are still normal respond with exaggerated natriuresis to hypertonic sodium chloride infusion. The exaggerated natriuresis is due to a decreased fractional proximal tubular sodium reabsorption in response to sodium loading.
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Sørensen et al. (1987) studied this question.
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