Mammalian kidney

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Mammalian kidney
Unipapillary, multilobar, smooth, bean-shaped camel kidney, in which the renal papillae are completely fused into the renal crest.[1]
Details
PrecursorUreteric bud, metanephrogenic blastema
SystemUrinary system and endocrine system
ArteryRenal artery
VeinRenal vein
NerveRenal plexus
LymphCollecting lymphatic vessels
Anatomical terminology

The mammalian kidneys are a pair of excretory organs of the urinary system of mammals,[2] being functioning kidneys in postnatal-to-adult individuals[3] (i. e. metanephric kidneys).[2] The kidneys in mammals are usually bean-shaped[4] or externally lobulated.[5] They are located behind the peritoneum (retroperitoneally)[6] on the back (dorsal) wall of the body.[7] The typical mammalian kidney consists of a renal capsule, a peripheral cortex, an internal medulla, one or more renal calyces, and a renal pelvis.[7] Although the calyces or renal pelvis may be absent in some species.[7] The medulla is made up of one or more renal pyramids,[8] forming papillae with their innermost parts.[9] 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.[7][10] Nitrogen-containing waste products are excreted by the kidneys in mammals mainly in the form of urea.[11]

The structure of the kidney differs between species.[12] The kidneys can be unilobar (a single lobe represented by a single renal pyramid) or multilobar,[13][14] unipapillary (a single or a common papilla), with several papillae or multipapillary,[14][15] may be smooth-surfaced or lobulated.[1][13] The multilobar kidneys can also be reniculate, which are found mainly in marine mammals.[16] The unipapillary kidney with a single renal pyramid is the simplest type of kidney in mammals, from which the more structurally complex kidneys are believed to have evolved.[17][6][18] Differences in kidney structure are the result of adaptations during evolution to variations in body mass and habitats (in particular, aridity) between species.[19][20][12]

The cortex and medulla of the kidney contain nephrons,[21] each of which consists of a glomerulus and a complex tubular system.[22] The cortex contains glomeruli and is responsible for filtering the blood.[7] The medulla is responsible for urine concentration[23] and contains tubules with short and long loops of Henle.[24] The loops of Henle are essential for urine concentration.[25] Amongst the vertebrates, only mammals and birds have kidneys that can produce urine more concentrated (hypertonic) than the blood plasma,[7] but only in mammals do all nephrons have the loop of Henle.[26]

The kidneys of mammals are vital organs[27] that maintain water, electrolyte and acid-base balance in the body, excrete nitrogenous waste products, regulate blood pressure, and participate in bone formation[28][29][30] and regulation of glucose levels.[31] The processes of blood plasma filtration, tubular reabsorption and tubular secretion occur in the kidneys, and urine formation is a result of these processes.[8] The kidneys produce renin[32] and erythropoietin[33] hormones, and are involved in the conversion of vitamin D to its active form.[34] Mammals are the only class of vertebrates in which only the kidneys are responsible for maintaining the homeostasis of the extracellular fluid in the body.[35] The function of the kidneys is regulated by the autonomic nervous system and hormones.[36]

The potential for regeneration in mature kidneys is limited[37][38] because new nephrons cannot be formed.[39] But in cases of limited injury, renal function can be restored through compensatory mechanisms.[40] The kidneys can have noninfectious and infectious diseases; in rare cases, congenital and hereditary anomalies occur in the kidneys of mammals.[41] Pyelonephritis is usually caused by bacterial infections.[42][43] Some diseases may be species specific,[44] and parasitic kidney diseases are common in some species.[45][46] The structural characteristics of the mammalian kidneys make them vulnerable to ischemic and toxic injuries.[47] Permanent damage can lead to chronic kidney disease.[48][49] Ageing of the kidneys also causes changes in them, and the number of functioning nephrons decreases with age.[50]

Structure[edit]

Gross anatomy[edit]

Didactic model of the multilobar mammalian kidney:[51]

Location and shape[edit]

In mammals, the kidneys are usually bean-shaped;[4] the shape is unique to mammals (fish, for example, have elongated kidneys).[52] Some species have externally lobulated kidneys, as in marine mammals, bovines and bears.[53][13] The lobulated kidneys of cetacians and pinnipeds have elongated oval shape.[54] The concave part of the bean-shaped kidneys is called the renal hilum, through which the renal artery and nerves enter the kidney. The renal vein, collecting lymphatic vessels and ureter exit the kidney through the renal hilum.[6][55]

The kidneys are located retroperitoneally[6] on the back (dorsal) wall of the body of mammals.[7] In the body, the kidney is surrounded or partially surrounded by a layer of fatty tissue (perirenal adipose capsule),[56][57][58] which separates the kidney from the perirenal fascia.[58]

General structure[edit]

The outer layer of each kidney is made up of a fibrous sheath called a renal capsule. The peripheral layer of the kidney is called the cortex, and the inner layer is called the medulla. The medulla consists of pyramids (also called malpighian pyramids), ascending with their base to the cortex and forming together with it the renal lobe.[59] The pyramids are separated from each other by renal columns (Bertin's columns) formed by cortical tissue.[60] The tips of the pyramids end with the renal papillae, from which urine is excreted into the calyces, pelvis, ureter, and, in most species, directly into the bladder,[59][10] after which it is excreted through the urethra.[61]

Parenchyma[edit]

Simplified structure of the mammalian kidney lobe:[21][62]
  • 1. Cortex
  • 2. Outer medulla
  • 3. Inner medulla
  • 4. Inner stripe
  • 5. Outer stripe
  • 6. Juxtamedullary nephron with long loop of Henle
  • 7. Medullary ray
  • 8. Renal capsule
  • 9. Renal papilla.
  Podocytes
  Proximal convoluted tubule
  Proximal straight tubule
  Intermediate tubule (loop of Henle)
  Distal straight tubule
  Macula densa
  Distal convoluted tubule
  Connecting tubule
  Collecting duct

The parenchyma, being the functional part of the kidneys, is visually divided into cortex and medulla.[63][64] The cortex itself is similar to the typical kidneys of less developed vertebrates, which cannot produce concentrated urine,[7] while the medulla is the main site of urine concentration.[23] The ratio of cortex to medulla varies between species, in domesticated animals the cortex usually occupies a third or fourth part of the parenchyma, while in desert animals it is only a fifth part.[13] Increased renal medulla thickness is associated with greater urine concentrating ability in desert mammals.[65]

The cortex and medulla are based on nephrons[66][22] together with an extensive network of blood vessels and capillaries, as well as collecting ducts, into which nephrons empty, and renal interstitium.[67] The nephron is composed of a renal corpuscle and a renal tubule. The renal corpuscle is a blood-filtering part of the nephron and is located in the cortex. The renal tubule extends from the renal corpuscle to the medulla into the loop of Henle and then returns back to the cortex. Finally, the renal tubule flows with its distal end into its collecting duct, which is common to several nephrons. The collecting ducts descend again into the medulla and fuse to wider collecting ducts, which pass through the inner medulla.[68][69]

Based on the location of the renal corpuscle in the cortex, nephrons are classified into 3 types: superficial (closer to the renal capsule), midcortical (in the middle part of the cortex) and juxtamedullary (closer to the medulla) nephrons.[24] Generally, they differ in the length of the loop of Henle. Superficial and midcortical nephrons typically have loops of Henle that are shorter than those of juxtamedullary nephrons.[70] According to the length of the loop of Henle, nephrons are classified into nephrons with a long loop and with a short loop of Henle.[24] Although those two classifications do not coincide. Usually, juxtamedullary nephrons have long loops of Henle, but there are more long-looped nephrons than juxtamedullary nephrons in the kidneys.[71]

Cortex[edit]

Structurally, the cortex consists of cortical labyrinth and medullary rays.[9] The cortical labyrinth contains interlobular arteries, vascular networks formed by afferent and efferent arterioles, renal corpuscles, proximal convoluted tubules, macula densa, distal convoluted tubules, connecting tubules and the initial parts of the collecting ducts.[72] The proximal convoluted tubules predominate in the cortical labyrinth.[73] The continuous layer of the cortex lying above the medullary rays is called the cortex corticis.[9] Cortex corticis differs from the rest of the cortical labyrinth in that it doesn't contain glomeruli.[74][75] Some mammals (for example, pig) have nephrons whose loops of Henle do not reach the medulla; such nephrons are called cortical nephrons.[68][76] Cortical nephrons have a very short thin segment of the loop of Henle, and this segment may even be absent.[76] The medullary rays of the cortex contain the proximal straight tubules, the cortical part of the thick ascending limb of the loops of Henle, and the cortical part of the collecting ducts.[72] The cortex is divided into lobules, each of which is a medullary ray in conjunction with connected to it nephrons, and interlobular arteries that pass between the lobules.[77]

Medulla[edit]

The medulla in mammals is divided into outer and inner regions. The outer region consists of short loops of Henle and collecting ducts, while the inner region consists of long loops and collecting ducts.[78] The outer region is also subdivided into outer[79] (lying directly under the cortex)[80] and inner stripes.[79] The stripes differ in that the outer stripe contains proximal straight tubules, while the inner stripe contains thin descending limbs of the loop of Henle (a section of the nephron following the proximal straight tubule).[80]

The ability to produce more concentrated urine is associated with the length of the inner medulla (with its long loops of Henle).[81] Most mammalian species have nephrons with both short and long loops of Henle, while some species may have only one type. For example, mountain beavers have only nephrons with a short loop, and, accordingly, there is no inner medulla in the kidneys and their ability to concentrate urine is low. Dogs and cats, on the other hand, have only long-loop nephrons with an average ability to concentrate urine. The ratio of nephrons with short loops of Henle to those with long loops also varies between species.[82] Previously, it was mistakenly believed that species with the highest urine concentration ability have only long-looped nephrons. But the kidney of species with high ability to concentrate urine have more short-looped nephrons than long-looped nephrons, so the highest concentration ability requires both types of nephrons.[83]

Variations[edit]

Variation of the kidney between domestic mammalian species:[84]
  • (A) Equine kidneys with heart-shaped right kidney
  • (B) Bovine kidneys with lobulated cortex and fused medulla
  • (C) Canine bean-shaped kidneys.

Structurally, kidneys vary between mammals.[85] What structural type a particular species will have depends generally on the body mass of the animals.[86] Small mammals have unilobar kidneys with a compact structure and a single renal papilla.[85][14] Larger animals have multilobar kidneys, such as those of bovines.[85][14] By itself, the lobe is equivalent to a simple unipapillary kidney, as in rats or mice.[73] Bovine kidneys also lack renal pelvis, urine from the major calyces is excreted directly into the ureter.[87]

Kidneys can be unipapillary,[14] as in rats and mice,[88] with few renal papillae, as in spider monkeys, or with many, as in pigs and humans.[14] Most animals have single renal papilla.[14] In some animals, such as horses, the tips of the renal pyramids fuse with each other to form a common renal papilla, called the renal crest.[15] Such kidneys are called crest kidneys and are also considered unipapillary kidneys (an enlarged modification).[89][86][19] The crest kidneys usually appear in species larger than the rabbit (for example, in monkeys and camels).[90][19]

Author's drawing of a dolphin reniculate kidney:[91]
  • 1. Renal artery
  • 2. Renal vein
  • 3. Common collecting duct that becomes the ureter.

The kidneys of the marine mammals, otters and bears are reniculate.[16] The reniculate kidneys consist of small reniculi,[16] each of which is comparable by its structure to a simple unipapillary kidney.[9] The kidneys of marine mammals can have hundreds[16] or thousands[49] of reniculi, each with its own cortex, medulla, and calyx.[16] For example, each whale kidney consist of about 7000 renculi which join a common collective system.[49] Although the kidneys of manatees are actually multilobar because their cortex is continuous rather than discrete.[16]

The size of the kidneys increases with the mass of mammals, and the number of nephrons in the kidneys between mammals increases allometrically.[92] In mice, the kidneys are approximately 1 cm (0.4 in) long, weighing 400 mg, with 16,000 nephrons, while in the killer whale, the kidney length exceeds 25 cm (10 in), the mass is approximately 4.5 kg (10 lb), with the number of nephrons of the order of 10,000,000. At the same time, the killer whale kidneys are reniculate, with each renicule about 430 mg in weight and 1 cm (0.4 in) in length, making renicule of the killer whale similar to the kidney of a mouse not only in structure, but also in size and mass.[93]

Microanatomy[edit]

By microanatomic structure, the kidney can be divided into several main elements: interstitium, renal corpuscles, tubules, and vasculature.[13] The interstitium is the cells and extracellular matrix in the space between the glomeruli, vessels, tubules, and collecting ducts.[94][95] The interstitial space surrounding cells is filled with interstitial fluid.[96] The interstitium between the tubules contains fibroblasts, dendritic cells, macrophages and lymphocytes. Cortical interstitium also includes the endothelial cells of the lymphatic capillaries,[96] which are considered part of the interstitium due to the lack of a basement membrane.[97] Interstitial fibroblasts form the tissue skeleton of the kidney.[98] Blood vessels, nerves and lymphatic vessels run through the interstitium.[99] The nephron, together with the collecting duct into which it empties, is called the uriniferous tubule. Each uriniferous tubule, along with the vasculature supplying it, is embedded in the interstitium.[13]

Approximately 18–26 different cell types have been described in mammalian kidneys, with a large variation in the range due to a lack of consensus on what counts as a particular cell type, and likely to species differences.[100] Renal corpuscles are composed of 4 cell types: fenestrated endothelium, mesangial cells, podocytes and parietal epithelial cells of Bowman's capsule.[101] At least 16 different cell types make up the renal tubules.[102] The tubules themselves are divided into at least 14 segments,[102] which differ in cell types and functions.[103] The normal functioning of the kidneys is provided by the complex of epithelial, endothelial, interstitial and immune cells.[104]

Blood supply[edit]

Equine kidney blood supply

The mammalian kidney is the organ that has the most complex vascular blood system compared to other organs.[105] Despite their small size, the kidneys of mammals account for a significant part of the minute volume of blood circulation.[106] It is believed that in land mammals, about a fifth of the volume of blood that passes through the heart passes through the kidneys.[107] In adult mice, for example, minute volume is about 9%–22%.[108]

Blood enters the kidney through the renal artery,[55] which in the multilobar kidney branches in the area of the renal pelvis into large interlobar arteries that pass through the renal columns.[10][109] The interlobar arteries branch at the base of the pyramid, giving rise to arcuate arteries, from which the interlobular arteries extend into the cortex.[109] The interlobar arteries supply the pyramids and the adjacent cortex with an extensive network of blood vessels.[10] The cortex itself is heavily permeated with arteries, while there are no arteries in the medulla.[17] The venous flow of blood runs back parallel to the arteries.[109] In some species, there are veins isolated from the arteries under the capsule in the cortex, which in humans are called stellate veins. These veins flow into the interlobular veins.[110] The renal portal system is absent in mammals,[111] with the exception of monotremes.[112] Mammals are the only class of vertebrates (with exception of some species) that does not have a renal portal system.[113]

The vascular glomeruli of nephrons receive blood from afferent arterioles, which originate in the interlobular arteries with intermediate formation of prearterioles. Each afferent arteriole divides into several renal glomeruli. Then these glomeruli join into the efferent arteriole, into which filtered blood goes from the nephrons. In nephrons with a long loop of Henle, the efferent arterioles branch, forming straight vessels called vasa recta, which descend into the medulla. The descending vasa recta, ascending vasa recta vessels, and the loop of Henle together form the countercurrent system of the kidney. In the afferent arteriole, blood is supplied at high pressure, which promotes filtration, and in the efferent arteriole, it is at low pressure, which promotes reabsorption.[109]

Lymphatic drainage[edit]

The kidney is well supplied with lymphatic vessels,[114] which remove excess fluid with substances and macromolecules dissolved in it from the interstitium that fills the space between the tubules and blood vessels.[115][116] The anatomy of the lymphatic system of the kidney is similar between mammals.[117] Lymphatics basically follow the path of blood vessels.[118]

The lymphatic system of the kidneys begins in the cortex with the initial blind-end intralobular lymphatic capillaries passing near the tubules and renal corpuscles, but the lymphatic vessels do not go inside the renal corpuscles. The intralobular lymphatic capillaries are connected to the arcuate lymphatics.[119] The arcuate lymphatics pass into the interlobar lymphatics, which pass near the interlobar arteries.[119][117] The arcuate and interlobar lymphatics are lymphatic precollectors.[97] Finally, the interlobar lymphatics join the collecting hilar lymphatics leaving the kidney through renal hilum.[119] Lymphatic vessels are usually absent in the medulla of the mammalian kidneys, and the role of lymphatic vessels is assumed to be performed by vasa recta.[120][121]

In some species, there may be differences in the anatomy of the lymphatic system of the kidney. For example, sheep lack lymphatics in the renal capsule, and rabbits lack interlobular lymphatics.[119] Most studies fail to detect lymphatic vessels in the renal medulla of animals, in particular, they are not found in sheep and rats. But some studies have found lymphatic vessels in the renal medulla of pigs and rabbits.[121] Depending on the species, there may or may not also be a connection between the lymphatics of the renal capsule and the internal renal lymphatic system.[122]

Nerve supply[edit]

The innervation of the kidney is provided by efferent sympathetic nerve fibers entering the kidney through the renal hilum,[55] originating in the celiac plexus,[123] and afferent, leaving the kidney to the spinal ganglion.[123] There is no reliable evidence for the innervation of the kidney by parasympathetic nerves,[123] while the existing evidence is controversial.[124] Efferent sympathetic nerve fibers reach the renal vasculature, renal tubules, juxtaglomerular cells, and the wall of the renal pelvis,[125] all parts of the nephron are innervated by sympathetic nerves.[123] Nerve fibers pass through the connective tissue around the arteries and arterioles. In the medulla, the descending vasa recta are innervated as long as they contain smooth muscle cells.[126] Most afferent nerve fibers are located in the renal pelvis.[127] The vast majority of nerves in the kidneys are unmyelinated.[128]

Normal physiological stimulation of the efferent sympathetic nerves of the kidney is involved in maintaining the balance of water and sodium in the body. Activation of the efferent sympathetic nerves of the kidney reduces its blood flow, and respectively, filtration and excretion of sodium in the urine, and also increases the rate of renin secretion.[129] The afferent nerves in the kidney are also involved in maintaining balance. Mechanosensory nerves of the kidney are activated by stretching of the tissue of the renal pelvis, which can occur with an increase in the rate of urine flow from the kidney, resulting in a reflex decrease in the activity of efferent sympathetic nerves. That is, activation of the afferent nerves in the kidney suppresses the activity of the efferent nerves.[130]

Functions[edit]

Excretory function[edit]

In mammals, nitrogenous metabolic products are excreted predominantly in the form of urea,[11] which is the end by-product of mammalian protein metabolism[131][132] and is highly soluble in water.[133] Most of the urea is excreted by the kidneys.[131] Blood filtration, as in other vertebrates, occurs in the renal glomeruli, where pressurized blood passes through a permeable barrier that filters out blood cells and large protein molecules, forming primary urine. The filtered primary urine is osmotically and ionically the same as blood plasma. In the tubules of the nephron, substances useful for the body, dissolved in the primary urine, are subsequently reabsorbed, as the urine is being concentrated.[134]

Osmoregulation[edit]

The mammalian kidneys maintain an almost constant level of plasma osmolarity. The main component of blood plasma, which determines its osmolarity, is sodium and its anions.[135] The key role in maintaining a constant level of osmolarity is managed by the control of the ratio of sodium and water in the blood.[135][136] Drinking large amounts of water can dilute the blood plasma. To remove excess water but keep salt in the blood, the kidneys produce more dilute urine than the plasma. If too little water is consumed, then urine is excreted more concentrated than blood plasma.[135] The concentration of urine is provided by an osmotic gradient that increases from the border between the cortex and medulla to the top of the pyramid of the medulla.[135]

In addition to the kidneys, the hypothalamus and neurohypophysis are involved in the regulation of water balance through a feedback system. The osmoreceptors of the hypothalamus respond to an increase in the osmolarity of the blood plasma, as a result of which the secretion of vasopressin by the posterior pituitary gland is stimulated, and thirst also arises. The kidneys respond via receptors to increased levels of vasopressin by increasing water reabsorption. As a result, plasma osmolarity decreases due to its dilution with water.[137]

Variation in the rate of water excretion is an important survival function for mammals that have limited access to water.[135] The loop of Henle is the most prominent feature of the mammalian kidney. These loops provide the most efficient way to reabsorb water and create concentrated urine, allowing mammals to save water in their bodies.[138] After passing through the loop of Henle, the fluid becomes hypertonic relative to the blood plasma.[139] Mammalian kidneys combine nephrons with short and long loops of Henle.[140] The ability to concentrate urine is determined mainly by the structure of the medulla and the length of the loops of Henle.[141]

Endocrine function[edit]

In addition to excretory, the kidneys also perform an endocrine function, they produce certain hormones. The juxtaglomerular cells of the kidneys produce renin, which is a key regulator of the renin–angiotensin system, which is responsible for blood pressure regulation.[32]

The production of erythropoietin by the kidneys is responsible for the differentiation of erythroid progenitor cells in the bone marrow into erythrocytes and is induced by hypoxia. Thus, with a lack of oxygen, the number of red blood cells in the blood increases, and they are responsible for transporting oxygen.[33]

The kidneys are involved in the metabolism of vitamin D. In the liver, vitamin D is converted to calcifediol (25OHD), while the kidneys convert calcifediol to calcitriol (1,25(OH)2D), which is the active form of the vitamin and is essentially a hormone. Vitamin D is involved in the formation of bones and cartilage, and also performs a number of other functions, for example, it is involved in the functioning of the immune system.[34]

Blood pressure regulation[edit]

Some mammalian internal organs, including the kidneys and lung, are designed to function within normal blood pressure levels and normal blood volume levels, and blood pressure itself is also affected by changes in blood volume levels. Therefore, maintaining a constant blood volume for mammals is a very important function of the body.[142] The stable level of blood volume is influenced by the glomerular filtration rate, the function of individual parts of the nephron, the sympathetic nervous system and the renin-angiotensin-aldosterone system.[143]

In the walls of the afferent arterioles at the entrance to the renal glomeruli, there are juxtaglomerular cells. These cells are sensitive to changes in the minute volume of blood circulation, and to the composition and volume of the extracellular fluid, producing renin in response to changes in their level.[144] Once in the bloodstream, renin converts angiotensinogen to angiotensin I. Angiotensin I is further cleaved by the angiotensin-converting enzyme to angiotensin II, which is a potent vasoconstrictor that increases blood pressure.[144] In addition to angiotensin II, other biologically active substances can be formed in mammals. Angiotensin II can be cleaved to angiotensin III, angiotensin IV and angiotensin (1–7).[145]

Acid-base balance[edit]

Maintaining acid-base balance is vital because changes in pH levels affect virtually every biological process in the body.[146] In a typical mammal, a normal average pH level is around 7.4.[147] As in the case of other vertebrates in mammals, the acid-base balance is maintained mainly by the bicarbonate buffer system (HCO3-/CO2), which allows maintaining a constant pH level of the blood and extracellular fluid.[148] This buffer system is described by the following equation:[149]

The regulation of the acid-base balance through the bicarbonate buffer system is provided by the lungs and kidneys.[148] The lungs regulate CO2 (carbon dioxide) level, while the kidneys regulate HCO3- and H+ (bicarbonate and hydrogen ions).[149] The kidneys play a key role in maintaining a constant level of acid-base balance in mammals.[30] In the glomeruli, HCO3- is completely filtered into primary urine.[149] To maintain a constant pH, the kidneys reabsorb almost all of the HCO3- from primary urine back into the bloodstream and secrete H+ into the urine, oxidizing the urine.[150]

Reabsorption of HCO3- occurs in the proximal tubule, in the ascending limb of the loop of Henle, and to a lesser extent in the distal convoluted tubule of the nephron. H+ secretion is carried out mainly through Na+/H+ exchangers in the tubules of the nephron.[150] The collecting ducts are involved in the energy-dependent secretion of H+.[151] When H+ ions enter the urine, they can combine with filtered HCO3- to form carbonic acid H2CO3, which is being converted into CO2 and H2O (water) by the luminal carbonic anhydrase. The formed CO2 diffuses into the cells of the tubules, where it combines with H2O with the help of cytosolic carbonic anhydrase and forms HCO3-, which then returns to the bloodstream, and the formed H+ ion is secreted into the urine. Some of the H+ ions are secreted at an energy cost through an ATP-dependent mechanism.[150]

The excreted urine is slightly acidic. The excretion of H+ together with urine also occurs through buffer systems, in particular, NH4+ (ammonium).[152] Only a small amount of NH4+ is filtered through the glomerulus; [152] most of the ammonium excreted is the result of H+ ion oxidation of NH3 (ammonia) formed in the cells of the proximal convoluted tubule, which is secreted into the lumen of the tubule either as NH3 or as NH4+.[153] The formation of ammonia is also accompanied by the formation of new HCO3-, which replenishes the extracellular buffer system.[153] In the thick ascending tubule of the loop of Henle, on the contrary, NH4+ is absorbed, which causes its accumulation in the interstitium.[154] The final stage of urine oxidation occurs in the collecting ducts, where H+ ions are secreted with the involvement of ATP, and NH3 is transported from the interstitium and secreted into the urine, where NH3 is oxidized by H+ to form NH4+.[151] By regulating HCO3- reabsorption and H+ secretion, the kidneys help maintain blood pH homeostasis.[149]

Glucose homeostasis[edit]

Together with the liver,[155] the kidneys are involved in maintaining glucose homeostasis in the body of mammals.[31][156] The processes of filtration, reabsorption and consumption of glucose, as well as the production of glucose through gluconeogenesis, occur in the kidneys.[31][156] Glucose consumption (glycolysis) occurs primarily in the medulla, while gluconeogenesis occurs in the cortex. Hormonally, the process of gluconeogenesis in the kidneys is regulated by insulin and catecholamines.[31]

Evolution[edit]

See also: Kidney (vertebrates) § Evolution

Mammalian metanephric kidney[edit]

See also: Evolution of mammals

The first mammals are believed to have appeared during the Permian period, which was characterized by cold nights in arid deserts and a strong seasonality with long, cold winters. It is likely that cold and aridity were significant factors of evolutionary pressure at that time. The development of warm-bloodedness in protomammals could lead to an increase in the intensity of blood circulation, and, accordingly, to an increase in blood pressure, which, in turn, increased the glomerular filtration rate of the kidneys. However, an increase in the glomerular filtration rate would also lead to an increase in the removal rate of water from the body.[157] All mammals have a thin segment of the tubule that is part of the loop of Henle. This segment is responsible for the concentration of urine and the reabsorption of water.[158] It can be assumed that the development of a water reabsorption mechanism could be part of the evolution of warm-bloodedness, rather than a direct adaptation to aridity.[157]

Adaptations to aridity[edit]

The ability to produce more concentrated urine is inversely dependent on the body mass of the mammals, that is, the smaller the mass of the animal, the more concentrated urine relative to animals with a larger mass its kidneys could produce during adaptation to an arid environment.[159] Some desert animals have evolved greater ability to concentrate urine than other animals.[160] The most concentrated urine among the studied species is produced by the Australian hopping mouse Notomys alexis,[159] whose kidneys have longer loops of Henley and an elongated renal papilla compared to the kidneys of other mammals.[161] The longer loops of Henley in the Australian hopping mouse make it possible to produce very concentrated urine[138] and survive in conditions of water scarcity.[159]

Adaptations to body mass[edit]

One of the key factors that determine the shape and morphology of the kidneys in mammals is their mass.[162] The simplest type of kidney in mammals is the unipapillary kidney, consisting of a cortex, medulla, and renal pelvis.[163] But the unipapillary kidney is limited by the number of nephrons at which it functions optimally.[20] It is assumed that unipapillary kidney was the original kidney structure in mammals, from which multilobar kidneys evolved.[19]

More complex multilobar kidneys likely emerged as an adaptation to the increased body mass of mammals and the corresponding need for an increase in the number of nephrons in the kidneys.[20] A further adaptation mechanism is an increase in the size of the renal glomeruli in large mammals (and, accordingly, an increase in the length of the tubules), as in elephants, in which the diameter of the glomerulus can be 2 times larger than in killer whales.[93] The appearance of reniculate kidneys was probably the result of adaptation to both an increase in body mass and habitats.[19][20]

Reniculate kidneys[edit]

Main article: Reniculate kidney

Reniculate kidneys are typical mainly for marine mammals. They are believed to be an adaptation both to the large body mass, allowing the number of nephrons to increase by increasing the number of renculi, and to a diet with large amounts of saline water, as well as an adaptation for long term diving.[19] Reniculate kidneys probably allow the number of nephrons to be increased by adding renculi without the need to increase tubule length as the organ size increases.[93] Consumption of excess salt in marine mammals leads to intracellular dehydration, resulting in a need for rapid removal of excess salt from the body, which in the case of reniculate kidneys is facilitated by an increase in the total surface area between the cortex and medulla.[19] The need to dive for long periods of time requires a reduction in the body's oxygen consumption,[164] while the kidneys are an energy-consuming organ,[165] so the glomerular filtration rate decreases during diving.[164] In contrast, the glomerular filtration rate is very high between dives.[19]

Development[edit]

Stages of kidney development[edit]

See also: Kidney development

In mammals, kidney development during embryonic period proceeds through three stages, with different type of kidney developing at each stage: pronephros, mesonephros and metanephros.[166][167] All three kidhey types develop from the intermediate mesoderm sequentially in the cranio-caudal direction (in the direction from the side of the head to the tail of the body).[168][167] First, the pronephros is formed, which is considered rudimentary in mammals, that is, it does not function.[166] Then, caudal to the pronephros, the mesonephros develops, which is the functioning kidney of the embryo.[166][167] Subsequently, the mesonephros degrades in females, and in males it participates in the development of the reproductive system. The third stage is the formation of the metanephros in the caudal part of the embryo. The metanephric kidney is the definitive (permanent) mammalian kidney, which persists in adults.[166]

Metanephros development[edit]

Schematic representation of nephrogenesis during embryologic development following induction of cap mesenchyme by the ureteric bud.[169]

The metanephros develops from the ureteric bud, which is an outgrowth on the caudal part of the nephric duct,[170][171] and the metanephrogenic blastema, which is part of the intermediate mesoderm surrounding the ureteral bud.[172][173] The development of metanephros begins with the induction of a metanephrogenic blastema by the ureteric bud.[173][166] While the kidney develops, the metanephrogenic blastema and ureteric bud reciprocally induce each other.[166] Growing into the mesoderm, the ureteric bud branches and transforms into a tree structure that will eventually become the ureter, renal pelvis, major and minor calyces, renal papillae, and collecting ducts.[174] At the same time, at the tips of the collecting ducts, the mesoderm differentiates into epithelial cells that form nephron tubules[175] (processes of epithelialization and tubulogenesis occur).[176] Vascular system of the kidney is also developed with the development of nephrons, with large vessels branching from the dorsal aorta.[176]

In some mammals, kidney organogenesis ends before birth, while in others it may continue for some time into the postpartum period[177] (for example, in rodents it ends about a week after birth).[178] When the formation of new nephrons (nephrogenesis) ends, the number of nephrons in the kidney becomes final.[177]

Postnatal maturation[edit]

After birth and in the postnatal period, the kidneys are functionally immature; functional development of the kidneys in all mammals lags behind the anatomical development.[179] In the postnatal period, the mass of the tubules is not large enough, so the ability to reabsorb fluids is reduced compared to the kidneys of adult mammals.[180] During this period, hypertrophy and hyperplasia of the tubules occurs, and the kidneys increase in size. The period during which fully functional kidneys form varies significantly between mammalian species. In rats, the kidneys quickly become fully functional, while in monkeys it takes 5 months.[179]

Injury and diseases[edit]

Kidney diseases or disorders may be congenital, inherited, non-infectious, and infectious.[41] Diseases vary between mammalian species. Some diseases may be specific only to some species, while the others may be more common in one species and less common in another.[44] For example, chronic progressive nephropathy is common in mice, rats and naked mole-rats,[181] but at the same time there is no analogous disease in humans.[182]

Congenital and inherited anomalies[edit]

Congenital anomalies and hereditary disorders of the kidneys among mammals are rare, but can have a significant impact on kidney function,[183] in some cases they can cause death in the early neonatal period.[184] Among the anomalies of kidney development are hypoplasia and dysplasia of the kidneys (dysplasia can be unilateral or bilateral), agenesis (absence) of one or both kidneys, polycystic kidney disease, simple renal cysts, perirenal pseudocysts, doubled or tripled renal arteries, malposition of the kidneys, horseshoe kidney and nephroblastoma.[184]

Non-infectious diseases[edit]

Non-infectious diseases of the kidney include acute kidney injury, chronic kidney disease,[185] glomerular diseases[186] and tubular diseases (renal tubular acidosis, Fanconi syndrome and renal glycosuria).[187] In small mammals, renal neoplasms are rare but usually are not benign.[188] Renal neoplasms and abscesses are rare in ruminants.[189] Obstructive uropathy (obstruction of urine flow from one or both kidneys) can lead to hydronephrosis with dilatation of the renal pelvis.[190] Kidney stones can also be formed in the kidneys (nephrolithiasis).[191]

The cause of acute kidney injury in most cases is ischemic or toxic injury. Mammalian kidneys are susceptible to ischemic injury because mammals lack a renal-portal system, and as a result, vascular vasoconstriction in the glomeruli can lead to decreased blood supply to the entire kidney. The kidneys are susceptible to toxic injury, since toxins are reabsorbed in the tubules along with most of the filtered substances.[47] The kidneys are able to restore their functionality after acute injury, but it also can progress into chronic kidney disease. Chronic kidney disease is characterised by loss of function of the kidney tissues, and the disease is usually progressive.[185]

Infectious diseases[edit]

Kidney infections in small mammals are usually caused by aerobic bacteria, including Escherichia coli, staphylococci, enterococci, and streptococci.[192] Fungal and parasitic infections of the kidney are rare in small mammals.[192] Pyelonephritis is usually caused by bacteria that enter the kidney through the ascending route from the lower parts of the urinary system, in rare cases through the blood (descending hematogenous route).[42] In ruminants, pyelonephritis is most often caused by the bacteria Corynebacterium renale and Escherichia coli.[43] Fish-eating mammals (such as minks and dogs) can become infected with the giant kidney worm Dioctophyme renale.[45] Pigs can become infected with the Stephanurus dentatus worm, which is found throughout the world, but is more common in the tropics and subtropics.[46][45] Kidney infections are considered rare among marine mammals.[193]

Ageing[edit]

After maturation, the kidneys slowly begin to undergo ageing processes, which are characterized by changes in anatomy, physiology, function and regenerative capabilities. During the life of mammals, glomerulosclerosis affects glomeruli, the basement membrane thickens, the tubules undergo atrophic changes, and the renal interstitium fibrosis increases. The number of functioning nephrons gradually decreases throughout the life. In terms of function, the glomerular filtration rate decreases and the ability to concentrate urine decreases, too. Age-related changes themselves may not be noticeable and may not lead to kidney failure or disease, but are a risk factor for kidney or urinary tract diseases.[50]

Repair and regeneration[edit]

Unlike more primitive vertebrates such as fish, in mammals nephrogenesis ends before or some time after birth,[39] caused by the loss of the condensed mesenchyme of the metanephrogenic blastema.[194] As a result, new nephrons cannot form in adults,[39] and after injuries, the kidneys of adult mammals cannot regenerate through the formation of new nephrons.[37] However, kidneys have other compensatory and regenerative mechanisms for restoring their function.[195]

Compensatory capabilities[edit]

In the case of unilateral nephrectomy, the load on the remaining kidney increases, increasing the rate of filtration and reabsorption and leading to changes in the nephrons themselves. The renal glomerulus may double or triple in diameter. These compensatory changes are similar to the changes in nephrons that occur after birth as the kidney grows.[196] Resection of kidney tissue also does not cause kidney regeneration,[197] however, compensatory changes can also occur after kidney damage if it leads to a significant decrease in the number of nephrons in the kidneys.[198]

Nephron regeneration[edit]

Within a single nephron, regenerative abilities differ between its parts.[199] In acute toxic and ischemic injuries, the tubules are able to regenerate and restore the function of the nephron.[196] In particular, the proximal part of the nephron, through which up to two-thirds of the primary urine is absorbed,[200] has the ability to regenerate.[201] This part of the nephron in mammals is most at risk of ischemic or toxic damage.[200] In addition, the repair of nephrons occurs in the course of normal physiological activity throughout the life due to the shedding of tubular epithelial cells.[202] The glomerulus has a complex structure, and its ability to recover after injury is limited.[203] Mesangial and endothelial cells are able to proliferate and restore their population after injury. On the contrary, podocytes do not proliferate under normal conditions.[204]

Healing after injury[edit]

If minor damage to the nephron tubules occurs, the lost cells are replaced by new ones, and the epithelium regenerates, restoring its structure and function. In moderate to severe injuries with large cell loss, the chances of regeneration of the tubular epithelium are reduced.[38] In such cases, damage leads to inflammatory and fibrotic responses, and regenerative tissue repair is impaired.[38] Such a reaction is typical for acute kidney injury.[49] Fibrosis is the second line of body defences,[205] which was supposed to reduce possible hemorrhage and fight possible infection during the evolution of mammals.[49] Renal fibrosis is the result of failed kidney healing and associated with renal dysfunction,[206] but it was suggested that it might support survival of non-injured and partially injured nephrons.[207] Chronic kidney injury is characterized by fibrosis, scarring, and loss of tissue function.[48]

See also[edit]

  • Human kidney – an example of mammalian kidney that filters blood in humans

References[edit]

  1. ^ a b Abdalla 2020, p. 1, Abstract.
  2. ^ a b Withers, Cooper, Maloney et al. 2016, p. 25, 1.2.8 Excretion.
  3. ^ Vidya K Nagalakshmi; Jing Yu (17 March 2015). "The ureteric bud epithelium: morphogenesis and roles in metanephric kidney patterning". Molecular Reproduction and Development. 82 (3): 151–166. doi:10.1002/MRD.22462. ISSN 1040-452X. PMC 4376585. PMID 25783232. Wikidata Q30300352.
  4. ^ a b Keogh, Kilroy, Bhattacharjee 2020, p. 8, 7.3. Mammals.
  5. ^ Seth M. Kisia (2011). Vertebrates: Structures and Functions. CRC Press. p. 436. doi:10.1201/B10502. ISBN 978-1-4398-4052-8. Wikidata Q124754122.
  6. ^ a b c d Eurell, Frappier 2006, Kidney : General Organisation.
  7. ^ a b c d e f g h Withers, Cooper, Maloney et al. 2016, p. 250, 3.6.3 The Kidney.
  8. ^ a b George A. Feldhamer; Lee C. Drickamer; Stephen H. Vessey; Joseph F. Merritt; C. Krajewski (2015). Mammalogy: Adaptation, Diversity, Ecology (4th ed.). Baltimore: Johns Hopkins University Press. p. 198. ISBN 978-1-4214-1588-8. Wikidata Q117041834.
  9. ^ a b c d Kriz, Kaissling 2012, p. 595, Kidney Types and Renal Pelvis.
  10. ^ a b c d Renal pyramid at the Encyclopædia Britannica
  11. ^ a b Fenton, Knepper 2007, p. 679, Abstract.
  12. ^ a b Jane C. Fenelon; M. Caleb; Geoff Shaw; Alistair Evans; M. Pyne; S. D. Johnston; Marilyn Renfree (19 April 2021). "The Unique Penile Morphology of the Short-Beaked Echidna, Tachyglossus aculeatus". Sexual Development. 15 (4): 262–271. doi:10.1159/000515145. ISSN 1661-5425. Wikidata Q117034134. Archived from the original on 9 March 2023.
  13. ^ a b c d e f Breshears, Confer 2017, p. 617, Structure.
  14. ^ a b c d e f g WHO 1991, p. 49, 3.4 Species, strain, and sex differences in renal structure and function.
  15. ^ a b R. Nickel; A. Schummer; E. Seiferle (1979). The Viscera of the Domestic Mammals (2nd ed.). Berlin. p. 286. doi:10.1007/978-1-4757-6814-5. ISBN 978-1-4757-6816-9. Wikidata Q117074872.{{cite book}}: CS1 maint: location missing publisher (link)
  16. ^ a b c d e f Ortiz 2001, p. 1832, Kidney structure.
  17. ^ a b Kriz, Kaissling 2012, p. 595, Renal vasculature.
  18. ^ Marcel F Williams (2 November 2005). "Morphological evidence of marine adaptations in human kidneys". Medical Hypotheses. 66 (2): 247–257. doi:10.1016/J.MEHY.2005.09.024. ISSN 0306-9877. PMID 16263222. Wikidata Q36303142.
  19. ^ a b c d e f g h Zhou, Rong, Guo et al. 2023, p. 2, Introduction.
  20. ^ a b c d Zhou, Rong, Guo et al. 2023, p. 6, The Evolution of Renal Structures Was Driven by Body Size and Habitats in Mammals.
  21. ^ a b Davidson 2009, Figure 1. Structure of the mammalian kidney.
  22. ^ a b Jia L. Zhuo; Xiao C. Li (July 2013). "Proximal nephron". Comprehensive Physiology. 3 (3): 1079–123. doi:10.1002/CPHY.C110061. ISSN 2040-4603. PMC 3760239. PMID 23897681. Wikidata Q28388052.
  23. ^ a b C Michele Nawata; Thomas L Pannabecker (24 May 2018). "Mammalian urine concentration: a review of renal medullary architecture and membrane transporters". Journal of Comparative Physiology B. 188 (6): 899–918. doi:10.1007/S00360-018-1164-3. ISSN 0174-1578. PMC 6186196. PMID 29797052. Wikidata Q88802057.
  24. ^ a b c Kriz, Kaissling 2012, p. 600, Nephrons and Collecting Duct System.
  25. ^ Casotti, Lindberg, Braun 2000, p. R1723.
  26. ^ Casotti, Lindberg, Braun 2000, p. R1722-R1723.
  27. ^ Little, McMahon 2012, p. 1, Summary.
  28. ^ Little, McMahon 2012, p. 2, An Overview of Cell Players and Cellular Processes in Metanephric Kidney Development.
  29. ^ Jing Yu; M. Todd Valerius; Mary Duah; et al. (1 May 2012). "Identification of molecular compartments and genetic circuitry in the developing mammalian kidney". Development. 139 (10): 1863–1873. doi:10.1242/DEV.074005. ISSN 0950-1991. PMC 3328182. PMID 22510988. Wikidata Q30419294. Archived from the original on 15 July 2022.
  30. ^ a b Bobulescu IA; Moe OW (September 2006). "Na+/H+ Exchangers in Renal Regulation of Acid-Base Balance". Seminars in Nephrology. 26 (5): 334–344. doi:10.1016/J.SEMNEPHROL.2006.07.001. ISSN 0270-9295. PMC 2878276. PMID 17071327. Wikidata Q28972309.
  31. ^ a b c d Vanessa Schein; Luiz C Kucharski; Pedro M. Guerreiro; Tiago Leal Martins; Isabel Morgado; Deborah M. Power; Adelino Canario; Roselis S M da Silva (15 July 2015). "Stanniocalcin 1 effects on the renal gluconeogenesis pathway in rat and fish". Molecular and Cellular Endocrinology. 414: 1–8. doi:10.1016/J.MCE.2015.07.010. ISSN 0303-7207. PMID 26187698. Wikidata Q57012122.
  32. ^ a b M. L. S. Sequeira Lopez; R. A. Gomez (1 July 2010). "The renin phenotype: roles and regulation in the kidney". Current Opinion in Nephrology and Hypertension. 19 (4): 366–371. doi:10.1097/MNH.0B013E32833AFF32. ISSN 1062-4821. PMC 3079389. PMID 20502328. Wikidata Q30431545.
  33. ^ a b S. Suresh; Praveen Kumar Rajvanshi; C. T. Noguchi (1 January 2019). "The Many Facets of Erythropoietin Physiologic and Metabolic Response". Frontiers in Physiology. 10: 1534. doi:10.3389/FPHYS.2019.01534. ISSN 1664-042X. PMC 6984352. PMID 32038269. Wikidata Q89620015. Archived from the original on 8 May 2022.
  34. ^ a b D. D. Bikle (1 January 2011). "Vitamin D: an ancient hormone". Experimental Dermatology. 20 (1): 7–13. doi:10.1111/J.1600-0625.2010.01202.X. ISSN 0906-6705. PMID 21197695. Wikidata Q33783519. Archived from the original on 14 July 2022.
  35. ^ D. H. Evans, ed. (18 November 2008). Osmotic and Ionic Regulation: Cells and Animals. CRC Press. p. 506. ISBN 978-0-8493-8030-3. Wikidata Q117043359.
  36. ^ Ó. C. Rodríguez; M. L. Suárez Rey (February 2018). 3D Nephrology in Small Animals. Translated by Owen Howard. Illustrator: Unknown. Grupo Asís Biomedia S.L. p. 5. ISBN 978-84-17225-34-6. Wikidata Q117043609.
  37. ^ a b Little, McMahon 2012, p. 12, 7 Reassessing Renal Disease, Repair, and Regeneration Using Developmental Biology.
  38. ^ a b c Kumar 2018, p. 28, Figure 1 Schematic illustration highlighting patchy regenerative/reparative processes after mammalian acute kidney injury.
  39. ^ a b c Davidson 2011, p. 1435, Introduction.
  40. ^ Davidson 2011, p. 1437-1439, Postnatal regenerative response of the mammalian kidney.
  41. ^ a b "Urinary System". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  42. ^ a b "Pyelonephritis in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 30 September 2023.
  43. ^ a b T Taghipur Bazargani; A Khodakaram-Tafti; I Ashrafi; A M Abbassi (1 January 2015). "Giant hydronephrosis and secondary pyelonephritis induced by Salmonella dublin in a Holstein calf". Iranian Journal of Veterinary Research. 16 (1): 114–116. ISSN 1728-1997. PMC 4789252. PMID 27175163. Wikidata Q38959395.
  44. ^ a b G. W. Richter; Kim Solez, eds. (1988). International Review of Experimental Pathology. Vol. 30. Academic Press. pp. 231–232. ISBN 0-12-364930-7. Wikidata Q122870348.
  45. ^ a b c Heinz Mehlhorn, ed. (28 November 2007). Encyclopedia of Parasitology (3rd ed.). Springer Science+Business Media. p. 1532. doi:10.1007/978-3-540-48996-2. ISBN 978-3-540-48996-2. LCCN 2007937942. OL 35464251M. Wikidata Q122851992.
  46. ^ a b "Swine Kidney Worm Infection". Merck Veterinary Manual. Archived from the original on 4 June 2023. Retrieved 30 September 2023.
  47. ^ a b Katja Berger; Marcus J. Moeller (13 June 2014). "Mechanisms of epithelial repair and regeneration after acute kidney injury". Seminars in Nephrology. 34 (4): 394–403. doi:10.1016/J.SEMNEPHROL.2014.06.006. ISSN 0270-9295. PMID 25217268. Wikidata Q38248788.
  48. ^ a b H. Haller; S. Sorrentino (2011). "Chapter 34 - Kidney". In Gustav Steinhoff (ed.). Regenerative Medicine: From Protocol to Patient. Springer Science+Business Media. p. 811. doi:10.1007/978-90-481-9075-1. ISBN 978-90-481-9075-1. Wikidata Q118139734.
  49. ^ a b c d e Robert L. Chevalier (31 January 2017). "Evolutionary Nephrology". KI reports. 2 (3): 302–317. doi:10.1016/J.EKIR.2017.01.012. ISSN 2468-0249. PMC 5568830. PMID 28845468. Wikidata Q43573882.
  50. ^ a b Breshears, Confer 2017, p. 637, Aging of the Kidney.
  51. ^ K. Apelt; Roel Bijkerk; Franck Lebrin; T. J. Rabelink (2 May 2021). "Imaging the Renal Microcirculation in Cell Therapy". Cells. 10 (5). doi:10.3390/CELLS10051087. ISSN 2073-4409. PMC 8147454. PMID 34063200. Wikidata Q117050923. Archived from the original on 10 March 2023.
  52. ^ L. Sherwood; Hillar Klandorf; P. H. Yancey (2012). Animal Physiology: From Genes to Organisms (2nd ed.). Cengage Group. p. 569. ISBN 978-0-8400-6865-1. Wikidata Q117048829.
  53. ^ Gwaltney-Brant, Sharon M. (15 March 2012). "Renal toxicology". In Ramesh C. Gupta (ed.). Veterinary Toxicology: Basic and Clinical Principles (2nd ed.). Academic Press. p. 264. doi:10.1016/C2010-0-67763-7. ISBN 978-0-12-385926-6. Wikidata Q124785280.
  54. ^ Edwin B. Howard, ed. (13 December 2017), Pathobiology Of Marine Mammal Diseases, vol. 1 (1st ed.), CRC Press, p. 14, Wikidata Q122880668
  55. ^ a b c Donald W. Linzey (13 February 2012). Vertebrate Biology (2nd ed.). p. 319. ISBN 978-1-4214-0040-2. Wikidata Q117048995.
  56. ^ De Martino, Cesare; Allen, Delmas; Accinni, Lidia (1985). "Microscopic structure of the kidney". In L. J. A. Didio; P. M. Motta (eds.). Basic, Clinical, and Surgical Nephrology. Unknown. Boston: Martinus Nijhoff Publishers. pp. 53–82. doi:10.1007/978-1-4613-2575-8. ISBN 978-1-4612-9616-4. Wikidata Q117050154.
  57. ^ Robin Sturtz; Lori Asprea (2012). "Chapter 7 Anatomy of the Urinary Tract". Anatomy and Physiology for Veterinary. Illustrator: Unknown. Wiley-Blackwell. p. 41. ISBN 978-0-8138-2264-8. Wikidata Q124819455.
  58. ^ a b C. Rouiller; A. F. Muller, eds. (1969). The Kidney: Morphology, Biochemistry, Physiology. Vol. 1. Academic Press. pp. 64–65. ISBN 978-1-4832-7174-3. Wikidata Q117068124.
  59. ^ a b Davidson 2009, Figure 1 Structure of the mammalian kidney.
  60. ^ D. B. Moffat (1975). The Mammalian Kidney. Unknown. Cambridge University Press. pp. 16–18. ISBN 0-521-20599-9. Wikidata Q117051109.
  61. ^ "Excretion - Mammals". Encyclopædia Britannica. Archived from the original on 3 June 2022. Retrieved 11 March 2023.
  62. ^ Kriz, Kaissling 2012, p. 602, Figure 20.9 Schematic of nephrons and collecting duct.
  63. ^ "Anatomy of the Kidney & Ureter". SEER Training. U. S. National Cancer Institute. Archived from the original on 11 March 2023. Retrieved 11 March 2023.
  64. ^ K. M. Dyce; W. O. Sack; C. J. G. Wensing (2010). Textbook of Veterinary Anatomy (4th ed.). Saunders. p. 177. ISBN 978-1-4160-6607-1. LCCN 2009033865. Wikidata Q117066071.
  65. ^ Joana L. Rocha; José C. Brito; Rasmus Nielsen; Raquel Godinho (13 September 2020), Convergent evolution of increased urine concentrating ability in desert mammals, doi:10.1101/2020.09.11.294124, Wikidata Q114590669
  66. ^ Davidson 2009, p. 2, Figure 1. Structure of the mammalian kidney.
  67. ^ Grant Maxie 2015, p. 379, Anatomy.
  68. ^ a b Sands, Layton 2012, p. 1464, Kidney Structure.
  69. ^ Sands, Verlander 2004, p. 4-5, Figure 1.1 A long-looped and short-looped nephron together with the collecting system.
  70. ^ Yu, Alan S. L.; Chertow, Glenn M.; Luyckx, Valerie; Marsden, Philip A.; Skorecki, Karl; Taal, Maarten W. (25 September 2019). Brenner and Rector's The Kidney E-Book. Elsevier Health Sciences. The Nephron. ISBN 978-0-323-55085-7.
  71. ^ Jamison RL (1 February 1987). "Short and long loop nephrons". Kidney International. 31 (2): 597–605. doi:10.1038/KI.1987.40. ISSN 0085-2538. PMID 3550229. Wikidata Q39762041.
  72. ^ a b Sands, Verlander 2004, p. 6, Cortex.
  73. ^ a b Xin J. Zhou; Zoltan G. Laszik; Tibor Nadasdy; Vivette D. D'Agati, eds. (2 March 2017), Silva's Diagnostic Renal Pathology, Cambridge University Press, p. 19, Wikidata Q117066851
  74. ^ Rouiller, Charles; Muller, Alex F. (12 May 2014). The Kidney: Morphology, Biochemistry, Physiology. Academic Press. p. 133. ISBN 978-1-4832-7174-3.
  75. ^ Moffat, D. B. (12 June 1975). The Mammalian Kidney. CUP Archive. p. 19. ISBN 978-0-521-20599-3.
  76. ^ a b Moffat, D. B. (12 June 1975). The Mammalian Kidney. CUP Archive. p. 21. ISBN 978-0-521-20599-3.
  77. ^ Grant Maxie 2015, p. 378, Anatomy.
  78. ^ Davidson 2009, Overview of kidney structure and embryonic development.
  79. ^ a b C. Rouiller; A. F. Muller, eds. (1969). The Kidney: Morphology, Biochemistry, Physiology. Vol. 1. Academic Press. p. 357. ISBN 978-1-4832-7174-3. Wikidata Q117068124.
  80. ^ a b Sands, Verlander 2004, p. 8, Outer Medulla.
  81. ^ Little, Melissa Helen (6 August 2015). Kidney Development, Disease, Repair and Regeneration. Academic Press. p. 122. ISBN 978-0-12-800438-8.
  82. ^ W. Kriz (1984). "Structure and Function of the Renal Medulla". Paediatric nephrology. Springer Science+Business Media. pp. 3–10. doi:10.1007/978-3-642-69863-7_1. ISBN 978-3-540-13598-2. Wikidata Q117072065.
  83. ^ E. Koushanpour; Wilhelm Kriz (1986). Renal Physiology: Principles, Structure, and Function. Springer Science+Business Media. p. 270. doi:10.1007/978-1-4757-1912-3. ISBN 978-1-4757-1914-7. Wikidata Q124729687.
  84. ^ Keogh, Kilroy, Bhattacharjee 2020, p. 9, 7.3.1. Mammalian kidneys: overall morphology.
  85. ^ a b c Casotti, Lindberg, Braun 2000, p. R1722.
  86. ^ a b Dantzler 2016, p. 20, 2.2.6 Mammals.
  87. ^ Abdalla 2020, p. 3, 3. Results and discussion.
  88. ^ K. S. Frazier; J. C. Seely; G. C. Hard; et al. (1 June 2012). "Proliferative and nonproliferative lesions of the rat and mouse urinary system". Toxicologic Pathology. 40 (4 Suppl): 14S–86S. doi:10.1177/0192623312438736. ISSN 0192-6233. PMID 22637735. Wikidata Q48636042. Archived from the original on 27 December 2022.
  89. ^ Miller, Rachel K. (13 April 2017). Kidney Development and Disease. Springer. p. 249. ISBN 978-3-319-51436-9.
  90. ^ Dantzler 2016, p. 19—20, 2.2.6 Mammals.
  91. ^ Roger L Sur; Jenny M Meegan; Cynthia R Smith; Todd Schmitt; James L'Esperance; Dean Hendrikson; Jason R Woo (1 May 2018). "Surgical Management of Nephrolithiasis in the Bottlenose Dolphin: Collaborations Between the Urologist and Veterinarian". Journal of endourology case reports. 4 (1): 62–65. doi:10.1089/CREN.2017.0143. ISSN 2379-9889. PMC 5944394. PMID 29756043. Wikidata Q54957107.
  92. ^ Keogh, Kilroy, Bhattacharjee 2020, p. 8, 7.3.1. Mammalian kidneys: overall morphology.
  93. ^ a b c M. H. Little (14 December 2020). "Returning to kidney development to deliver synthetic kidneys". Developmental Biology. doi:10.1016/J.YDBIO.2020.12.009. ISSN 0012-1606. PMC 8052282. PMID 33333068. Wikidata Q104492546. Archived from the original on 12 March 2023.
  94. ^ Russell, Hong, Windsor et al. 2019, p. 6, Detailed Features of Human and Mammalian Renal Lymphatic Anatomy : Renal Interstitium.
  95. ^ Kriz, Kaissling 2012, p. 602, Interstitium : Definition.
  96. ^ a b Michael Zeisberg; Raghu Kalluri (26 March 2015). "Physiology of the Renal Interstitium". Clinical Journal of the American Society of Nephrology. 10 (10): 1831–1840. doi:10.2215/CJN.00640114. ISSN 1555-9041. PMC 4594057. PMID 25813241. Wikidata Q36123584.
  97. ^ a b Russell, Hong, Windsor et al. 2019, p. 6, Detailed Features of Human and Mammalian Renal Lymphatic Anatomy : Morphology of Renal Lymph Vessels.
  98. ^ Kriz, Kaissling 2012, p. 602, Interstitial Fibroblasts.
  99. ^ Breshears, Confer 2017, p. 622, Interstitium.
  100. ^ A. Schumacher; M. B. Rookmaaker; J. A. Joles; R. Kramann; T. Q. Nguyen; M. van Griensven; V. L. S. LaPointe (11 August 2021). "Defining the variety of cell types in developing and adult human kidneys by single-cell RNA sequencing". NPG Regenerative Medicine. 6. doi:10.1038/S41536-021-00156-W. ISSN 2057-3995. Wikidata Q117085458. Archived from the original on 13 March 2023.
  101. ^ C Schell; N Wanner; T B Huber (18 August 2014). "Glomerular development--shaping the multi-cellular filtration unit". Seminars in Cell & Developmental Biology. 36: 39–49. doi:10.1016/J.SEMCDB.2014.07.016. ISSN 1084-9521. PMID 25153928. Wikidata Q34434949.
  102. ^ a b Lihe Chen; Jevin Z Clark; Jonathan W Nelson; Brigitte Kaissling; David H. Ellison; Mark A Knepper (28 June 2019). "Renal-Tubule Epithelial Cell Nomenclature for Single-Cell RNA-Sequencing Studies". Journal of the American Society of Nephrology. 30 (8): 1358–1364. doi:10.1681/ASN.2019040415. ISSN 1046-6673. PMID 31253652. Wikidata Q93115184. Archived from the original on 13 March 2023.
  103. ^ Jae Wook Lee; Chung-Lin Chou; Mark A Knepper (27 March 2015). "Deep Sequencing in Microdissected Renal Tubules Identifies Nephron Segment-Specific Transcriptomes". Journal of the American Society of Nephrology. 26 (11): 2669–2677. doi:10.1681/ASN.2014111067. ISSN 1046-6673. PMC 4625681. PMID 25817355. Wikidata Q35589079. Archived from the original on 13 March 2023.
  104. ^ Balzer, Rohacs, Susztak 2022, p. 1, Introduction.
  105. ^ Schwartz, Colin J. (6 December 2012). Structure and Function of the Circulation. Springer. p. 631. ISBN 978-1-4615-7924-3.
  106. ^ Knut Schmidt-Nielsen (9 June 1997). Animal Physiology (5th ed.). Cambridge University Press. p. 371. ISBN 0-521-57098-0. Wikidata Q117089453.
  107. ^ John E. Reynolds, ed. (2013). Biology of Marine Mammals. Smithsonian Institution. p. 299. ISBN 978-1-58834-420-5. Wikidata Q117089734.
  108. ^ David A D Munro; Peter Hohenstein; Jamie A. Davies (12 June 2017). "Cycles of vascular plexus formation within the nephrogenic zone of the developing mouse kidney". Scientific Reports. 7 (1): 3273. doi:10.1038/S41598-017-03808-4. ISSN 2045-2322. PMC 5468301. PMID 28607473. Wikidata Q42177011.
  109. ^ a b c d Grant Maxie 2015, p. 379, Vascular supply.
  110. ^ Kriz, Kaissling 2012, p. 596, Renal vasculature.
  111. ^ P. H. Holz (1 January 1999). "The Reptilian Renal Portal System - A Review". Bulletin of the Association of Reptilian and Amphibian Veterinarians. 9 (1): 4–14. doi:10.5818/1076-3139.9.1.4. ISSN 1076-3139. Wikidata Q117088499.
  112. ^ R. L. Kotpal (2010). Modern Text Book of Zoology: Vertebrates. Vol. 2. Rastogi Publications. p. 782. ISBN 978-81-7133-891-7. Wikidata Q117088647.
  113. ^ Keogh, Kilroy, Bhattacharjee 2020, p. 6, 6. Renal portal system.
  114. ^ Russell, Hong, Windsor et al. 2019, p. 1, Introduction.
  115. ^ Elaine L. Shelton; Hai-Chun Yang; Jianyong Zhong; Michele M. Salzman; Valentina Kon (26 October 2020). "Renal lymphatic vessel dynamics". American Journal of Physiology - Renal Physiology. doi:10.1152/AJPRENAL.00322.2020. ISSN 1931-857X. PMC 7792696. PMID 33103446. Wikidata Q100995658. Archived from the original on 13 March 2023.
  116. ^ Russell, Hong, Windsor et al. 2019, p. 7, Renal Lymphatic Physiology under Normal Conditions : Formation of Renal Lymph.
  117. ^ a b Harald Seeger; Marco Bonani; Stephan Segerer (23 May 2012). "The role of lymphatics in renal inflammation". Nephrology Dialysis Transplantation. 27 (7): 2634–2641. doi:10.1093/NDT/GFS140. ISSN 0931-0509. PMID 22622451. Wikidata Q84203623. Archived from the original on 13 March 2023.
  118. ^ Russell, Hong, Windsor et al. 2019, p. 2, Anatomy of Renal Lymphatics : Renal Vascular Anatomy.
  119. ^ a b c d Russell, Hong, Windsor et al. 2019, p. 3, Comparative Renal Lymphatic Anatomy : Mammalian Renal Lymphatic Anatomy.
  120. ^ Russell, Hong, Windsor et al. 2019, p. 9, Renal Lymphatic Physiology under Normal Conditions : Interstitial Fluid and Protein Drainage in the Medulla.
  121. ^ a b Russell, Hong, Windsor et al. 2019, p. 5, Detailed Features of Human and Mammalian Renal Lymphatic Anatomy : Medullary Lymphatics.
  122. ^ Russell, Hong, Windsor et al. 2019, p. 5, Table 1. Comparison of renal lymphatic anatomy between species.
  123. ^ a b c d Kopp 2018, p. 6, 2.2 Intrarenal Distribution of Efferent Renal Sympathetic Nerves.
  124. ^ Yasuna Nakamura; Tsuyoshi Inoue (8 July 2020). "Neuroimmune Communication in the Kidney". JMA Journal. 3 (3): 164–174. doi:10.31662/JMAJ.2020-0024. ISSN 2433-328X. PMC 7590379. PMID 33150250. Wikidata Q101322955.
  125. ^ Kopp 2011, Abstract.
  126. ^ Kriz, Kaissling 2012, p. 610, Nerves.
  127. ^ Kopp 2011c, 7.1. Kidney.
  128. ^ Kopp 2011b, 2.1. Neural Pathways.
  129. ^ Kopp 2018, p. 1, Introduction.
  130. ^ Kopp 2011, 8.1. Activation of Afferent Renal Sensory Nerves by Physiological Stimuli.
  131. ^ a b Knepper MA; Roch-Ramel F (1 February 1987). "Pathways of urea transport in the mammalian kidney". Kidney International. 31 (2): 629–633. doi:10.1038/KI.1987.44. ISSN 0085-2538. PMID 3550233. Wikidata Q39762062.
  132. ^ Robert A. Fenton; Mark A Knepper (March 2007). "Urea and renal function in the 21st century: insights from knockout mice". Journal of the American Society of Nephrology. 18 (3): 679–88. doi:10.1681/ASN.2006101108. ISSN 1046-6673. PMID 17251384. Wikidata Q28284934. Archived from the original on 9 March 2023.
  133. ^ "Excretion - General features of excretory structures and functions". Britannica. Archived from the original on 4 June 2022. Retrieved 14 March 2023.
  134. ^ Bradley 2009, p. 121, 8.4 Terrestrial vertebrates.
  135. ^ a b c d e Sands, Layton 2009, Introduction.
  136. ^ Bernard C Rossier (23 February 2016). "Osmoregulation during Long-Term Fasting in Lungfish and Elephant Seal: Old and New Lessons for the Nephrologist". The Nephron Journals. 134 (1): 5–9. doi:10.1159/000444307. ISSN 1660-8151. PMID 26901864. Wikidata Q57865766. Archived from the original on 22 September 2022.
  137. ^ Mark A Knepper; Tae-Hwan Kwon; Soren Nielsen (1 April 2015). "Molecular physiology of water balance". The New England Journal of Medicine. 372 (14): 1349–1358. doi:10.1056/NEJMRA1404726. ISSN 0028-4793. PMC 6444926. PMID 25830425. Wikidata Q38399100.
  138. ^ a b Schulte, Kunter, Moeller 2014, p. 718, Adapting to living on dry land: the water-retaining kidney was invented twice.
  139. ^ C. J. Lote (22 June 2012). "The loop of Henle, distal tubule and collecting duct". Principles of Renal Physiology (5th ed.). Springer New York. pp. 70–85. doi:10.1007/978-1-4614-3785-7. ISBN 978-1-4614-3785-7. Wikidata Q117104227. Retrieved 14 March 2023.
  140. ^ Liu W; Morimoto T; Kondo Y; Iinuma K; Uchida S; Imai M (1 August 2001). ""Avian-type" renal medullary tubule organization causes immaturity of urine-concentrating ability in neonates". Kidney International. 60 (2): 680–693. doi:10.1046/J.1523-1755.2001.060002680.X. ISSN 0085-2538. PMID 11473651. Wikidata Q43688352. Archived from the original on 14 March 2022.
  141. ^ Abdalla 2020, p. 1—2, 1. Introduction.
  142. ^ Bradley 2009, p. 164, 11.5 The mammalian kidney.
  143. ^ David Fournier; Friedrich C Luft; Michael Bader; Detlev Ganten; Miguel A Andrade-Navarro (May 2012). "Emergence and evolution of the renin-angiotensin-aldosterone system". Journal of Molecular Medicine. 90 (5): 495–508. doi:10.1007/S00109-012-0894-Z. ISSN 0946-2716. PMC 3354321. PMID 22527880. Wikidata Q28729911.
  144. ^ a b Sequeira-Lopez, Maria Luisa S.; Gomez, R. Ariel (2 April 2021). "Renin Cells, the Kidney, and Hypertension". Circulation Research. 128 (7): 887–907. doi:10.1161/CIRCRESAHA.121.318064. ISSN 0009-7330. PMC 8023763. PMID 33793334.
  145. ^ N. Hazon; F. B. Eddy; G. Flik, eds. (6 December 2012). Ionic Regulation in Animals: A Tribute to Professor W.T.W.Potts. Springer Science+Business Media. p. 153. doi:10.1007/978-3-642-60415-7. ISBN 978-3-642-64396-5. Wikidata Q117104121.
  146. ^ Eladari 2014, p. 1623, Introduction.
  147. ^ L. Sherwood; Hillar Klandorf; P. H. Yancey (2012). Animal Physiology: From Genes to Organisms (2nd ed.). Cengage Group. p. 637. ISBN 978-0-8400-6865-1. Wikidata Q117048829.
  148. ^ a b Carsten A. Wagner; Stefan Broer, eds. (31 March 2004). Membrane Transporter Diseases. Springer Science+Business Media. p. 66. doi:10.1007/978-1-4419-9023-5. ISBN 978-1-4613-4761-3. Wikidata Q117190520.
  149. ^ a b c d James L. Lewis III (July 2021), "Acid-Base Regulation", MSD Manuals - Medical Professional Version, archived from the original on 17 March 2023, retrieved 17 March 2023
  150. ^ a b c Eladari, Hasler, Féraille 2012, p. 84, Bicarbonate Absorption.
  151. ^ a b Eladari 2014, p. 1629, Renal ammonia handling : Fig. 3.
  152. ^ a b Eladari 2014, p. 1627, Renal ammonia handling.
  153. ^ a b Eladari 2014, p. 1627-1628, Renal ammonia handling.
  154. ^ Eladari 2014, p. 1628, Renal ammonia handling : Fig.2.
  155. ^ Klaus Urich (17 April 2013). Comparative Animal Biochemistry. Translated by P. J. King. Illustrator: Unknown. Springer Berlin Heidelberg. p. 534. doi:10.1007/978-3-662-06303-3. ISBN 978-3-642-08181-1. OL 37213388M. Wikidata Q123236759.
  156. ^ a b Leszek Szablewski (14 April 2011). Glucose Homeostasis and Insulin Resistance. Bentham Science Publishers. pp. 77–78. ISBN 978-1-60805-189-2. Wikidata Q123237143.
  157. ^ a b Vize, Smith 2004, p. 352.
  158. ^ Vize, Smith 2004, p. 351.
  159. ^ a b c Joana L. Rocha; José C. Brito; Rasmus Nielsen; Raquel Godinho (1 March 2021). "Convergent evolution of increased urine‐concentrating ability in desert mammals". Mammal Review. 51 (4): 482–491. doi:10.1111/MAM.12244. ISSN 1365-2907. Wikidata Q112795614.
  160. ^ William H. Dantzler (February 1982). "Renal Adaptations of Desert Vertebrates". BioScience. 32 (2): 108–113. doi:10.2307/1308563. ISSN 0006-3568. JSTOR 1308563. Wikidata Q121096094.
  161. ^ Abraham Allan Degen (1997). John Cloudsley-Thompson (ed.). Ecophysiology of Small Desert Mammals. Springer Science+Business Media. doi:10.1007/978-3-642-60351-8. ISBN 978-3-642-64366-8. OL 34372464M. Wikidata Q122965291.
  162. ^ C. Thigpen; L. Best; T. Camarata (28 September 2019). "Comparative morphology and allometry of select extant cryptodiran turtle kidneys". Zoomorphology. 139: 111–121. doi:10.1007/S00435-019-00463-3. ISSN 0720-213X. Wikidata Q117048961. Archived from the original on 22 May 2022.
  163. ^ Zhou, Rong, Guo et al. 2023, p. 1, Introduction.
  164. ^ a b Ortiz 2001, p. 1838, Apnea/simulated diving.
  165. ^ Ying Chen; Brendan C Fry; Anita T Layton (1 July 2016). "Modeling Glucose Metabolism in the Kidney". Bulletin of Mathematical Biology. 78 (6): 1318–1336. doi:10.1007/S11538-016-0188-7. ISSN 0092-8240. PMC 5431085. PMID 27371260. Zbl 1348.92055. Wikidata Q33683963.
  166. ^ a b c d e f Bush, Sakurai, Nigam 2012, p. 859, Overview.
  167. ^ a b c Jamie A. Davies (19 September 2013). Kidney Development. doi:10.1002/9780470015902.A0001152.PUB3. ISBN 978-0-470-01590-2. Wikidata Q117156103. {{cite book}}: |journal= ignored (help)
  168. ^ Davidson 2009, 1. Overview of kidney structure and embryonic development.
  169. ^ A. Schumacher; M. B. Rookmaaker; J. A. Joles; R. Kramann; T. Q. Nguyen; M. van Griensven; V. L. S. LaPointe (11 August 2021). "Defining the variety of cell types in developing and adult human kidneys by single-cell RNA sequencing". NPG Regenerative Medicine. 6. doi:10.1038/S41536-021-00156-W. ISSN 2057-3995. Wikidata Q117085458.
  170. ^ C. Cebrián; K. Borodo; N. Charles; D. A. Herzlinger (1 November 2004). "Morphometric index of the developing murine kidney". Developmental Dynamics. 231 (3): 601–608. doi:10.1002/DVDY.20143. ISSN 1058-8388. PMID 15376282. Wikidata Q50792365.
  171. ^ Joseph M Chambers; Rebecca A Wingert (22 October 2020). "Advances in understanding vertebrate nephrogenesis". Tissue Barriers: 1832844. doi:10.1080/21688370.2020.1832844. ISSN 2168-8362. PMID 33092489. Wikidata Q100943416.
  172. ^ Bush, Sakurai, Nigam 2012, pp. 859–860, Overview.
  173. ^ a b A. Kispert; Seppo Vainio; A. P. McMahon (1 November 1998). "Wnt-4 is a mesenchymal signal for epithelial transformation of metanephric mesenchyme in the developing kidney". Development. 125 (21): 4225–4234. doi:10.1242/DEV.125.21.4225. ISSN 0950-1991. PMID 9753677. Wikidata Q41006079.
  174. ^ Bush, Sakurai, Nigam 2012, p. 861-862, Development of the Metanephros.
  175. ^ Bush, Sakurai, Nigam 2012, p. 860, Development of the Metanephros.
  176. ^ a b Bush, Sakurai, Nigam 2012, p. 861, Development of the Metanephros.
  177. ^ a b Bush, Sakurai, Nigam 2012, p. 882, Termination of the Kidney Development.
  178. ^ D. R. Abrahamson (1 January 2009). "Development of kidney glomerular endothelial cells and their role in basement membrane assembly". Organogenesis. 5 (1): 275–287. doi:10.4161/ORG.7577. ISSN 1547-6278. PMC 2659369. PMID 19568349. Wikidata Q42235704.
  179. ^ a b John Curtis Seely (11 February 2017). "A brief review of kidney development, maturation, developmental abnormalities, and drug toxicity: juvenile animal relevancy". Journal of Toxicologic Pathology. 30 (2): 125–133. doi:10.1293/TOX.2017-0006. ISSN 0914-9198. PMC 5406591. PMID 28458450. Wikidata Q33607543.
  180. ^ Kendall S. Frazier (2 August 2017). "Species Differences in Renal Development and Associated Developmental Nephrotoxicity". Birth Defects Research. 109 (16): 1243–1256. doi:10.1002/BDR2.1088. ISSN 2472-1727. PMID 28766875. Wikidata Q88659637.
  181. ^ Karen A. Terio; Denise McAloose; Judy St. Leger, eds. (8 October 2018). Pathology of Wildlife and Zoo Animals. Academic Press. p. 503. ISBN 978-0-12-805306-5. OL 30587122M. Wikidata Q122849312.
  182. ^ Gordon C. Hard; Kent J. Johnson; Samuel M. Cohen (1 January 2009). "A comparison of rat chronic progressive nephropathy with human renal disease-implications for human risk assessment". Critical Reviews in Toxicology. 39 (4): 332–346. doi:10.1080/10408440802368642. ISSN 1040-8444. PMID 19514917. Wikidata Q37514291.
  183. ^ "Overview of Congenital and Inherited Anomalies of the Urinary System". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  184. ^ a b "Renal Anomalies". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  185. ^ a b "Renal Dysfunction in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  186. ^ "Glomerular Disease in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  187. ^ "Renal Tubular Defects in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  188. ^ "Neoplasia of the Urinary System in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  189. ^ Bradford P. Smith, ed. (April 2014). Large Animal Internal Medicine (5th ed.). Elsevier. p. 768. ISBN 978-0-323-08839-8. OL 26438715M. Wikidata Q122886585.
  190. ^ "Obstructive Uropathy in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  191. ^ "Urolithiasis in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 29 September 2023.
  192. ^ a b "Overview of Infectious Diseases of the Urinary System in Small Animals". Merck Veterinary Manual. Archived from the original on 27 September 2023. Retrieved 30 September 2023.
  193. ^ Edwin B. Howard, ed. (13 December 2017), Pathobiology Of Marine Mammal Diseases, vol. 1 (1st ed.), CRC Press, p. 30, Wikidata Q122880668
  194. ^ Davidson 2011, p. 1436, Cessation of mammalian nephrogenesis.
  195. ^ Davidson 2011, pp. 1437–1439, Postnatal regenerative response of the mammalian kidney.
  196. ^ a b Davidson 2011, p. 1437, Postnatal regenerative response of the mammalian kidney.
  197. ^ Ariela Benigni; Marina Morigi; Giuseppe Remuzzi (1 April 2010). "Kidney regeneration". The Lancet. 375 (9722): 1310–1317. doi:10.1016/S0140-6736(10)60237-1. ISSN 0140-6736. PMID 20382327. Wikidata Q37728655.
  198. ^ Davidson 2011, p. 1441, Conclusions and perspectives.
  199. ^ Yang, Liu, Fogo 2014, What Is Kidney Regeneration?.
  200. ^ a b David F. Williams; Giuseppe Orlando; Giuseppe Remuzzi, eds. (8 June 2017). "Nephron Repair in Mammals and Fish". Kidney Transplantation in the Regenerative Medicine Era: Kidney Transplantation in the Regenerative Medicine Era. Academic Press. p. 997. ISBN 978-0-12-801734-0. LCCN 2017285658. Wikidata Q118136559.
  201. ^ Hai-Chun Yang; Shao-Jun Liu; Agnes B. Fogo (19 May 2014). "Kidney regeneration in mammals". The Nephron Journals. 126 (2): 50. doi:10.1159/000360661. ISSN 1660-8151. PMC 4337834. PMID 24854640. Wikidata Q55210136.
  202. ^ Davidson 2011, p. 1438, Postnatal regenerative response of the mammalian kidney.
  203. ^ Yang, Liu, Fogo 2014, Introduction.
  204. ^ Yang, Liu, Fogo 2014, Mechanisms of Kidney Regeneration.
  205. ^ Qi Cao; David C H Harris; Yiping Wang (1 May 2015). "Macrophages in kidney injury, inflammation, and fibrosis". Physiology. 30 (3): 183–194. doi:10.1152/PHYSIOL.00046.2014. ISSN 1548-9213. PMID 25933819. Wikidata Q38453872.
  206. ^ Nogueira, Pires, Oliveira 2017, p. 3, Impact of Renal Fibrosis on Human Health.
  207. ^ Nogueira, Pires, Oliveira 2017, p. 2, Renal Fibrosis: Aetiology and Pathophysiology.

Bibliography[edit]

Books

Article in scientific journals

External links[edit]

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