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Nutrition
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
2.17. Biochemical abnormalities in kwashiorkor includehypernatraemia.aminoaciduria.lactase deficiency.low serum albumin.potassium deficiency.
Hepatorenal tyrosinemia/fumarylacetoacetate hydrolase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Increased quantities are also excreted in the urine. Of the tyrosyl compounds found in the urine, p-hydroxyphenyllactic acid is the most prominent; p-hydroxyphenylpyruvic acid and p-hydroxyphenylacetic acid are also present in appreciable quantities. Patients often have elevated concentrations of methionine in the blood. Hypoglycemia is common, especially in the acute illness. In chronic cirrhosis or after treatment, tyrosine concentrations may be normal. On the other hand, during the acute stages of hepatocellular damage many other amino acids may be found in elevated amounts in the serum, including cystathionine, proline and hydroxyproline. These patterns, along with the tyrosine, are reflected in the urinary excretion of amino acids. They are superimposed on the generalized aminoaciduria that results from the renal tubular aspects of the disease. Patients also have phosphaturia and hypophosphatemia. The presence of reducing substance completes the picture of the renal Fanconi syndrome. The sugar is usually glucose, but other sugars have been reported [4, 68]. With progression, there is systemic acidosis, increased potassium loss, and hypokalemia.
Renal Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
In patients with Itai-itai disease the renal tubular dysfunction was evident also in the form of decreased excretion of phenolsulfonphtalein (PSP).146 The lower normal limit of excretion is 25% after 15 min, but in seven of the ten patients tested the excretion was 10 to 22.5% and for the other three patients it was 25%.146 Many of the patients also had aminoaciduria, reduced ability to dilute and concentrate urine and to reabsorb phosphorus.151 The thiosulfate and PAH clearance were low.146
Partial Fanconi syndrome induced by ifosfamide
Published in Baylor University Medical Center Proceedings, 2019
Muhammad Ajmal Panezai, Charles Owen, Harold M. Szerlip
Over the course of his hospitalization, the patient experienced a gradual worsening of serum electrolyte levels requiring large amounts of replacement potassium and phosphorus (Figure 1). His renal function and serum bicarbonate remained normal and his urine pH was <6.0 throughout the admission. A urine protein–creatinine ratio was 5.3 g/g with a urine albumin–creatinine ratio of 329 mg/g; 24-hour urine collection revealed excretion of 126 mmol potassium, 2.2 g phosphorus 5338 mg protein, and 343 mg albumin. Urine amino acid quantitative test showed marked generalized aminoaciduria. Until his death on day 60 of the hospitalization, he required continued electrolyte supplementation.
The safety of current pharmacotherapeutic strategies for osteosarcoma
Published in Expert Opinion on Drug Safety, 2021
Mariella Spalato, Antoine Italiano
IFO is an alkylating chemotherapeutic agent of the oxaphosphorines. It is a nitrogen mustard-like alkylating agent that requires activation in the liver to form its active intermediaries, which act by modifying and cross-linking purine bases in DNA, thus inhibiting DNA, RNA, and protein synthesis and leading to programmed cell death (apoptosis) in rapidly dividing cells. IFO causes clinical nephrotoxicity in up to 30% of patients[36]. Nevertheless, the reported prevalence of nephrotoxicity ranges from 15% to 60%, according to the definition of kidney injury, the duration of follow-up, and the therapeutic protocols[36]. IFO-induced renal injury derives from the inhibition of oxidative phosphorylation, which results in a spectrum of nephrotoxic phenotypes. The clinical presentation depends on the type, the severity, and the reversibility of the kidney injury, as well as on the time to onset after the administration of the treatment. The inhibition of renal thioredoxin reductase activity can induce an AKI[37], which can progress to chronic kidney injury (CKI). The most frequent damage is type 2 proximal renal tubular acidosis (RTA) [38,39]. In one study of 120 patients who received a median cumulative IFO dose of 30 g/m2, evidence of proximal tubular dysfunction was seen in 66% of patients 3 months after completing treatment, and 7% of patients had Fanconi syndrome[40]. Fanconi syndrome is a proximal tubule defect in which resorption of glucose, amino acids, phosphate, and bicarbonate is impaired, causing excessive urinary losses, and consequently metabolic acidosis, hypophosphatemia, and hypokalemia. Aminoaciduria and glucosuria are usually not clinically significant. Distal or type 1 RTA tubular involvement is rare[41]. Nephrogenic diabetes insipidus, clinically represented by marked polyuria, is also uncommon. Nephrotoxicity is generally reversible, but in some patients glomerular and tubular function can continue to deteriorate even after the end of treatment[42].