Growth rate in infants with impaired renal function

doi:10.1016/S0022-3476(88)80661-9

The Journal of Pediatrics

Volume 113, Issue 3, September 1988, Pages 594-600

https://doi.org/10.1016/S0022-3476(88)80661-9 Get rights and content

We report changes in renal function and growth rate in children with reduced renal function who were kept on a low normal phosphorus formula until 18 months of age. The relationship between serum creatinine values and derived creatinine clearance and residual renal function is reviewed regarding the risk of progressive loss of function. Expressing growth as growth velocity standard deviation scores over 6-moth intervals gave a more accurate description of growth performance than did change in height standard deviation scores. A relationship between residual clearance and growth velocity was inferred. However, the growth of children with a less severe reduction in function was affected intermittently by intercurrent infections and inadequately treated acidosis and salt wasting. Children with a more severe reduction in function, despite maintenance on the low-phosphorus formula, had elevated serum parathormone levels. We conclude that following growth (as serial growth velocity standard deviation scores) in relation to other variables gives more insight into factors affecting growth in these children; the level of residual function affects growth potential but other complicating factors also have an effect.

References (21)

RizzoniG et al.
Growth in children with chronic renal failure on conservative management
Kidney Int
(1984)
HollidayMA et al.
Pitressin-resistant hyposthenuria in chronic renal disease
Am J Med
(1967)
ShemeshO et al.
Limitations of creatinine as a filtration marker in glomerulonephritis patients
Kidney Int
(1985)
Rodriguez-SorianoJ et al.
Fluid and electrolyte imbalances in children with chronic renal failure
Am J Kidney Dis
(1986)
ChantlerC et al.
Growth in children with renal disease
Clin Nephron
(1973)
BettsPR et al.
Growth pattern and dietary intake of children with chronic renal insufficiency
Br Med J
(1974)
HostetterTH et al.
Hypofiltration in remnant nephrons: a potentially adverse response to renal ablation
Am J Physiol
(1981)
KleinknechtC et al.
Growth and development of nondialyzed children with chronic renal failure
Kidney Int
(1983)
BarrattTM et al.
Assessment of growth
Am J Kidney Dis
(1986)
SchwartzGJ et al.
A simple estimate of glomerular filtration rate in children derived from body length and plasma creatinine
Pediatrics
(1976)

There are more references available in the full text version of this article.

Cited by (10)

Analysis of novel heterozygous mutations in the CYP11B2 gene causing congenital aldosterone synthase deficiency and literature review
2019, Steroids
Citation Excerpt :
Consistent with previous studies, this patient illustrates a relationship between hyponatremia and failure to thrive. Salt wasting could be a factor leading to impaired growth [26,27], possibly due to insulin-like growth factor-1 (IGF-1) suppression or reduced extracellular fluid volume [28,29], but the exact mechanism of this association is not clear. In contrast to the common dose of 100 μg/d in other cases, our patient underwent fludrocortisone therapy initiated at 75 μg/d, and gradually reduced to 50 μg/d. Fludrocortisone treatment is essential for patients with ASD, but symptoms of salt wasting improve with age; eventually, the therapy can be discontinued for most children when they grow older.
Aldosterone synthase deficiency (ASD) is a rare autosomal recessive disorder characterized by severe hyperkalemia, salt loss, vomiting, severe dehydration and failure to thrive. ASD is a life-threatening electrolyte imbalance in infants resulting from mutations in CYP11B2. We described ASD in a Chinese male infant with vomiting, poor feeding and failure to thrive. He was mildly dehydrated, with a weight of 6 kg (−3.45 SDS) and length of 67 cm (−3.10 SDS). Laboratory tests showed hyponatremia (119 mmol/L), serum potassium 5.4 mmol/L, low plasma aldosterone and plasma renin activity (PRA) levels. Next-generation sequencing of his DNA revealed compound heterozygous mutations in CYP11B2, a known variant c.1391_1393delTGC (p.Leu464del, rs776404064) and a novel variant c.1294delA (p.Arg432Glyfs*37). The HEK-293T expression system was used to investigate the variants, demonstrating negligible aldosterone synthesis compared with WT CYP11B2. The patient started fludrocortisone and subsequently gained 3.2 kg of weight and normalized serum sodium (137 mmol/L). We further reviewed reported cases of ASD, summarizing clinical features and CYP11B2 mutations; missense and nonsense mutations are most frequent. Fludrocortisone treatment is essential for ASD, and the need for mineralocorticoid replacement wanes with age; eventually, therapy can be discontinued for many affected children. Our study broadens the ASD phenotypic spectrum and shows the efficiency of next-generation sequencing for patients with atypical clinical manifestations.
Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats
2001, Kidney International
Citation Excerpt :
Even less is known about the effect of potassium depletion on BP in infants. The requirements of K+ and other electrolytes are increased during this period of rapid growth27-29, and the infants' growth rate is sensitive to subtle changes in electrolyte intake and extracellular fluid volume status. Therefore, we examined the effects of chronic dietary potassium depletion on BP using young rats as a model system to mimic the clinical situation frequently encountered in rapidly growing infants.
Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats.
Chronic hypokalemia has been associated with renal hypertrophy, interstitial disease, and hypertension in both adult animals and humans. However, the effects of potassium (K⁺) depletion on the rapidly growing infant have not been well studied. The purpose of this study was to determine the effects of severe chronic dietary K⁺ depletion on blood pressure (BP) and renal structural changes in young rats.
Sprague-Dawley rats (50 ± 5 g) were fed either a control or a potassium-deficient diet (<0.05% K⁺) for 14 to 21 days. At the end of this period, the blood pressure (BP) was measured in all rats, and six rats in each group were sacrificed to determine changes in renal histology and renin-angiotensin system (RAS) activity. The remaining rats in each group were then switched to a high-salt (6% NaCl)-normal-K⁺ (0.5%) diet or were continued on their respective control or K⁺-deficient diet for an additional six days. Blood pressure measurements were done every three days until the end of the study.
K⁺-depleted animals had significant growth retardation and increased RAS activity, manifested by high plasma renin activity, recruitment of renin-producing cells along the afferent arterioles, and down-regulation of angiotensin II receptors in renal glomeruli and ascending vasa rectae. K⁺-depleted kidneys also showed tubulointerstitial injury with tubular cell proliferation, osteopontin expression, macrophage infiltration, and early fibrosis. At week 2, K⁺-depleted rats had higher systolic BP than control rats. Switching to a high-salt (6% NaCl)-normal-K⁺ diet resulted in further elevation of systolic BP in K⁺-depleted rats, which persisted even after the serum K⁺ was normalized.
Dietary potassium deficiency per se increases the BP in young rats and induces salt sensitivity that may involve at least two different pathogenic pathways: increased RAS activity and induction of tubulointerstitial injury.
High-calorie nutrition for infants with chronic renal disease
1996, Journal of Renal Nutrition
Objective: This report describes the administration of high-calorie formula (HCF), with caloric densities between 40 kcal/oz and 60 kcal/oz, to children with renal disease and severe fluid restrictions.
Design: Retrospective Descriptive Analyses.
Setting: Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Patients: Records of all infants with chronic renal disease treated at Children's Hospital between 1984 and 1991 and who received supplemental formulas with a minimal caloric density of 40 kcal/oz were reviewed.
Intervention: Commercial formulas were modified with glucose polymers and corn oil to attain caloric densities of 40 kcal/oz to 60 kcal/oz. The target caloric density for each patient was selected based on each infant's fluid restrictions and recommended daily allowance requirements. Patients were evaluated monthly for compliance, and formula changes were adjusted to ensure adequate caloric intake and fluid balance.
Main outcome measures: Patient tolerance of the HCF was defined by the absence of noninfectious diarrhea and vomiting while receiving the HCF. Progression of formula advancement (either in volume or concentration) required the stools be tested negative for reducing substances. The review was discontinued when the following occurred: fluid liberalization, transplantation, or death.
Results: Seventeen infants given the HCF were reviewed. Sixteen infants required nasogastric feedings (usually given continuously at night). The mean average daily caloric intake achieved was 113.2 kcal/kg/d. Fifty-nine percent of the patients were tolerant of the HCF. The type and duration of dialysis did not affect tolerance of the HCF.
Conclusion: The HCF was well tolerated with minimal side effects and should be considered for any infant with severe fluid restrictions.
Effects of reduced renal function and dietary protein on muscle protein synthesis
1991, Kidney International
Effects of reduced renal function and dietary protein on muscle protein synthesis. We describe a rat model of renal failure that separates catabolic and anabolic states from each other. Muscle protein synthesis was compared during the anabolic period between sham (S) operated and renal failure (RF) rats that were fed different levels of dietary protein. Male rats weighing between 60 and 80 g first had a partial left nephrectomy and then were given a tryptophan deficient diet from four to six days to induce weight loss. On the second day of the diet either a renal decapsulation (S rats) or a simple right nephrectomy (RF rats) was done to enhance the catabolic response in both and to induce renal failure in the RF rats. Following the period of feeding the deficient diet, both groups were fed a nutritionally complete 14, 17, 20 or 30% protein diet for three to five days. This induced a brisk anabolic response as measured by weight gain. Differences in body weight between the S and RF rats after three to five days on the repletion diet generally was less than 10%. The rats then were fasted overnight, fed a standard meal and muscle protein synthesis (Sm%) was measured two hours post-feeding. Sm% was estimated from the incorporation of ³H phenylalanine (PHE) into muscle 10 minutes following the i.v. injection of ³HPHE (25 µCi/100 g body wt) with carrier PHE to flood all the precursor amino acid pools. Weight loss in the catabolic phase was greater and the net weight gain for the two phases was less in the RF group. Overall, renal failure resulted in a significant reduction in Sm% (P < 0.001). When Sm% for each S and RF rat, expressed as percent of the average of the S group for that study, was compared with the reciprocal of serum creatinine (1/S_Cr) for that rat a curvilinear relationship was observed. Sm% in RF rats whose S_Cr values were between 0.6 and 1.0 mg/dl did not differ from the S rats. Those with values >1.0 mg/dl showed a definite decrease in Sm%. We conclude that the anabolic response to a given meal as measured by Sm% during nutritional rehabilitation was depressed when the renal function decreased to 30% of normal. There was a tendency in the RF rats on the high protein diet to depress Sm% further, however, this finding was inconclusive.
American Society of Pediatric Nephrology position paper on linking reimbursement to quality of care
2005, Journal of the American Society of Nephrology
Measuring nutritional status in children with chronic kidney disease
2004, American Journal of Clinical Nutrition

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SupplementGrowth rate in infants with impaired renal function

Kidney Int

Am J Med

Kidney Int

Am J Kidney Dis

Growth in children with renal disease

Clin Nephron

Growth pattern and dietary intake of children with chronic renal insufficiency

Br Med J

Hypofiltration in remnant nephrons: a potentially adverse response to renal ablation

Am J Physiol

Growth and development of nondialyzed children with chronic renal failure

Kidney Int

Assessment of growth

Am J Kidney Dis

A simple estimate of glomerular filtration rate in children derived from body length and plasma creatinine

Pediatrics

Supplement
Growth rate in infants with impaired renal function