China
Africa
Explore chapters and articles related to this topic
Renal Disease
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Molly Wong Vega, Poyyapakkam Srivaths
In renal tubular acidosis, nutrition therapy may include similar nutrition therapies as seen in nephrolithiasis. Rare disorders like Bartter’s syndrome and Gitelman syndrome may require high amounts of electrolyte supplementation including that of sodium, chloride, potassium, and magnesium. In nephrogenic diabetes insipidus, nutrition therapy focuses on prevention of hypernatremia due to impaired water reabsorption in the kidney. Avoidance of excessive intake of solutes (primarily sodium and protein) that may increase water/urine excretion is important. Water supplementation via tube feedings is often necessary due to the high total fluid volumes (150–200 mL/kg per day) required to maintain adequate serum sodium levels. Growth can also be challenging as fluid intake may displace nutrient intake for oral feeders.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Second decade (∼40%): Primarily neurological symptoms (silent cirrhosis).Movement disorders: dystonia, parkinsonism, chorea, myoclonus.Rubral (midbrain) tremor, “wing beating,” rest, postural, intention tremor.Bulbar symptoms early and prominent.Psychiatric (psychosis, depression).Cognitive decline.Articular and muscular symptoms: arthritis, proximal weakness.Renal tubular acidosis.
Nephrology, including fluid and electrolytes
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
10.25. Hypokalemia is likely to occur indiarrhoea.renal tubular acidosis.infants of diabetic mothers.infantile pyloric stenosis.neonatal asphyxia.
Established and recent developments in the pharmacological management of urolithiasis: an overview of the current treatment armamentarium
Published in Expert Opinion on Pharmacotherapy, 2020
Mohamed Abou Chakra, Athanasios E. Dellis, Athanasios G. Papatsoris, Mohamad Moussa
Nephrolithiasis, which may occur in any of the subsets of type I renal tubular acidosis, accounts for most of the morbidity in adults and adolescents. Major risk factors in this case include alkaline urine, hypercalciuria, and hypocitraturia. The most frequently occurring risk factor, hypocitraturia, is due to decreased filtered load and/or to increased tubular reabsorption of filtered citrate. While increased tubular reabsorption may be due to systemic acidosis, hypocitraturia occurs in incomplete renal tubular acidosis. Furthermore, alkali therapy increases citrate excretion in complete and incomplete type I renal tubular acidosis. Potassium citrate appears to reduce calcium excretion in both types of hypercalciuric type I renal tubular acidosis [105].
Pediatric primary calcific band keratopathy with or without glaucoma from biallelic SLC4A4 mutations
Published in Ophthalmic Genetics, 2018
Proximal renal tubular acidosis, an impairment of bicarbonate (HCO3−) reabsorption in the proximal renal tubules, can be a transient isolated phenomenon in young children. When permanent, it is usually one of multiple defects in proximal renal tubular function (Fanconi syndrome) that can be secondary to a variety of systemic diseases. Permanent proximal renal tubular acidosis without other proximal tubular dysfunction is a rare phenomenon (3). In 1970 Donckerwolcke and colleagues described such a case in a 20-month-old girl (4). In addition to having permanent proximal renal tubular acidosis, she was developmentally delayed (small for age and hypotonic) and had progressive band keratopathy. Several years later Wisnes and colleagues described a familial form of proximal renal tubular acidosis with co-existent developmental delay and ocular findings (corneal opacities, glaucoma, cataract) (5). In 1999 Igarashi and colleagues demonstrated that this phenotype is caused by biallelic mutations in SLC4A4 (6), and since then several additional cases confirmed to harbor biallelic mutations in the gene have been published (7). SLC4A4 encodes a Na+/HCO3– cotransporter that has prominent function in the proximal renal tubule and corneal endothelium. Mutations in SLC4A4 lead to increased HCO3– in the corneal stroma, which facilitates Ca2+ deposition and thus primary calcific band keratopathy. In addition, the disruption of ion balance in the aqueous humor from mutations in the gene likely contributes to the development of glaucoma and, as described in some case reports, cataract.
Target association rule mining to explore novel paediatric illness patterns in emergency settings
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Pradeep Kumar Dabla, Kamal Upreti, Divakar Singh, Anju Singh, Jitender Sharma, Aashima Dabas, Damien Gruson, Bernard Gouget, Sergio Bernardini, Evgenija Homsak, Sanja Stankovic
A total of 197 children were screened, of which 25, 4 and 7 had diarrhoea, malabsorption and serious malnourishment, respectively. Three other individuals with renal tubular acidosis were exempted. Finally, the study included 158 children with 66.4% of boy), median (IQR) aged 11 (6–10) months. Only 138 children’s consequences were available, while others were still admitted at the conclusion of the study. The levels for sodium were determined to be 135–145 mmol/L and potassium was determined to be 3.5–5.5 mmol/L, meanwhile the normal range for BUN and Lactate was determined to have an upper reference limit of 18 mg/dL and 2 mmol/L, respectively [30].