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Characteristics of Presentation and Metabolic Risk Factors in Relation to Extent of Involvement in Infants with Nephrolithiasis
DOI: 10.14744/ejmi.2019.87741 EJMI 2020;4(1):78–85 Research Article Characteristics of Presentation and Metabolic Risk Factors in Relation to Extent of Involvement in Infants with Nephrolithiasis Kenan Yilmaz,1 Mustafa Erman Dorterler2 1Department of Pediatric Nephrolog, Sanliurfa Training and Research Hospital, Sanliurfa, Turkey 2Department of Pediatric Surgery, Harran University Faculty of Medicine, Sanliurfa, Turkey Abstract Objectives: To evaluate the characteristics of presentation and metabolic risk factors in relation to the extent of in- volvement in infants with nephrolithiasis. Methods: A total of 111 infants (age range 0.3–11.8 months, 58.6% were girls) diagnosed with nephrolithiasis in the first year of life were included in this retrospective study. Data on age at diagnosis, gender, family history of nephrolithiasis, parental consanguinity, symptoms on admission, urinary abnormalities, surgery, size of renal calculi, and metabolic risk factors (hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, cystinuria, hypercalcemia) were recorded for each patient and compared with the number of kidneys affected (bilateral vs. unilateral), the number of kidney stones (multiple vs. single), and the kidney stone size (microlithiasis vs. larger stones). Results: Overall, 58.6% of the infants were girls. Irritability was the most common symptom on admission (34.2%). Microlithiasis (62.2%), bilateral kidney involvement (61.3%), multiple kidney stones (73.9%), and metabolic risk fac- tors (45.0%, hypercalciuria in 31.5%) were commonly noted. Bilateral nephrolithiasis was associated with significantly higher rates of hypercalciuria than unilateral nephrolithiasis (39.7% vs. 18.6%, respectively; p=0.022). The presence of multiple kidney stones was associated with a significantly higher rate of hyperuricosuria than the presence of a single kidney stone (20.7% vs. -
Oxalate Loading Test: a Screening Test for Steatorrhoea
Gut: first published as 10.1136/gut.20.12.1089 on 1 December 1979. Downloaded from Gut, 1979, 20, 1089-1094 Oxalate loading test: a screening test for steatorrhoea D. S. RAMPTON', G. P. KASIDAS, G. ALAN ROSE, AND MARTIN SARNER2 From University College Hospital, London, St. Peter's Hospitals and Institute of Urology, London SUMMARY To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4-44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0-33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19-186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0 25 mmol/24 h, range 0-08-059 mmol) (normal <0 20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0-91 mmol/24 h, range 046- 1P44 mmol) (normal <0-44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r=0*73, P <0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 58+09% (±1 SD) in normal subjects and 14-7+6-0% (P <0.002) in patients with steatorrhoea. -
Acute Kidney Injury in Cancer Patients
Acute kidney injury in cancer patients Bruno Nogueira César¹ Marcelino de Souza Durão Júnior¹ ² 1. Disciplina de Nefrologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil 2. Unidade de Transplante Renal Hospital Israelita Albert Einstein, São Paulo, SP, Brasil http://dx.doi.org/10.1590/1806-9282.66.S1.25 SUMMARY The increasing prevalence of neoplasias is associated with new clinical challenges, one of which is acute kidney injury (AKI). In addition to possibly constituting a clinical emergency, kidney failure significantly interferes with the choice and continuation of antineoplastic therapy, with prognostic implications in cancer patients. Some types of neoplasia are more susceptible to AKI, such as multiple myeloma and renal carcinoma. In cancer patients, AKI can be divided into pre-renal, renal (intrinsic), and post-renal. Conventional platinum-based chemotherapy and new targeted therapy agents against cancer are examples of drugs that cause an intrinsic renal lesion in this group of patients. This topic is of great importance to the daily practice of nephrologists and even constitutes a subspecialty in the field, the onco-nephrology. KEYWORDS: Acute Kidney Injury. Neoplasia. Malignant tumor. Chemotherapy. INTRODUCTION With the epidemiological transition of recent de- (CT), compromises the continuation of treatment, cades, cancer has become the object of several clini- and limits the participation of patients in studies cal studies that resulted in more options for the diag- with new drugs. nosis and treatment of the disease. Thus, there was an increase in the survival of patients, and handling EPIDEMIOLOGY complications of the disease and treatment adverse effects also became more common1. -
Blueprint Genetics Primary Hyperoxaluria Panel
Primary Hyperoxaluria Panel Test code: KI0801 Is a 3 gene panel that includes assessment of non-coding variants. Is ideal for patients with a clinical suspicion of hyperoxaluria. About Primary Hyperoxaluria The primary hyperoxalurias are rare disorders of glyoxylate metabolism, which result in markedly increased endogenous oxalate synthesis by the liver. They are characterized by an excess of oxalate resulting in manifestations ranging from occasional renal stones, recurrent nephrolithiasis and nephrocalcinosis to end-stage renal disease (ESRD) and systemic oxalosis. Presenting ranges from the neonatal period to adulthood. Among disorders causing hyperoxaluria, the primary hyperoxalurias are the most severe, ultimately leading to ESRD and if untreated, death in most patients. Type I primary hyperoxaluria (PH1), is caused by deficient or absent activity of liver-specific peroxisomal alanine glyoxylate aminotransferase (AGT). In some patients with PH1 type disease, the enzyme is present but mistargeted to mitochondria where it is metabolically inactive. The severe infantile form is characterized by a failure to thrive, nephrocalcinosis with or without nephrolithiasis and early ESRD. Onset in childhood and adolescence is often characterized by recurrent urolithiasis (with or without nephrocalcinosis) and progressive renal failure. The late onset form is characterized by occasional renal stones with onset in adulthood, but acute renal failure caused by bilateral obstruction of the kidneys by oxalate stones may occur. Other manifestations include urinary tract infections, dysuria and hematuria. The ongoing systemic oxalosis also may lead to other clinical manifestations such as cardiac conduction defects, vascular calcification with distal gangrene, disturbed vision, specific brown colored retinal deposits, skin nodules, joint involvement and bone disease leading to fractures in long-term dialysis-dependent patients. -
High Urinary Calcium Excretion and Genetic Susceptibility to Hypertension and Kidney Stone Disease
High Urinary Calcium Excretion and Genetic Susceptibility to Hypertension and Kidney Stone Disease Andrew Mente,* R. John D’A. Honey,† John M. McLaughlin,* Shelley B. Bull,* and Alexander G. Logan* *Prosserman Centre for Health Research, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Public Health Sciences, and †St. Michael’s Hospital, Division of Urology, Department of Surgery, University of Toronto, Toronto, Ontario, Canada Increased urinary calcium excretion commonly is found in patients with hypertension and kidney stone disease (KSD). This study investigated the aggregation of hypertension and KSD in families of patients with KSD and hypercalciuria and explored whether obesity, excessive weight gain, and diabetes, commonly related conditions, also aggregate in these families. Consec- utive patients with KSD, aged 18 to 50 yr, were recruited from a population-based Kidney Stone Center, and a 24-h urine and their spouse were interviewed by telephone (333 ؍ sample was collected. The first-degree relatives of eligible patients (n to collect demographic and health information. Familial aggregation was assessed using generalized estimating equations. Multivariate-adjusted odds ratios (OR) revealed significant associations between hypercalciuria in patients and hypertension (OR 2.9; 95% confidence interval 1.4 to 6.2) and KSD (OR 1.9; 95% confidence interval 1.03 to 3.5) in first-degree relatives, specifically in siblings. No significant associations were found in parents or spouses or in patients with hyperuricosuria. Similarly, no aggregation with other conditions was observed. In an independent study of siblings of hypercalciuric patients with KSD, the adjusted mean fasting urinary calcium/creatinine ratio was significantly higher in the hypertensive siblings compared with normotensive siblings (0.60 ؎ 0.32 versus 0.46 ؎ 0.28 mmol/mmol; P < 0.05), and both sibling groups had significantly higher values than the unselected study participants (P < 0.001). -
Redalyc.The Nutritional Limitations of Plant-Based Beverages in Infancy
Nutrición Hospitalaria ISSN: 0212-1611 [email protected] Sociedad Española de Nutrición Parenteral y Enteral España Vitoria, Isidro The nutritional limitations of plant-based beverages in infancy and childhood Nutrición Hospitalaria, vol. 34, núm. 5, 2017, pp. 1205-1214 Sociedad Española de Nutrición Parenteral y Enteral Madrid, España Available in: http://www.redalyc.org/articulo.oa?id=309253341026 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Nutr Hosp. 2017; 34(5):1205-1214 ISSN 0212-1611 - CODEN NUHOEQ S.V.R. 318 Nutrición Hospitalaria Revisión The nutritional limitations of plant-based beverages in infancy and childhood Limitaciones nutricionales de las bebidas vegetales en la lactancia y la infancia Isidro Vitoria Unit of Nutrition and Metabolopathies. Hospital Universitario y Politécnico La Fe. Valencia, Spain Abstract Breastfeeding, infant formula and cow’s milk are basic foods in infant nutrition. However, they are being increasingly replaced either totally or partially by plant-based beverages. The composition of 164 plant-based beverages available in Spain was reviewed based on the nutritional labeling of the package and the man- ufacturers’ webpages. This was compared to the composition of cow’s milk and infant formula. In addition, the nutritional disease associated with consumption of plant-based beverages in infants and children was reviewed by means of a literature search in Medline and Embase since 1990 based on the key words “plant-based beverages” or “rice beverages” or “almond beverages” or “soy beverages” and “infant” or “child”. -
Fructose As an Endogenous Toxin
HEPATOCYTE MOLECULAR CYTOTOXIC MECHANISM STUDY OF FRUCTOSE AND ITS METABOLITES INVOLVED IN NONALCOHOLIC STEATOHEPATITIS AND HYPEROXALURIA By Yan (Cynthia) Feng A thesis submitted in the conformity with the requirements for the degree of Master of Science Graduate Department of Pharmaceutical Sciences University of Toronto © Copyright by Yan (Cynthia) Feng 2010 ABSTRACT HEPATOCYTE MOLECULAR CYTOTOXIC MECHANISM STUDY OF FRUCTOSE AND ITS METABOLITES INVOLVED IN NONALCOHOLIC STEATOHEPATITIS AND HYPEROXALURIA Yan (Cynthia) Feng Master of Science, 2010 Department of Pharmaceutical Sciences University of Toronto High chronic fructose consumption is linked to a nonalcoholic steatohepatitis (NASH) type of hepatotoxicity. Oxalate is the major endpoint of fructose metabolism, which accumulates in the kidney causing renal stone disease. Both diseases are life-threatening if not treated. Our objective was to study the molecular cytotoxicity mechanisms of fructose and some of its metabolites in the liver. Fructose metabolites were incubated with primary rat hepatocytes, but cytotoxicity only occurred if the hepatocytes were exposed to non-toxic amounts of hydrogen peroxide such as those released by activated immune cells. Glyoxal was most likely the endogenous toxin responsible for fructose induced toxicity formed via autoxidation of the fructose metabolite glycolaldehyde catalyzed by superoxide radicals, or oxidation by Fenton’s hydroxyl radicals. As for hyperoxaluria, glyoxylate was more cytotoxic than oxalate presumably because of the formation of condensation product oxalomalate causing mitochondrial toxicity and oxidative stress. Oxalate toxicity likely involved pro-oxidant iron complex formation. ii ACKNOWLEDGEMENTS I would like to dedicate this thesis to my family. To my parents, thank you for the sacrifices you have made for me, thank you for always being there, loving me and supporting me throughout my life. -
Article Twenty-Four Hour Urine Testing and Prescriptions For
CJASN ePress. Published on November 11, 2019 as doi: 10.2215/CJN.03580319 Article Twenty-Four Hour Urine Testing and Prescriptions for Urinary Stone Disease–Related Medications in Veterans Shen Song,1 I-Chun Thomas,2 Calyani Ganesan,1 Ericka M. Sohlberg ,3 Glenn M. Chertow,1 Joseph C. Liao,2,3 Simon Conti,2,3 Christopher S. Elliott,3,4 Alan C. Pao,1,2,3 and John T. Leppert1,2,3 Abstract Background and objectives Current guidelines recommend 24-hour urine testing in the evaluation and treatment 1Division of of persons with high-risk urinary stone disease. However, how much clinicians use information from 24-hour Nephrology, urine testing to guide secondary prevention strategies is unknown. We sought to determine the degree to which Departments of clinicians initiate or continue stone disease–related medications in response to 24-hour urine testing. Medicine and 3Urology, Stanford Design, setting, participants, & measurements We examined a national cohort of 130,489 patients with incident University School of Medicine, Stanford, urinary stone disease in the Veterans Health Administration between 2007 and 2013 to determine whether California; 2Veterans prescription patterns for thiazide diuretics, alkali therapy, and allopurinol changed in response to 24-hour urine Affairs Palo Alto testing. Health Care System, Palo Alto, California; 4 fi and Division of Results Stone formers who completed 24-hour urine testing (n=17,303; 13%) were signi cantly more likely to be Urology, Santa Clara prescribed thiazide diuretics, alkali therapy, and allopurinol compared with those who did not complete a 24-hour Valley Medical Center, urine test (n=113,186; 87%). -
Peroxisomal Alanine:Glyoxylate Aminotransferase Deficiency in Primary Hyperoxaluria Type I
Volume 201, number 1 FEBS 3672 May 1986 Peroxisomal alanine:glyoxylate aminotransferase deficiency in primary hyperoxaluria type I C.J. Danpure and P.R Jennings Divisum of Inherited Metabolic Diseases, Clinical Research Centre, Watford Road, Harrow HA1 3UJ, England Received 1 April 1986 Activities of alanine:glyoxylate aminotransferase in the livers of two patients with primary hyperoxaluria type I were substantially lower than those found in five control human livers. Detailed subcellular fractiona- tion of one of the hyperoxaluric livers, compared with a control liver, showed that there was a complete absence of peroxisomal alanine:glyoxylate aminotransferase. This enzyme deficiency explains most of the biochemical characteristics of the disease and means that primary hyperoxaluria type I should be added to the rather select list of peroxisomal disorders. Hyperoxaluria Alanine:glyoxylate aminotransferase Glutamate:glyoxylate aminotransferase Peroxisomal disorder Glyoxylate metabolism (Human) Liver pathology 1. INTRODUCTION transamination in primary hyperoxaluria type I. Our results suggest that the basic biochemical Primary hyperoxaluria type I is a rare inborn er- defect in the disease is the absence of peroxisomal ror of metabolism caused by an accumulation of alanine : glyoxylate aminotransferase. glyoxylate, which leads to increased synthesis and excretion of oxalate and glycolate. Clinically the disease is characterized by recurrent calcium ox- 2. EXPERIMENTAL alate kidney stones, resulting in progressive renal insufficiency and death usually before the age of 2.1. Livers 20 [l]. Numerous in vivo studies in the 1960s sug- The subcellular fractionation experiments were gested that there might be an abnormality in the carried out on the liver of a patient with transamination of glyoxylate to glycine [2-41 in pyridoxine-resistant primary hyperoxaluria type I the type I disease, but the observations made in and a normal human liver. -
Hypouricaemia and Hyperuricosuria in Familial Renal Glucosuria
Clin Kidney J (2013) 6: 523–525 doi: 10.1093/ckj/sft100 Advance Access publication 5 September 2013 Clinical Report Hypouricaemia and hyperuricosuria in familial renal glucosuria Inês Aires1,2, Ana Rita Santos1, Jorge Pratas3, Fernando Nolasco1 and Joaquim Calado1,2 1Department of Medicine and Nephrology, Faculdade de Ciências Médicas, Universidade NOVAde Lisboa-Hospital de Curry Cabral, Lisboa, Portugal, 2Department of Genetics, Faculdade de Ciências Médicas, Universidade NOVAde Lisboa, Lisboa, Portugal and 3Department of Nephrology, Hospitais Universitários de Coimbra, Coimbra, Portugal Correspondence and offprint requests to: Joaquim Calado; E-mail: [email protected] Abstract Familial renal glucosuria is a rare co-dominantly inherited benign phenotype characterized by the presence of glucose in the urine. It is caused by mutations in the SLC5A2 gene that encodes SGLT2, the Na+-glucose cotransporter responsible for the reabsorption of the bulk of glucose in the proxi- mal tubule. We report a case of FRG displaying both severe glucosuria and renal hypouricaemia. We hypothesize that glucosuria can disrupt urate reabsorption in the proximal tubule, directly causing hyperuricosuria. Keywords: glucose; kidney; SGLT2; urate Background urate values were found to be raised, with an excretion of 7.33 mmol (1242 mg)/1.73 m2/24 h or 0.13 mmol (21.5 mg)/kg of body weight and a fractional excretion of 20%. Familial renal glucosuria (FRG) is characterized by the Phosphorus (urinary and serum), bicarbonate (plasma) presence of glucose in the urine in the absence of dia- and immunoglobulin light chains (urine) were all within betes mellitus or generalized proximal tubular dysfunc- normal range (data not shown). -
Antenatal Diagnosis of Inborn Errors Ofmetabolism
816 ArchivesofDiseaseinChildhood 1991;66: 816-822 CURRENT PRACTICE Arch Dis Child: first published as 10.1136/adc.66.7_Spec_No.816 on 1 July 1991. Downloaded from Antenatal diagnosis of inborn errors of metabolism M A Cleary, J E Wraith The introduction of experimental treatment for Sample requirement and techniques used in lysosomal storage disorders and the increasing prenatal diagnosis understanding of the molecular defects behind By far the majority of antenatal diagnoses are many inborn errors have overshadowed the fact performed on samples obtained by either that for many affected families the best that can amniocentesis or chorion villus biopsy. For be offered is a rapid, accurate prenatal diag- some disorders, however, the defect is not nostic service. Many conditions remain at best detectable in this material and more invasive only partially treatable and as a consequence the methods have been applied to obtain a diagnos- majority of parents seek antenatal diagnosis in tic sample. subsequent pregnancies, particularly for those disorders resulting in a poor prognosis in terms of either life expectancy or normal neurological FETAL LIVER BIOPSY development. Fetal liver biopsy has been performed to The majority of inborn errors result from a diagnose ornithine carbamoyl transferase defi- specific enzyme deficiency, but in some the ciency and primary hyperoxaluria type 1. primary defect is in a transport system or Glucose-6-phosphatase deficiency (glycogen enzyme cofactor. In some conditions the storage disease type I) could also be detected by biochemical defect is limited to specific tissues this method. The technique, however, is inva- only and this serves to restrict the material avail- sive and can be performed by only a few highly able for antenatal diagnosis for these disorders. -
Metabolic Disturbance As a Cause of Recurrent Hematuria in Children
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 39 (1991), pp. 707—710 Metabolic disturbance as a cause of recurrent hematuria in children HELOISA CATTINI PERRONE, HoRAclo AJZEN, JULIO ToPoRovsKI, and NESTOR SCHOR Nephrology Division, Facu/dade de Cjéncias Médicas da Santa Casa de São Paulo and Escola Paulista de Medicina, São Paulo, Brazil Metabolic disturbance as a cause of recurrent hematuria in children. be distinguished utilizing an oral calcium load test [9]. The To evaluate metabolic disturbance as a cause of hematuria, 250 chil- characterization of these groups of IH have been reported to be dren, aged eight months to fourteen years, with recurrent hematuria were studied. In the present series, metabolic disturbance was mainly of clinical value in formulating a rational therapeutic regimen due to idiopathic hypercalciuria (IH), the most common etiology of for children with IH associated with hematuria and/or urolithi- hematuria without proteinuria in childhood. Sixty-seven (27%) of the asis [10]. This paper therefore, was undertaken to analyze children had IH, ten children (4%) had hyperuricosuria, and 27 (11%) metabolic disturbances associated with hematuria and to assess had nephrolithiasis. To better characterize the IH into renal (RH) or the clinical value of the oral calcium load test in characterizing absorptive hypercalciuria (AH) subtypes, 45 of the 67 children (ranging age from six to twelve years) were further submitted to an oral calcium IH subtypes in children. Furthermore, we examined the clinical load test. Eighteen patients (40%) had AH, 7(15.5%) RH and 20(44.4%) evolution of children with IH, who were submitted to different could not be classified as having AH or RH [indeterminant (ID)therapeutic approaches based upon classification by the oral idiopathic hypercalciuria group].