Sodium and urea urinary saving patterns in the elderly can change according to circumstances

MUSSO, C.G.; JAUREGUI, R.; ANDRESIK, D.; VILAS, M.; SEGALINI, A.; VAZQUEZ, C.

INTERNATIONAL UROLOGY AND NEFROLOGY

Springer

Año: 2011 vol. 43 p. 611 - 612

0301-1623

Among the main physiological differences between the healthy young and old people is an increased sodium and urea urinary loss in the elderly patients in comparison with young ones. This difference becomes clearer during states of renal hypoperfusion where young patients show a sodium and urea saving patterns (fractional excretion of sodium 50%) [1, 2]. However, over many years of practicing geriatric nephrology, we have observed on certain occasions, such as states of severe dehydration, sodium depletion or cardiogenic shock, old patients may reach saving fractional excretion of sodium and urea values similar to those in young persons.In order to illustrate the above-mentioned phenomenon, we present a patient with such exceptional finding: this 78?year-old woman, with a past history of gastro-oesophageal reflux (on omeprazol 40 mg/day), osteoporosis (calcium-carbonate 2 g/day), chronic malnutrition due to anorexia secondary to psychological negativism (she was neither suffering from chronic sepsis nor an oncologic disease), was admitted in our nursing home. In order to improve her nutritional status, she was started on tube feeding with 2 l/day of hypotonic enteric nutrition. Two weeks later, she developed asymptomatic hyponatremia. Her serum potassium, acid?base status, creatinine and urea were within normal range, and she had no oedema. She was not suffering from congestive cardiac failure, cirrhosis, or hypothyroidism. Her urinary indices showed low fractional excretion of sodium and urea (Table 1). Due to the clinical situation, urinary indices and the persistence of her hyponatremia despite the implementation of water restriction, we suspected that she developed hyponatremia secondary to sodium depletion. Consequently, sodium (3 g NaCl/day was added to her feeding bottles) and after that her serum sodium normalized, and her urinary indices values rose (Table 1) without developing either oedema or hypertension. It has already been demonstrated that the above-mentioned senile sodium urinary loss in the elderly is the result of the combination of many mechanisms such as [2, 3, 4]: (A) Reduction of sodium reabsorption in the thick ascending loop of Henle, which is attributed to the reduction in the number of sodium transport mechanism (sodium?potassium-2chloride: NK2Cl) in this segment. (B) Serum renin and aldosterone levels and their response to hypovolemia are both diminished in old age. (C) The elevated serum and urinary natriuretic peptide levels may be another cause for the characteristic urinary sodium loss of this population. Regarding urea handling by the senile kidney, it has already been described that basal fractional excretion of urea value is increased in the aged people compared with young ones: 65% vs. 50%, respectively [3]. It was proposed that this phenomenon could be explained by reduced distal urea reabsorption secondary to diminished number of urea channels (UT1) in senile collecting tubules.