URINARY SODIUM-EXCRETION IN PATIENTS WITH NEPHROTIC SYNDROME, AND ITSCIRCADIAN VARIATION

We analysed sodium excretion and its circadian variation in 70 patient s with nephrotic syndrome and 19 healthy controls over 1-3 days, with a regimen of bed rest and constant sodium intake around the clock. We sampled urine and blood and took their blood pressure every 3 h. We al so scored 60 renal biopsies for presence of interstitial fibrosis and tubular atrophy. Peripheral oedema was estimated in 37 patients. Fifty -nine patients excreted >10 mmol sodium per 24 h, in equilibrium with dietary intake. In group A (n=24),sodium excretion followed a normal c ircadian rhythm, with a daytime peak. In group B (n=35), 29 had revers ed circadian rhythm with a night-time peak, and 6 had no apparent rhyt hm. Nephrotic syndrome was more severe in group B than in A (serum alb umin 19.5 vs. 24.1 g/l, p<0.05; oedema 7.0 vs. 3.8 kg, p<0.01). Group B also had signs of more advanced renal disease (GFR 49 vs. 99 ml/min; number of biopsies with tubulointerstitial damage: 20/28 vs. 4/23; p< 0.001). Reversed sodium rhythm was associated with reversed circadian rhythms for GFR, effective renal plasma flow and urine flow, and blunt ing or reversal of the day-night differences in blood pressure and pla sma renin activity. Eleven patients had urinary sodium excretion <1 mm ol/24 h. With respect to severity of nephrosis, they resembled group B , but GFR and incidence of tubulointerstitial lesions were like group A. Half of the patients with nephrotic syndrome had reversed circadian rhythm for sodium excretion. This nocturnal peak in natriuresis (and diuresis) may be due to re-entry of oedema fluid into the circulation, with a subsequent increase in renal blood flow and GFR, and especiall y occurs in patients with structural tubulointerstitial damage, where sodium reabsorption is incomplete.