Nutrition, acid-base status and growth in early childhood

Abstract

Optimal growth is only possible in a well-balanced "inner milieu". Premature infants are especially vulnerable for disturbances of acid-base metabolism with a predisposition to metabolic acidosis due to a transient disproportion between age-related low renal capacity for net acid excretion (NAE) and an unphysiologically high actual renal NAE on nutrition with standard formulas. During a 50 month period, 452 low birth-weight infants were screened for spontaneous development of incipient late metabolic acidosis (ILMA), an early stage during the development of retention acidosis, characterized by maximum renal acid stimulation (MRAS, urine-pH < 5.4) on two consecutive days but still compensated systemic acid-base status. Compared with controls, patients with ILMA showed higher serum creatinine values, an increased urinary excretion of sodium, aldosterone and nitrogen, but only slightly lower blood pH (7.38 vs 7.41) and base excess (-2.8 vs. 0.2 mmol/l) with respiratory compensation (PCO2 35 vs 37 mm Hg). Patients with altogether 149 episodes of ILMA were subsequently randomly allocated to either treatment with NaHCO3 2 mmol/kg/d for 7 days or no special therapy in protocol I, or NaHCO3 vs NaCl each 2 mmol/kg/d for 7 days in protocol II. Patients of protocol I with persistent MRAS for 7 days showed lowest weight gain and a tendency for a further increase in urinary aldosterone and nitrogen excretion. NaCl supplementation (protocol II) seemed to promote weight gain without affecting either impaired mineralization or suboptimal nitrogen retention. Patients with alkali therapy under both protocols showed normal weight gain and normalization of hormonal stimulation, mineralization (protocol II) and nitrogen assimilation. Modification of the mineral content of a standard preterm formula decreased renal NAE to the low level seen on alimentation with human milk and reduced the incidence of ILMA in preterm and small-for-gestational-age infants to 1%. The data show that ILMA is associated with impaired growth. Activation of secondary homeostatic mechanisms (extracellular volume contraction, depletion of disposable net base pools) might be important for impaired growth. Production of new formulas for reduced renal NAE could be an effective general preventive measure to reduce the clinical importance of one component of mixed acid-base disorders in early childhood.

Regulated acid–base transport in the collecting duct

“…The renin -angiotensin II -aldosterone system (RAAS) appears to be a major stimulator. RAAS activation occurs during metabolic acidosis (13,66,80,153) and blockade of the RAAS impairs renal acid excretion during acidosis (72,161). Moreover, deficiency of aldosterone secretion or signaling causes hyperkalemic distal renal tubular acidosis (60,104,161 …”

Food Composition and Acid-Base Balance: Alimentary Acid Load and Clinical Implications in Neonates

“…When net acid excretion is unable to match the non-volatile acids produced daily, positive acid balance leads to incipient or latent metabolic acidosis, and finally may result in manifest metabolic acidosis [2,3].…”

“…Although this diet-induced incipient metabolic acidosis does not produce major changes in the blood pH, it is associated with ongoing consumption of endogenous buffer reserves, clinically characterized by e.g. impaired bone mineralization and impaired growth [3]. The results of a prospective study in preterm neonates with birth weight below 1,500 g suggested that impaired acid-base homeostasis with a tendency towards metabolic acidosis might contribute to hypercalciuria and thus development of nephrocalcinosis in preterm infants [4].…”

“…Renal NAE in preterm infants is low on nutrition with human milk [3]. Moreover, human milk may contribute positively to a preterm infant's health and development [5], provided that the nutritional inadequacies of human milk for preterm infants are corrected, e.g.…”

The effect of dietary factors on the risk of developing urinary tract infection

“…Although scientists have known for several decades that the composition of the diet influences the urine pH, only recently has experimental and theoretical evidence been provided that it is possible to reliably calculate the potential renal acid load of foods and thus to estimate its influence on urine pH [2]. Patients with reduced renal function (e.g., preterm neonates and elderly persons) have a risk of suffering pathophysiological sequelae ("incipient late metabolic acidosis", chronic low-grade metabolic acidosis) of a food with a high acid load [3]. A possible chronic impact of food-borne acid load on urinary stone disease is generally accepted [4], and, for example, the effect on osteoporosis is still under discussion [5].…”