Renal Morphogenesis and Development of Renal Function

Guignard, J; Sulyok, E.

doi:10.1016/b978-1-4377-0134-0.10081-2

Cited by 4 publications

(4 citation statements)

References 92 publications

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“…The other risk factors include male gender, cesarean delivery and multiple pregnancy (14). RDS is observed with a rate of 60-80% in preterm infants younger than 28 weeks or below, with a rate of 50% in infants with a gestational age of 28-32 weeks and with a rate of 15-30% in infants with a gestational age of 32-36 weeks (1,14). In infants in whom surfactant and mechanical ventilation are used because of RDS, the most severe early complications include air leaks, pneumoniae, central nervous system bleedings and sepsis (1).…”

Section: Discussionmentioning

confidence: 99%

“…Since body functions of the newborns have not developed fully yet in this period, physiologic and biochemical changes involving all systems occur. Premature delivery is defined as birth of the baby before the 37 th week starting with the first day of the last mensturation (1). Although the number of the nephrons reach a normal value after the 32nd week, they are short and functionally immature; the development of renal vessels is not completed and renal blood flow is very low (2).…”

Section: Introductionmentioning

confidence: 99%

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Erken doğmuş yenidoğanlarda total parenteral beslenmenin böbrek işlevleri üzerine etkileri

Tabel¹,

Öncül²,

Akın³

et al. 2012

Tpa

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Aim:The aim of this study was to establish serum sistatine C, urine β 2 microglobulin, gluthatione-S -transferase π and N-acetyle β-D glucosaminidase levels in order to evaluate the effect of total parenteral nutrition on renal function in premature infants. In addition, we aimed to compare the renal functions between premature infants receiving total parenteral nutrition and control groups receiving enteral feeding. Material and Method: A hundred four premature infants with a gestational age between 28 and 34 weeks were included in the study. The parenteral nutrition group consisted of 50 infants (male/female; 23/27 and mean weight 1258±212.3 g) and the enteral nutrition group consisted of 54 infants (male/female; 20/34 and mean weight 1608±206.1 g). In the parenteral nutrition group; total parenteral group nutrition was initiated on the 3 rd day in the enteral nutrition group, minimal enteral nutrition was started on a mean of 6.3±2.4 days and total enteral nutrition was started on a mean of 24.5±6.3 days. Breastmilk was given orally or by orogastric/nasogastric tube at first day of life in the enteral group. On the 3 rd and 30 th day of life, blood samples of all patients were obtained for evaluating biochemical parameters and cystatin C and urine samples were obtained for evaluation of N-acetyl β-D glucosaminidase, gluthatione-S-transferase π, β 2 microglobulin, sodium, creatinin levels, density and pH of the urine. The study was approved by the ethics commite (2008/16). Results: When we compared the patients who received total parenteral nutrition and enteral nutrition on the 3 rd and 30 th days, serum cystatin C, urinary β 2 microglobulin, gluthatione-S-transferase π and N-acetyl-β-D glucosaminidase excretions were similar on the 3 rd day however were significantly higher on the 30 th day in samples of the patients receiving total parenteral nutrition (p<0.05 for each parameter on each day). Conclusions: This study shows that total parenteral nutrition in premature infants can have adverse effects on glomerular and tubular functions of the kidney which can be manifested at an early time with cystatin C, β 2 microglobulin, gluthatione-S-transferase π and N-acetyl β-D glucosaminidase. (Turk Arch Ped 2012; 47: 244-249)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Erken doğmuş yenidoğanlarda total parenteral beslenmenin böbrek işlevleri üzerine etkileri

Tabel¹,

Öncül²,

Akın³

et al. 2012

Tpa

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show abstract

“…The ureteric bud grows and branches repeatedly and forms the renal collecting system and induces mesenchymal transformation to form the glomeruli and renal tubules. These complex processes are under the control of metanephric mesenchyme-derived inductive signals (Wilms' tumor gene1-WT1 and glial cell line-derived neurotrophic factor-GDNF) and transcription factors, including Pax2, Lim1 and the Formin gene [167].…”

Section: Nephrogenesis-fetal Nephron Endowmentmentioning

confidence: 99%

Pathomechanisms of Prenatally Programmed Adult Diseases

2023

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Based on epidemiological observations Barker et al. put forward the hypothesis/concept that an adverse intrauterine environment (involving an insufficient nutrient supply, chronic hypoxia, stress, and toxic substances) is an important risk factor for the development of chronic diseases later in life. The fetus responds to the unfavorable environment with adaptive reactions, which ensure survival in the short run, but at the expense of initiating pathological processes leading to adult diseases. In this review, the major mechanisms (including telomere dysfunction, epigenetic modifications, and cardiovascular–renal–endocrine–metabolic reactions) will be outlined, with a particular emphasis on the role of oxidative stress in the fetal origin of adult diseases.

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“… 83–85 NHE3 inhibitors reduce sodium absorption in the gut, leading to increased water secretion into the intestinal lumen. 52 , 86 This may accelerate intestinal transit time and result in softer stool consistency. 52 An NHE3 inhibitor has been shown to increase stool sodium excretion and soften stool consistency in human trials; the effects of irritable bowel syndrome with constipation (IBS-C), a common GI condition characterized by abdominal pain and prolonged GI transit, were alleviated in trial participants.…”

Section: Disease Targets For Nhe3 Inhibitionmentioning

confidence: 99%

Novel Treatments from Inhibition of the Intestinal Sodium–Hydrogen Exchanger 3

Kövesdy¹,

Adebiyi²,

Rosenbaum³

et al. 2021

IJNRD

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Plasma membrane sodium–hydrogen exchangers (NHE) transport Na + into cells in exchange for H + . While there are nine isoforms of NHE in humans, this review focuses on the NHE3 isoform, which is abundantly expressed in the gastrointestinal tract, where it plays a key role in acid–base balance and water homeostasis. NHE3 inhibition in the small intestine results in luminal sodium and water retention, leading to a general decrease in paracellular water flux and diffusional driving force, reduced intestinal sodium absorption, and increased stool sodium excretion. The resulting softer and more frequent stools are the rationale for the development of tenapanor as a novel, first-in-class NHE3 inhibitor to treat irritable bowel syndrome with constipation. NHE3 also has additional therapeutic implications in nephrology. Inhibition of intestinal NHE3 also lowers blood pressure by reducing intestinal sodium absorption. Perhaps, the most novel effect is its ability to decrease intestinal phosphate absorption by inhibiting the paracellular phosphate absorption pathway. Therefore, selective pharmacological inhibition of NHE3 could be a potential therapeutic strategy to treat not only heart failure and hypertension but also hyperphosphatemia. This review presents an overview of the molecular and physiological functions of NHE3 and discusses how these functions translate to potential clinical applications in nephrology.

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Renal Morphogenesis and Development of Renal Function

Cited by 4 publications

References 92 publications

Erken doğmuş yenidoğanlarda total parenteral beslenmenin böbrek işlevleri üzerine etkileri

Erken doğmuş yenidoğanlarda total parenteral beslenmenin böbrek işlevleri üzerine etkileri

Pathomechanisms of Prenatally Programmed Adult Diseases

Novel Treatments from Inhibition of the Intestinal Sodium–Hydrogen Exchanger 3

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