1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known.
2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet.
3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate.
4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis.
5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels.
6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.