Splay (physiology)

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In physiology, splay is the difference between urine threshold (the amount of a substance required in the kidneys before it appears in the urine) and saturation, or TM, where saturation is the exhausted supply of renal reabsorption carriers. [1] [2] [3] [4] [5] In simpler terms, splay is the concentration difference between a substance's maximum renal reabsorption vs. appearance in the urine. [6] Splay is usually used in reference to glucose; [1] other substances, such as phosphate, have virtually no splay at all.

The splay in the glucose titration curve is likely a result of both anatomical and kinetic differences among nephrons. [7] A particular nephron's filtered load of glucose may be mismatched to its capacity to reabsorb glucose. For example, a nephron with a larger glomerulus has a larger load of glucose to reabsorb. [7] Also, different nephrons may have different distributions and densities of SGLT2 and SGLT1 along the proximal tubule and, thus, have different tubular maximum for glucose (TmG). [7] Therefore, some nephrons may excrete before others [8] [9] [10] and also because "the maximum reabsorption rate (or Tm) cannot be achieved until the amount/min of glucose being presented to the renal tubules is great enough to fully saturate the receptor sites". [11] John Field of the American Physiological Society said "Since the splay may occur when the residual nephrons are said to be free of anatomic abnormalities, the possibility exists that changes in the kinetics of glucose reabsorption may have been induced". [12]

One study found that glucose reabsorption exhibited low splay and another also found that the titration curves for glycine showed a large amount of splay whereas those for lysine showed none [13] and the kinetics of carrier-mediated glucose transport possibly explains the level of splay in renal titration curves. As splay can be clinically important, patients with proximal tubule disease, mainly caused by hereditary nature and often in children, have a lower threshold but a normal Tm. Therefore, splay is suggested, probably because "some individual cotransporters have a low glucose affinity but maximal transport rate (renal glycosuria). [14] Studies also show that if sulfate is reabsorbed by a Tm-limited process, it will have low splay and, in animals, the limits of citrate concentration normal in the body, citrate titration curves show a large amount of splay therefore a Tm for citrate reabsorption may actually happen. Also, tubular transport is Tm-limited and the reabsorption mechanism being saturated at a plasma concentration more than 20 times than usual shows a low level of splay. [13] Renal abnormalities of glucose excretion, causing glycosuria, [15] may happen as either a result of reduced Tm for glucose or because of an abnormally wide range of nephron heterogeneity so splay of the glucose excretion curve is increased. [16] [17] Two causes are also listed for splay: "heteroginicity in glomerular size, proximal tubular length and number of carrier proteins for glucose reabsorption" and variability of TmG nephrons. [18] Splay also occurs between 180 and 350 mg/dL %. [18] [19] [20]

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<span class="mw-page-title-main">Kidney</span> Organ that filters blood and produces urine in humans

In humans, the kidneys are two reddish-brown bean-shaped blood-filtering organs that are a multilobar, multipapillary form of mammalian kidneys, usually without signs of external lobulation. They are located on the left and right in the retroperitoneal space, and in adult humans are about 12 centimetres in length. They receive blood from the paired renal arteries; blood exits into the paired renal veins. Each kidney is attached to a ureter, a tube that carries excreted urine to the bladder.

<span class="mw-page-title-main">Nephron</span> Microscopic structural and functional unit of the kidney

The nephron is the minute or microscopic structural and functional unit of the kidney. It is composed of a renal corpuscle and a renal tubule. The renal corpuscle consists of a tuft of capillaries called a glomerulus and a cup-shaped structure called Bowman's capsule. The renal tubule extends from the capsule. The capsule and tubule are connected and are composed of epithelial cells with a lumen. A healthy adult has 1 to 1.5 million nephrons in each kidney. Blood is filtered as it passes through three layers: the endothelial cells of the capillary wall, its basement membrane, and between the foot processes of the podocytes of the lining of the capsule. The tubule has adjacent peritubular capillaries that run between the descending and ascending portions of the tubule. As the fluid from the capsule flows down into the tubule, it is processed by the epithelial cells lining the tubule: water is reabsorbed and substances are exchanged ; first with the interstitial fluid outside the tubules, and then into the plasma in the adjacent peritubular capillaries through the endothelial cells lining that capillary. This process regulates the volume of body fluid as well as levels of many body substances. At the end of the tubule, the remaining fluid—urine—exits: it is composed of water, metabolic waste, and toxins.

<span class="mw-page-title-main">Collecting duct system</span> Kidney system

The collecting duct system of the kidney consists of a series of tubules and ducts that physically connect nephrons to a minor calyx or directly to the renal pelvis. The collecting duct participates in electrolyte and fluid balance through reabsorption and excretion, processes regulated by the hormones aldosterone and vasopressin.

<span class="mw-page-title-main">Renal physiology</span> Study of the physiology of the kidney

Renal physiology is the study of the physiology of the kidney. This encompasses all functions of the kidney, including maintenance of acid-base balance; regulation of fluid balance; regulation of sodium, potassium, and other electrolytes; clearance of toxins; absorption of glucose, amino acids, and other small molecules; regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D.

<span class="mw-page-title-main">Proximal tubule</span> Segment of nephron in kidneys

The proximal tubule is the segment of the nephron in kidneys which begins from the renal pole of the Bowman's capsule to the beginning of loop of Henle. At this location, the glomerular parietal epithelial cells (PECs) lining bowman’s capsule abruptly transition to proximal tubule epithelial cells (PTECs). The proximal tubule can be further classified into the proximal convoluted tubule (PCT) and the proximal straight tubule (PST).

<span class="mw-page-title-main">Renal medulla</span> Innermost part of the kidney

The renal medulla is the innermost part of the kidney. The renal medulla is split up into a number of sections, known as the renal pyramids. Blood enters into the kidney via the renal artery, which then splits up to form the segmental arteries which then branch to form interlobar arteries. The interlobar arteries each in turn branch into arcuate arteries, which in turn branch to form interlobular arteries, and these finally reach the glomeruli. At the glomerulus the blood reaches a highly disfavourable pressure gradient and a large exchange surface area, which forces the serum portion of the blood out of the vessel and into the renal tubules. Flow continues through the renal tubules, including the proximal tubule, the loop of Henle, through the distal tubule and finally leaves the kidney by means of the collecting duct, leading to the renal pelvis, the dilated portion of the ureter.

In physiology, the renal threshold is the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine. When the renal threshold of a substance is exceeded, reabsorption of the substance by the proximal convoluted tubule is incomplete; consequently, part of the substance remains in the urine. Renal thresholds vary by substance – the low potency poison urea, for instance, is removed at much lower concentrations than glucose. Indeed, the most common reason for the glucose renal threshold ever being exceeded is diabetes, which is called glycosuria.

<span class="mw-page-title-main">Glycosuria</span> Medical condition

Glycosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys, producing a condition termed renal glycosuria. Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis.

<span class="mw-page-title-main">Renal tubular acidosis</span> Medical condition

Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine. The metabolic acidosis that results from RTA may be caused either by insufficient secretion of hydrogen ions into the latter portions of the nephron or by failure to reabsorb sufficient bicarbonate ions from the filtrate in the early portion of the nephron. Although a metabolic acidosis also occurs in those with chronic kidney disease, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes. RTA is usually an incidental finding based on routine blood draws that show abnormal results. Clinically, patients may present with vague symptoms such as dehydration, mental status changes, or delayed growth in adolescents.

<span class="mw-page-title-main">Reabsorption</span>

In renal physiology, reabsorption or tubular reabsorption is the process by which the nephron removes water and solutes from the tubular fluid (pre-urine) and returns them to the circulating blood. It is called reabsorption (and not absorption) because these substances have already been absorbed once (particularly in the intestines) and the body is reclaiming them from a postglomerular fluid stream that is on its way to becoming urine (that is, they will soon be lost to the urine unless they are reabsorbed from the tubule into the peritubular capillaries. This happens as a result of sodium transport from the lumen into the blood by the Na+/K+ATPase in the basolateral membrane of the epithelial cells. Thus, the glomerular filtrate becomes more concentrated, which is one of the steps in forming urine. Nephrons are divided into five segments, with different segments responsible for reabsorbing different substances. Reabsorption allows many useful solutes (primarily glucose and amino acids), salts and water that have passed through Bowman's capsule, to return to the circulation. These solutes are reabsorbed isotonically, in that the osmotic potential of the fluid leaving the proximal convoluted tubule is the same as that of the initial glomerular filtrate. However, glucose, amino acids, inorganic phosphate, and some other solutes are reabsorbed via secondary active transport through cotransport channels driven by the sodium gradient.

<span class="mw-page-title-main">Peritubular capillaries</span>

In the renal system, peritubular capillaries are tiny blood vessels, supplied by the efferent arteriole, that travel alongside nephrons allowing reabsorption and secretion between blood and the inner lumen of the nephron. Peritubular capillaries surround the cortical parts of the proximal and distal tubules, while the vasa recta go into the medulla to approach the loop of Henle.

In the physiology of the kidney, tubuloglomerular feedback (TGF) is a feedback system inside the kidneys. Within each nephron, information from the renal tubules is signaled to the glomerulus. Tubuloglomerular feedback is one of several mechanisms the kidney uses to regulate glomerular filtration rate (GFR). It involves the concept of purinergic signaling, in which an increased distal tubular sodium chloride concentration causes a basolateral release of adenosine from the macula densa cells. This initiates a cascade of events that ultimately brings GFR to an appropriate level.

Sodium-dependent glucose cotransporters are a family of glucose transporter found in the intestinal mucosa (enterocytes) of the small intestine (SGLT1) and the proximal tubule of the nephron. They contribute to renal glucose reabsorption. In the kidneys, 100% of the filtered glucose in the glomerulus has to be reabsorbed along the nephron. If the plasma glucose concentration is too high (hyperglycemia), glucose passes into the urine (glucosuria) because SGLT are saturated with the filtered glucose.

In physiology, transport maximum refers to the point at which increase in concentration of a substance does not result in an increase in movement of a substance across a cell membrane.

Renal reabsorption of sodium (Na+) is a part of renal physiology. It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor). It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide.

Renal glucose reabsorption is the part of kidney (renal) physiology that deals with the retrieval of filtered glucose, preventing it from disappearing from the body through the urine.

Renal oligopeptide reabsorption is the part of renal physiology that deals with the retrieval of filtered oligopeptides, preventing them from disappearing from the body through the urine.

Fanconi syndrome or Fanconi's syndrome is a syndrome of inadequate reabsorption in the proximal renal tubules of the kidney. The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity, or by adverse drug reactions. It results in various small molecules of metabolism being passed into the urine instead of being reabsorbed from the tubular fluid. Fanconi syndrome affects the proximal tubules, namely, the proximal convoluted tubule (PCT), which is the first part of the tubule to process fluid after it is filtered through the glomerulus, and the proximal straight tubule, which leads to the descending limb of loop of Henle.

<span class="mw-page-title-main">Diuretic</span> Substance that promotes the production of urine

A diuretic is any substance that promotes diuresis, the increased production of urine. This includes forced diuresis. A diuretic tablet is sometimes colloquially called a water tablet. There are several categories of diuretics. All diuretics increase the excretion of water from the body, through the kidneys. There exist several classes of diuretic, and each works in a distinct way. Alternatively, an antidiuretic, such as vasopressin, is an agent or drug which reduces the excretion of water in urine.

<span class="mw-page-title-main">Mammalian kidney</span> Paired organ in the urinary system of mammals

The mammalian kidneys are a pair of excretory organs of the urinary system of mammals, being functioning kidneys in postnatal-to-adult individuals. The kidneys in mammals are usually bean-shaped or externally lobulated. They are located behind the peritoneum (retroperitoneally) on the back (dorsal) wall of the body. The typical mammalian kidney consists of a renal capsule, a peripheral cortex, an internal medulla, one or more renal calyces, and a renal pelvis. Although the calyces or renal pelvis may be absent in some species. The medulla is made up of one or more renal pyramids, forming papillae with their innermost parts. Generally, urine produced by the cortex and medulla drains from the papillae into the calyces, and then into the renal pelvis, from which urine exits the kidney through the ureter. Nitrogen-containing waste products are excreted by the kidneys in mammals mainly in the form of urea.

References

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  3. ↑ Rhoades, Rodney A.; Bell, David R. (2012). Medical Physiology: Principles for Clinical Medicine. Lippincott Williams & Wilkins. pp. 399–406. ISBN   978-1609134273 . Retrieved September 11, 2015.
  4. ↑ USMLE Step 1 Physiology Lecture Notes. Kaplan, Inc. 2015. p. 213. ISBN   978-1625236920 . Retrieved September 11, 2015.
  5. ↑ Costanzo, Linda S. (2013). Physiology. Elsevier. ISBN   978-1455728138 . Retrieved September 11, 2015.
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  7. 1 2 3 Medical Physiology. Walter F. Boron, Emile L. Boulpaep (3rd ed.). Philadelphia, PA. 2017. p. 773. ISBN   978-1-4557-3328-6. OCLC   951680737.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link)
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  10. ↑ Sanoop, K. S.; Mridul, G. S.; Nishanth, P. S. (2012). Physicon - The Reliable Icon In Physiology. JP Medical. pp. 125–359. ISBN   978-9350259009 . Retrieved September 11, 2015.
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  12. ↑ Field, John, Handbook of Physiology: Renal physiology, page 598, American Physiological Society
  13. 1 2 Koushanpour, Esmail; Kriz, Wilhelm (2013). Renal Physiology: Principles, Structure, and Function. Springer Publishing. pp. 218–234. ISBN   978-1475719123 . Retrieved September 11, 2015.
  14. ↑ Boron, Walter F.; Boulpaep, Emile L. (2012). Medical Physiology, 2e Updated Edition: with STUDENT CONSULT Online Access. Elsevier. ISBN   978-1455711819 . Retrieved September 11, 2015.
  15. ↑ Johnson, Leonard R. (2 October 2003). Essential Medical Physiology. Academic Press. pp. 385–387. ISBN   0123875846 . Retrieved September 11, 2015.
  16. ↑ Lote, Christopher (22 June 2012). Principles of Renal Physiology. Springer Publishers. pp. 57–58. ISBN   978-1461437857 . Retrieved September 11, 2015.
  17. ↑ Stave, Uwe (2013). Perinatal Physiology. Springer Publishers. p. 599. ISBN   978-1468423167 . Retrieved September 11, 2015.
  18. 1 2 Kharana, Indu (2014). Textbook of Human Physiology for Dental Students. Elsevier. pp. 282–283. ISBN   978-8131238134 . Retrieved September 11, 2015.
  19. ↑ Premanik, Debasis; Premanik, Aparna (2006). Principles of Physiology. Academic Publishers India. pp. 271–272. ISBN   8189781340 . Retrieved September 11, 2015.
  20. ↑ Dudek, Ronald W. (2008). High-yield Physiology, Part 845, Volume 2008. Lippincott Williams & Wilkins. p. 83. ISBN   978-0781745871 . Retrieved September 11, 2015.
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