Log in

Relevant bibliographies by topics / Proximal renal tubules / Books

To see the other types of publications on this topic, follow the link: Proximal renal tubules.

Books on the topic 'Proximal renal tubules'

Author: Grafiati

Published: 10 September 2021

Last updated: 29 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 18 books for your research on the topic 'Proximal renal tubules.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Najjar, Samer. Effects of ischemia and reperfusion on mitochondrial phosphate uptake in rat renal proximal tubules. s.n.], 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

Wong, P. S. K. The use of NMR spectroscopy to follow intracellular sodium content in rat rental proximal tubules. University of Birmingham, 1994.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Jones, Caroline Elizabeth Mary. The development, evaluation and use of freshly isolated renal proxinal tubule systems in the fischer rat. Aston University. Department of Pharmaceutical Sciences, 1990.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Speeckaert, Marijn, and Joris Delanghe. Tubular function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0008.

Full text

Abstract:

Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is char

APA, Harvard, Vancouver, ISO, and other styles

5

Bockenhauer, Detlef, and Robert Kleta. Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0041_update_001.

Full text

Abstract:

Up to 80% of filtered salt and water is returned back into the circulation in the proximal tubule. Several solutes, such as phosphate, glucose, low-molecular weight proteins, and amino acids are exclusively reabsorbed in this segment, so their appearance in urine is a sign of proximal tubular dysfunction. An entire orchestra of specialized apical and basolateral transporters, as well as paracellular molecules, mediate this reabsorption. Defects in proximal tubular function can be isolated (e.g. isolated renal glycosuria, aminoacidurias, or hypophosphataemic rickets) or generalized. In the latt

APA, Harvard, Vancouver, ISO, and other styles

6

Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.

Full text

Abstract:

Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanc

APA, Harvard, Vancouver, ISO, and other styles

7

Schreuder, Michiel F. Renal tubular dysgenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0350.

Full text

Abstract:

Renal tubular dysgenesis involves the absence or incomplete differentiation of proximal tubular nephron segments. Due to the lack of a patent nephron, it is characterized by (fetal) anuria and subsequent oligohydramnios, pulmonary hypoplasia, premature birth with severe and refractory arterial hypotension, and fetal or neonatal death. The main cause for renal tubular dysgenesis is a genetic mutation in the renin–angiotensin system, which has shown an autosomal recessive trait. Maternal use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers during pregnancy can have

APA, Harvard, Vancouver, ISO, and other styles

8

Horst-Liu, Zeya. PDZ proteins based heteromultimeric complexes in the renal proximal tubule. 2006.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

Walsh, Stephen B. Approach to the patient with renal tubular acidosis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0036.

Full text

Abstract:

The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α‎‎‎-intercalated cells in

APA, Harvard, Vancouver, ISO, and other styles

10

Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

Full text

Abstract:

Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and

APA, Harvard, Vancouver, ISO, and other styles

11

Wagner, Carsten A., and Olivier Devuyst. Renal acid–base homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0024.

Full text

Abstract:

The kidney is central to acid–base homeostasis. Major processes are reabsorption of filtered bicarbonate, de novo synthesis of bicarbonate from ammoniagenesis, and net excretion of protons. The latter requires buffers such as ammonium, phosphate, citrate and other bases binding protons (so-called titratable acids). The proximal tubule is the major site of bicarbonate reabsorption and only site of ammoniagenesis. The thick ascending limb and the distal convoluted tubule handle ammonia/ammonium and complete bicarbonate reabsorption. The collecting duct system excretes protons and ammonium, but m

APA, Harvard, Vancouver, ISO, and other styles

12

Chapman, Hannah, and Christine Elwell. Renal and bladder cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0167.

Full text

Abstract:

This chapter addresses the diagnosis and management of bladder and renal cancers. In the UK, bladder cancer is the fourth most common cancer in men, and the eighth most common cancer in women. Bladder cancer arises from the bladder urothelium, and is typically a papillary transitional cell carcinoma. Chronic infection with the parasite Schistosoma haematobium is associated with squamous cell carcinoma of the bladder, and is most prevalent in Egypt and sub-Saharan Africa. Renal cancer accounts for 3% of cancers in adults in the UK and, in most cases, is a renal cell carcinoma arising from proxi

APA, Harvard, Vancouver, ISO, and other styles

13

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

Full text

Abstract:

Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease

APA, Harvard, Vancouver, ISO, and other styles

14

Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

Full text

Abstract:

Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine st

APA, Harvard, Vancouver, ISO, and other styles

15

Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

Full text

Abstract:

Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably red

APA, Harvard, Vancouver, ISO, and other styles

16

Stewart, Douglas, Gaurav Shah, Jeremiah R. Brown, and Peter A. McCullough. Contrast-induced acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0246.

Full text

Abstract:

Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a tr

APA, Harvard, Vancouver, ISO, and other styles

17

Servais, Aude, and Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.

Full text

Abstract:

Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately

APA, Harvard, Vancouver, ISO, and other styles

18

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

Full text

Abstract:

Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal pheno

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!