Low Creatininuria due to Hyponatremia Is Reversible in Many Patients

Abstract

<b><i>Background:</i></b> Chronic hyponatremia has been reported to be associated with low solute intake and low creatinine excretion (reflecting likely sarcopenia). We wanted to study the effect, on the long term, of correction of hyponatremia on solute and creatinine excretion in chronic SIADH. <b><i>Methods:</i></b> We made a retrospective review of clinical and biochemical data of patients with euvolemic hyponatremia. We analyzed 24-h urine solute and creatinine excretion in volunteers with hyponatremia induced by dDAVP over 4 days, in 12 patients with chronic SIADH (>1 month) before and after a few days of SNa correction and in 12 patients (6 women and 6 men) before and after 3 months of SNa correction by a vaptan or urea. <b><i>Results:</i></b> We confirm a low urine creatinine and solute excretion only in patients with chronic hyponatremia (>1 month). Correction of SNa (from 127 ± 2.3 mEq/L to 139 ± 2.8 mEq/L) for >3 months, in the 12 patients (mean age 58 ± 18), was associated with an increase in 24-h creatinine excretion (from 986 ± 239 to 1,238 ± 220 mg; <i>p</i> < 0.02) and in patients treated with a vaptan (<i>n</i> = 5) solute excretion increased from 656 ± 207 mmol/24 h to 960 ± 193 mmol/24 h (<i>p</i> < 0.02). Sodium excretion increased also in the 12 patients (from 100 ± 53 mEq/24 h to 169 ± 38 mEq/24 h; <i>p</i> < 0.01). <b><i>Conclusion:</i></b> Chronic hyponatremia (>1 month) is associated with a decrease in solute output (or intake) and in creatinine excretion. In many patients, these abnormalities are reversible in the long term.

What an Internist Need to Know About Hyponatremia?

“…Patients with chronic hyponatremia are frequently considered asymptomatic and left untreated when fluid restriction fails (WR). Hyponatremia has been associated with attention deficit gait disturbances falls [44,45] bone fractures [2] osteoporosis [46], sarcopenia [47] and an excess mortality [48]. The unstable gait and propensity to fall, observed in hyponatremia could result from nerve conduction velocity alterations [49].…”

“…The other therapeutic option consists of administering urea [47]. Urea which diffuses slowly into the brain (4 to 10 hours to equilibrate), allows a rapid reduction in brain oedema and in intracranial pressure, before any increase in serum sodium (see Figure 4).…”