Key result
Infusion of atrial natriuretic peptide at 16 ng/kg/min increased urinary sodium excretion from 0.12 to 0.42 mEq/min in patients with chronic renal failure and from 0.13 to 0.73 in those without.
Why the study?
Does stepwise infusion of atrial natriuretic peptide improve natriuresis in glomerulonephritic patients with or without moderate renal failure?
Does stepwise infusion of atrial natriuretic peptide improve natriuresis in glomerulonephritic patients with or without moderate renal failure?
In patients with glomerulonephritis and chronic renal failure, ANP retains its natriuretic efficacy, and supraphysiological doses lead to significant natriuresis and extranatriuretic effects.
Answers are grounded in this paper and cite their sources.
ANP may retain natriuretic efficacy in glomerulonephritis with renal failure; hypothesis-generating for therapeutic use pending controlled trials.
It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP). In this study, plasma ANP (pANP) and renal function were evaluated during stepwise infusion of low ANP doses (2, 4, 8, and 16 ng/kg per min) in glomerulonephritic patients with (CRF) or without (GN) moderate renal failure, and in normal subjects (NOR), kept at low-sodium diet (LSD; 35 mEq NaCl/day). To assess the physiological ANP levels, pANP was also measured in the three groups after normal-sodium diet (NSD; 235 mEq NaCl/day). ANP did not affect systemic and renal perfusion at any of the doses tested; a significant increment of GFR was observed only in NOR and GN. The 2-, 4-, and 8-ng/kg doses increased pANP to values overlapping the physiological concentrations measured at NSD; this was associated with a dose-dependent increment of urinary excretion of sodium (UNaV) that reached analogous levels in the three groups. ANP accounted for approximately 40% of the UNaV increment evoked by NSD in patients and in normal subjects. The 16-ng/kg dose led to supraphysiological levels that induced a similar marked enhancement of UNaV (from the basal value of 0.12 +/- 0.02 to 0.42 +/- 0.08 mEq/min in CRF, from 0.13 +/- 0.02 to 0.73 +/- 0.08 in GN, and from 0.09 +/- 0.02 to 0.49 +/- 0.11 in NOR). In CRF, the normal natriuretic response to the highest dose was caused by a larger increase of fractional UNaV that was strictly dependent on the greater pANP increment, as demonstrated by similar changes in the fractional excretion of cGMP, and, in part, on the greater aldosterone decrease. In all groups, ANP also induced a dose-dependent urinary loss of phosphate, potassium, and urea, resulting in a significant 15 to 25% decrease in the plasma levels. Thus, in GN and CRF patients, ANP plays a significant role in the renal handling of sodium; moreover, the achievement of low supraphysiological pANP levels leads to a conspicuous natriuresis associated with unique extranatriuretic effects.
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Nicola et al. (1997) studied Glomerulonephritis with or without moderate renal failure. Atrial natriuretic peptide (ANP) vs. Basal values was evaluated on Urinary excretion of sodium (UNaV). Infusion of atrial natriuretic peptide at 16 ng/kg/min increased urinary sodium excretion from 0.12 to 0.42 mEq/min in patients with chronic renal failure and from 0.13 to 0.73 in those without.
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