Supergravity

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Supergravity 

Beyond the Standard Model
Simulated Large Hadron Collider CMS particle detector data depicting a Higgs boson produced by colliding protons decaying into hadron jets and electrons

String theory

In theoretical physics, supergravity (supergravity theory; SUGRA for short) is a modern field theory that combines the principles of supersymmetry and general relativity; this is in contrast to non-gravitational supersymmetric theories such as the Minimal Supersymmetric Standard Model. Supergravity is the gauge theory of local supersymmetry. Since the supersymmetry (SUSY) generators form together with the Poincaré algebra a superalgebra, called the super-Poincaré algebra, supersymmetry as a gauge theory makes gravity arise in a natural way.

Gravitons

Like any field theory of gravity, a supergravity theory contains a spin-2 field whose quantum is the graviton. Supersymmetry requires the graviton field to have a superpartner. This field has spin 3/2 and its quantum is the gravitino. The number of gravitino fields is equal to the number of supersymmetries.

History

Gauge supersymmetry

The first theory of local supersymmetry was proposed by Dick Arnowitt and Pran Nath in 1975 and was called gauge supersymmetry.

Supergravity

The first model of 4-dimensional supergravity (without this denotation) was formulated by Dmitri Vasilievich Volkov and Vyacheslav A. Soroka in 1973, emphasizing the importance of spontaneous supersymmetry breaking for the possibility of a realistic model. The minimal version of 4-dimensional supergravity (with unbroken local supersymmetry) was constructed in detail in 1976 by Dan Freedman, Sergio Ferrara and Peter van Nieuwenhuizen. In 2019 the three were awarded a special Breakthrough Prize in Fundamental Physics for the discovery. The key issue of whether or not the spin 3/2 field is consistently coupled was resolved in the nearly simultaneous paper, by Deser and Zumino, which independently proposed the minimal 4-dimensional model. It was quickly generalized to many different theories in various numbers of dimensions and involving additional (N) supersymmetries. Supergravity theories with N>1 are usually referred to as extended supergravity (SUEGRA). Some supergravity theories were shown to be related to certain higher-dimensional supergravity theories via dimensional reduction (e.g. N=1, 11-dimensional supergravity is dimensionally reduced on T⁷ to 4-dimensional, ungauged, N=8 Supergravity). The resulting theories were sometimes referred to as Kaluza–Klein theories as Kaluza and Klein constructed in 1919 a 5-dimensional gravitational theory, that when dimensionally reduced on a circle, its 4-dimensional non-massive modes describe electromagnetism coupled to gravity.

mSUGRA

mSUGRA means minimal SUper GRAvity. The construction of a realistic model of particle interactions within the N = 1 supergravity framework where supersymmetry (SUSY) breaks by a super Higgs mechanism carried out by Ali Chamseddine, Richard Arnowitt and Pran Nath in 1982. Collectively now known as minimal supergravity Grand Unification Theories (mSUGRA GUT), gravity mediates the breaking of SUSY through the existence of a hidden sector. mSUGRA naturally generates the Soft SUSY breaking terms which are a consequence of the Super Higgs effect. Radiative breaking of electroweak symmetry through Renormalization Group Equations (RGEs) follows as an immediate consequence. Due to its predictive power, requiring only four input parameters and a sign to determine the low energy phenomenology from the scale of Grand Unification, its interest is a widely investigated model of particle physics

See also: Gravity-Mediated Supersymmetry Breaking in the MSSM

11D: the maximal SUGRA

One of these supergravities, the 11-dimensional theory, generated considerable excitement as the first potential candidate for the theory of everything. This excitement was built on four pillars, two of which have now been largely discredited:

• Werner Nahm showed 11 dimensions as the largest number of dimensions consistent with a single graviton, and more dimensions will show particles with spins greater than 2. However, if two of these dimensions are time-like, these problems are avoided in 12 dimensions. Itzhak Bars gives this emphasis.
• In 1981 Ed Witten showed 11 as the smallest number of dimensions big enough to contain the gauge groups of the Standard Model, namely SU(3) for the strong interactions and SU(2) times U(1) for the electroweak interactions. Many techniques exist to embed the standard model gauge group in supergravity in any number of dimensions like the obligatory gauge symmetry in type I and heterotic string theories, and obtained in type II string theory by compactification on certain Calabi–Yau manifolds. The D-branes engineer gauge symmetries too.
• In 1978 Eugène Cremmer, Bernard Julia and Joël Scherk (CJS) found the classical action for an 11-dimensional supergravity theory. This remains today the only known classical 11-dimensional theory with local supersymmetry and no fields of spin higher than two. Other 11-dimensional theories known and quantum-mechanically inequivalent reduce to the CJS theory when one imposes the classical equations of motion. However, in the mid 1980s Bernard de Wit and Hermann Nicolai found an alternate theory in D=11 Supergravity with Local SU(8) Invariance. While not manifestly Lorentz-invariant, it is in many ways superior, because it dimensionally-reduces to the 4-dimensional theory without recourse to the classical equations of motion.

• In 1980 Peter Freund and M. A. Rubin showed that compactification from 11 dimensions preserving all the SUSY generators could occur in two ways, leaving only 4 or 7 macroscopic dimensions, the others compact. The noncompact dimensions have to form an anti-de Sitter space. There are many possible compactifications, but the Freund-Rubin compactification's invariance under all of the supersymmetry transformations preserves the action.

Finally, the first two results each appeared to establish 11 dimensions, the third result appeared to specify the theory, and the last result explained why the observed universe appears to be four-dimensional.

Many of the details of the theory were fleshed out by Peter van Nieuwenhuizen, Sergio Ferrara and Daniel Z. Freedman.

The end of the SUGRA era

The initial excitement over 11-dimensional supergravity soon waned, as various failings were discovered, and attempts to repair the model failed as well. Problems included:

• The compact manifolds which were known at the time and which contained the standard model were not compatible with supersymmetry, and could not hold quarks or leptons. One suggestion was to replace the compact dimensions with the 7-sphere, with the symmetry group SO(8), or the squashed 7-sphere, with symmetry group SO(5) times SU(2).
• Until recently, the physical neutrinos seen in experiments were believed to be massless, and appeared to be left-handed, a phenomenon referred to as the chirality of the Standard Model. It was very difficult to construct a chiral fermion from a compactification — the compactified manifold needed to have singularities, but physics near singularities did not begin to be understood until the advent of orbifold conformal field theories in the late 1980s.
• Supergravity models generically result in an unrealistically large cosmological constant in four dimensions, and that constant is difficult to remove, and so require fine-tuning. This is still a problem today.
• Quantization of the theory led to quantum field theory gauge anomalies rendering the theory inconsistent. In the intervening years physicists have learned how to cancel these anomalies.

Some of these difficulties could be avoided by moving to a 10-dimensional theory involving superstrings. However, by moving to 10 dimensions one loses the sense of uniqueness of the 11-dimensional theory.

The core breakthrough for the 10-dimensional theory, known as the first superstring revolution, was a demonstration by Michael B. Green, John H. Schwarz and David Gross that there are only three supergravity models in 10 dimensions which have gauge symmetries and in which all of the gauge and gravitational anomalies cancel. These were theories built on the groups SO(32) and ${\displaystyle E_{8}\times E_{8}}$, the direct product of two copies of E₈. Today we know that, using D-branes for example, gauge symmetries can be introduced in other 10-dimensional theories as well.

The second superstring revolution

Initial excitement about the 10-dimensional theories, and the string theories that provide their quantum completion, died by the end of the 1980s. There were too many Calabi–Yaus to compactify on, many more than Yau had estimated, as he admitted in December 2005 at the 23rd International Solvay Conference in Physics. None quite gave the standard model, but it seemed as though one could get close with enough effort in many distinct ways. Plus no one understood the theory beyond the regime of applicability of string perturbation theory.

There was a comparatively quiet period at the beginning of the 1990s; however, several important tools were developed. For example, it became apparent that the various superstring theories were related by "string dualities", some of which relate weak string-coupling - perturbative - physics in one model with strong string-coupling - non-perturbative - in another.

Then the second superstring revolution occurred. Joseph Polchinski realized that obscure string theory objects, called D-branes, which he discovered six years earlier, equate to stringy versions of the p-branes known in supergravity theories. String theory perturbation didn't restrict these p-branes. Thanks to supersymmetry, p-branes in supergravity gained understanding well beyond the limits of string theory.

Armed with this new nonperturbative tool, Edward Witten and many others could show all of the perturbative string theories as descriptions of different states in a single theory that Witten named M-theory. Furthermore, he argued that M-theory's long wavelength limit, i.e. when the quantum wavelength associated to objects in the theory appear much larger than the size of the 11th dimension, need 11-dimensional supergravity descriptors that fell out of favor with the first superstring revolution 10 years earlier, accompanied by the 2- and 5-branes.

Therefore, supergravity comes full circle and uses a common framework in understanding features of string theories, M-theory, and their compactifications to lower spacetime dimensions.

Relation to superstrings

The term "low energy limits" labels some 10-dimensional supergravity theories. These arise as the massless, tree-level approximation of string theories. True effective field theories of string theories, rather than truncations, are rarely available. Due to string dualities, the conjectured 11-dimensional M-theory is required to have 11-dimensional supergravity as a "low energy limit". However, this doesn't necessarily mean that string theory/M-theory is the only possible UV completion of supergravity; supergravity research is useful independent of those relations.

4D N = 1 SUGRA

Before we move on to SUGRA proper, let's recapitulate some important details about general relativity. We have a 4D differentiable manifold M with a Spin(3,1) principal bundle over it. This principal bundle represents the local Lorentz symmetry. In addition, we have a vector bundle T over the manifold with the fiber having four real dimensions and transforming as a vector under Spin(3,1). We have an invertible linear map from the tangent bundle TM to T. This map is the vierbein. The local Lorentz symmetry has a gauge connection associated with it, the spin connection.

The following discussion will be in superspace notation, as opposed to the component notation, which isn't manifestly covariant under SUSY. There are actually many different versions of SUGRA out there which are inequivalent in the sense that their actions and constraints upon the torsion tensor are different, but ultimately equivalent in that we can always perform a field redefinition of the supervierbeins and spin connection to get from one version to another.

In 4D N=1 SUGRA, we have a 4|4 real differentiable supermanifold M, i.e. we have 4 real bosonic dimensions and 4 real fermionic dimensions. As in the nonsupersymmetric case, we have a Spin(3,1) principal bundle over M. We have an R^4|4 vector bundle T over M. The fiber of T transforms under the local Lorentz group as follows; the four real bosonic dimensions transform as a vector and the four real fermionic dimensions transform as a Majorana spinor. This Majorana spinor can be reexpressed as a complex left-handed Weyl spinor and its complex conjugate right-handed Weyl spinor (they're not independent of each other). We also have a spin connection as before.

We will use the following conventions; the spatial (both bosonic and fermionic) indices will be indicated by M, N, ... . The bosonic spatial indices will be indicated by μ, ν, ..., the left-handed Weyl spatial indices by α, β,..., and the right-handed Weyl spatial indices by ${\displaystyle {\dot {\alpha }}}$, ${\displaystyle {\dot {\beta }}}$, ... . The indices for the fiber of T will follow a similar notation, except that they will be hatted like this: ${\displaystyle {\hat {M}},{\hat {\alpha }}}$. See van der Waerden notation for more details. ${\displaystyle M=(\mu ,\alpha ,{\dot {\alpha }})}$. The supervierbein is denoted by ${\displaystyle e_{N}^{\hat {M}}}$, and the spin connection by ${\displaystyle \omega _{{\hat {M}}{\hat {N}}P}}$. The inverse supervierbein is denoted by ${\displaystyle E_{\hat {M}}^{N}}$.

The supervierbein and spin connection are real in the sense that they satisfy the reality conditions

${\displaystyle e_{N}^{\hat {M}}(x,{\overline {\theta }},\theta )^{*}=e_{N^{*}}^{{\hat {M}}^{*}}(x,\theta ,{\overline {\theta }})}$ where ${\displaystyle \mu ^{*}=\mu }$, ${\displaystyle \alpha ^{*}={\dot {\alpha }}}$, and ${\displaystyle {\dot {\alpha }}^{*}=\alpha }$ and ${\displaystyle \omega (x,{\overline {\theta }},\theta )^{*}=\omega (x,\theta ,{\overline {\theta }})}$.

The covariant derivative is defined as

${\displaystyle D_{\hat {M}}f=E_{\hat {M}}^{N}\left(\partial _{N}f+\omega _{N}[f]\right)}$.

The covariant exterior derivative as defined over supermanifolds needs to be super graded. This means that every time we interchange two fermionic indices, we pick up a +1 sign factor, instead of -1.

The presence or absence of R symmetries is optional, but if R-symmetry exists, the integrand over the full superspace has to have an R-charge of 0 and the integrand over chiral superspace has to have an R-charge of 2.

A chiral superfield X is a superfield which satisfies ${\displaystyle {\overline {D}}_{\hat {\dot {\alpha }}}X=0}$. In order for this constraint to be consistent, we require the integrability conditions that ${\displaystyle \left\{{\overline {D}}_{\hat {\dot {\alpha }}},{\overline {D}}_{\hat {\dot {\beta }}}\right\}=c_{{\hat {\dot {\alpha }}}{\hat {\dot {\beta }}}}^{\hat {\dot {\gamma }}}{\overline {D}}_{\hat {\dot {\gamma }}}}$ for some coefficients c.

Unlike nonSUSY GR, the torsion has to be nonzero, at least with respect to the fermionic directions. Already, even in flat superspace, ${\displaystyle D_{\hat {\alpha }}e_{\hat {\dot {\alpha }}}+{\overline {D}}_{\hat {\dot {\alpha }}}e_{\hat {\alpha }}\neq 0}$. In one version of SUGRA (but certainly not the only one), we have the following constraints upon the torsion tensor:

${\displaystyle T_{{\hat {\underline {\alpha }}}{\hat {\underline {\beta }}}}^{\hat {\underline {\gamma }}}=0}$

${\displaystyle T_{{\hat {\alpha }}{\hat {\beta }}}^{\hat {\mu }}=0}$

${\displaystyle T_{{\hat {\dot {\alpha }}}{\hat {\dot {\beta }}}}^{\hat {\mu }}=0}$

${\displaystyle T_{{\hat {\alpha }}{\hat {\dot {\beta }}}}^{\hat {\mu }}=2i\sigma _{{\hat {\alpha }}{\hat {\dot {\beta }}}}^{\hat {\mu }}}$

${\displaystyle T_{{\hat {\mu }}{\hat {\underline {\alpha }}}}^{\hat {\nu }}=0}$

${\displaystyle T_{{\hat {\mu }}{\hat {\nu }}}^{\hat {\rho }}=0}$

Here, ${\displaystyle {\underline {\alpha }}}$ is a shorthand notation to mean the index runs over either the left or right Weyl spinors.

The superdeterminant of the supervierbein, ${\displaystyle \left|e\right|}$, gives us the volume factor for M. Equivalently, we have the volume 4|4-superform${\displaystyle e^{{\hat {\mu }}=0}\wedge \cdots \wedge e^{{\hat {\mu }}=3}\wedge e^{{\hat {\alpha }}=1}\wedge e^{{\hat {\alpha }}=2}\wedge e^{{\hat {\dot {\alpha }}}=1}\wedge e^{{\hat {\dot {\alpha }}}=2}}$.

If we complexify the superdiffeomorphisms, there is a gauge where ${\displaystyle E_{\hat {\dot {\alpha }}}^{\mu }=0}$, ${\displaystyle E_{\hat {\dot {\alpha }}}^{\beta }=0}$ and ${\displaystyle E_{\hat {\dot {\alpha }}}^{\dot {\beta }}=\delta _{\dot {\alpha }}^{\dot {\beta }}}$. The resulting chiral superspace has the coordinates x and Θ.

R is a scalar valued chiral superfield derivable from the supervielbeins and spin connection. If f is any superfield, ${\displaystyle \left({\bar {D}}^{2}-8R\right)f}$ is always a chiral superfield.

The action for a SUGRA theory with chiral superfields X, is given by

${\displaystyle S=\int d^{4}xd^{2}\Theta 2{\mathcal {E}}\left[{\frac {3}{8}}\left({\bar {D}}^{2}-8R\right)e^{-K({\bar {X}},X)/3}+W(X)\right]+c.c.}$

where K is the Kähler potential and W is the superpotential, and ${\displaystyle {\mathcal {E}}}$ is the chiral volume factor.

Unlike the case for flat superspace, adding a constant to either the Kähler or superpotential is now physical. A constant shift to the Kähler potential changes the effective Planck constant, while a constant shift to the superpotential changes the effective cosmological constant. As the effective Planck constant now depends upon the value of the chiral superfield X, we need to rescale the supervierbeins (a field redefinition) to get a constant Planck constant. This is called the Einstein frame.

N = 8 supergravity in 4 dimensions

N=8 Supergravity is the most symmetric quantum field theory which involves gravity and a finite number of fields. It can be found from a dimensional reduction of 11D supergravity by making the size of 7 of the dimensions go to zero. It has 8 supersymmetries which is the most any gravitational theory can have since there are 8 half-steps between spin 2 and spin -2. (A graviton has the highest spin in this theory which is a spin 2 particle). More supersymmetries would mean the particles would have superpartners with spins higher than 2. The only theories with spins higher than 2 which are consistent involve an infinite number of particles (such as string theory and higher-spin theories). Stephen Hawking in his A Brief History of Time speculated that this theory could be the Theory of Everything. However, in later years this was abandoned in favour of string theory. There has been renewed interest in the 21st century with the possibility that this theory may be finite.

Higher-dimensional SUGRA

Main article: Higher-dimensional supergravity

Higher-dimensional SUGRA is the higher-dimensional, supersymmetric generalization of general relativity. Supergravity can be formulated in any number of dimensions up to eleven. Higher-dimensional SUGRA focuses upon supergravity in greater than four dimensions.

The number of supercharges in a spinor depends on the dimension and the signature of spacetime. The supercharges occur in spinors. Thus the limit on the number of supercharges cannot be satisfied in a spacetime of arbitrary dimension. Some theoretical examples in which this is satisfied are:

• 12-dimensional two-time theory
• 11-dimensional maximal SUGRA
• 10-dimensional SUGRA theories
  • Type IIA SUGRA: N = (1, 1)
  • IIA SUGRA from 11d SUGRA
  • Type IIB SUGRA: N = (2, 0)
  • Type I gauged SUGRA: N = (1, 0)
• 9d SUGRA theories
  • Maximal 9d SUGRA from 10d
  • T-duality
  • N = 1 Gauged SUGRA

The supergravity theories that have attracted the most interest contain no spins higher than two. This means, in particular, that they do not contain any fields that transform as symmetric tensors of rank higher than two under Lorentz transformations. The consistency of interacting higher spin field theories is, however, presently a field of very active interest.

Chronic kidney disease

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Chronic_kidney_disease 

 

Chronic kidney disease
Other names	Chronic renal disease, kidney failure, impaired kidney function
Uremic frost on the head in someone with chronic kidney disease
Specialty	Nephrology
Symptoms	Early: None Later: Leg swelling, feeling tired, vomiting, loss of appetite, confusion
Complications	Heart disease, high blood pressure, anemia
Duration	Long-term
Causes	Diabetes, high blood pressure, glomerulonephritis, polycystic kidney disease
Diagnostic method	Blood tests, urine tests
Treatment	Medications to manage blood pressure, blood sugar, and lower cholesterol, renal replacement therapy, kidney transplant
Frequency	753 million (2016)
Deaths	1.2 million (2015)

Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months to years. Initially there are generally no symptoms; later, symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications include an increased risk of heart disease, high blood pressure, bone disease, and anemia.

Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of chronic kidney disease. Diagnosis is by blood tests to measure the estimated glomerular filtration rate (eGFR), and a urine test to measure albumin. Ultrasound or kidney biopsy may be performed to determine the underlying cause. Several severity-based staging systems are in use.

Screening at-risk people is recommended. Initial treatments may include medications to lower blood pressure, blood sugar, and cholesterol. Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are generally first-line agents for blood pressure control, as they slow progression of the kidney disease and the risk of heart disease. Loop diuretics may be used to control edema and, if needed, to further lower blood pressure. NSAIDs should be avoided. Other recommended measures include staying active, and certain dietary changes such as a low-salt diet and the right amount of protein. Treatments for anemia and bone disease may also be required. Severe disease requires hemodialysis, peritoneal dialysis, or a kidney transplant for survival.

Chronic kidney disease affected 753 million people globally in 2016: 417 million females and 336 million males. In 2015 it caused 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

Signs and symptoms

CKD is initially without symptoms, and is usually detected on routine screening blood work by either an increase in serum creatinine, or protein in the urine. As the kidney function decreases:

• Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin–angiotensin system, increasing the risk of developing hypertension and heart failure.
• Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost").
• Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 ml/min/1.73 m², at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.
• Fluid overload symptoms may range from mild edema to life-threatening pulmonary edema.
• Hyperphosphatemia results from poor phosphate elimination in the kidney. Hyperphosphatemia contributes to increased cardiovascular risk by causing vascular calcification. Circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the kidney capacity for phosphate excretion declines which may contribute to left ventricular hypertrophy and increased mortality in people with CKD .
• Hypocalcemia results from 1,25 dihydroxyvitamin D₃ deficiency (caused by high FGF-23 and reduced kidney mass) and resistance to the action of parathyroid hormone. Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D₃). Later, this progresses to secondary hyperparathyroidism, kidney osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis.
• Changes in mineral and bone metabolism that may cause 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (kidney osteodystrophy); and 3) vascular or other soft-tissue calcification. CKD-mineral and bone disorders have been associated with poor outcomes.
• Metabolic acidosis may result from decreased capacity to generate enough ammonia from the cells of the proximal tubule. Acidemia affects the function of enzymes and increases excitability of cardiac and neuronal membranes by the promotion of hyperkalemia.
• Anemia is common and is especially prevalent in those requiring haemodialysis. It is multifactorial in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone marrow suppression. Hypoproliferative anemia occurs due to inadequate production of erythropoietin by the kidneys.
• In later stages, cachexia may develop, leading to unintentional weight loss, muscle wasting, weakness and anorexia.
• Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.
• People with CKD are more likely than the general population to develop atherosclerosis with consequent cardiovascular disease, an effect that may be at least partly mediated by uremic toxins. People with both CKD and cardiovascular disease have significantly worse prognoses than those with only cardiovascular disease.

Causes

The three most common causes of CKD in order of frequency as of 2015 are diabetes mellitus, hypertension, and glomerulonephritis. About one of five adults with hypertension and one of three adults with diabetes have CKD. If the cause is unknown, it is called idiopathic.

By anatomical location

• Vascular disease includes large vessel disease such as bilateral kidney artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome, and vasculitis.
• Glomerular disease comprises a diverse group and is classified into:
  • Primary glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis)
  • Secondary glomerular disease such as diabetic nephropathy and lupus nephritis
• Tubulointerstitial disease includes drug- and toxin-induced chronic tubulointerstitial nephritis, and reflux nephropathy.
• Obstructive nephropathy, as exemplified by bilateral kidney stones and benign prostatic hyperplasia of the prostate gland. Rarely, pinworms infecting the kidney can cause obstructive nephropathy.

Other

• Genetic congenital disease such as polycystic kidney disease or 17q12 microdeletion syndrome.
• Mesoamerican nephropathy, is "a new form of kidney disease that could be called agricultural nephropathy". A high and so-far unexplained number of new cases of CKD, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugar cane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures of about 36 °C (96 °F) is suspected, as are agricultural chemicals

Diagnosis

A 12-lead ECG of a person with CKD and a severe electrolyte imbalance: hyperkalemia (7.4 mmol/l) with hypocalcemia (1.6 mmol/l). The T-waves are peaked and the QT interval is prolonged.

Diagnosis of CKD is largely based on history, examination and urine dipstick combined with the measurement of the serum creatinine level (see above). It is important to differentiate CKD from acute kidney injury (AKI) because AKI can be reversible. One diagnostic clue that helps differentiate CKD from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). In many people with CKD, previous kidney disease or other underlying diseases are already known. A significant number present with CKD of unknown cause.

Screening

Screening those who have neither symptoms nor risk factors for CKD is not recommended. Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with African American ancestry, those with a history of kidney disease in the past, and subjects who have relatives who had kidney disease requiring dialysis.

Screening should include calculation of the estimated GFR (eGFR) from the serum creatinine level, and measurement of urine albumin-to-creatinine ratio (ACR) in a first-morning urine specimen (this reflects the amount of a protein called albumin in the urine), as well as a urine dipstick screen for hematuria.

The glomerular filtration rate (GFR) is derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship:the higher the creatinine, the lower the GFR. It reflects one aspect of kidney function: how efficiently the glomeruli - the filtering units - work. Normal GFR is 90-120 mLs/min. The units of creatinine vary from country to country. But since the glomeruli make up <5% of the mass of the kidney, the GFR does not indicate all aspects of kidney health and function. This can be done by combining the GFR level with the clinical assessment of the person, including fluid status, and measuring the levels of hemoglobin, potassium, phosphate and parathyroid hormone (PTH).

Ultrasound

Kidney ultrasonography is useful for diagnostic and prognostic purposes in chronic kidney disease. Whether the underlying pathologic change is glomerular sclerosis, tubular atrophy, interstitial fibrosis or inflammation, the result is often increased echogenicity of the cortex. The echogenicity of the kidney should be related to the echogenicity of either the liver or the spleen (Figure 22 and Figure 23). Moreover, decreased kidney size and cortical thinning are also often seen and especially when disease progresses (Figure 24 and Figure 25). However, kidney size correlates to height, and short persons tend to have small kidneys; thus, kidney size as the only parameter is not reliable.

• 

  Chronic renal disease caused by glomerulonephritis with increased echogenicity and reduced cortical thickness. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.

• 

  Nephrotic syndrome. Hyperechoic kidney without demarcation of cortex and medulla.

• 

  Chronic pyelonephritis with reduced kidney size and focal cortical thinning. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.

• 

  End-stage chronic kidney disease with increased echogenicity, homogenous architecture without visible differentiation between parenchyma and renal sinus and reduced kidney size. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.

Additional imaging

Additional tests may include nuclear medicine MAG3 scan to confirm blood flow and establish the differential function between the two kidneys. Dimercaptosuccinic acid (DMSA) scans are also used in kidney imaging; with both MAG3 and DMSA being used chelated with the radioactive element technetium-99.

Stages

Chronic kidney disease (CKD) staging - CKD G1-5 A1-3 glomerular filtration rate (GFR) and albumin/creatinine ratio (ACR)
				ACR
				A1	A2	A3
				Normal to mildly increased	Moderately increased	Severely increased
				<30	30-300	>300
G F R
	G1	Normal	≥ 90	1 if kidney damage present	1	2
	G2	Mildly decreased	60-89	1 if kidney damage present	1	2
	G3a	Mildly to moderately decreased	45-59	1	2	3
	G3b	Moderately to severely decreased	30-44	2	3	3
	G4	Severely decreased	15-29	3	4+	4+
	G5	Kidney failure	<15	4+	4+	4+
Numbers 1 - 4 indicates risk of progression as well as frequency of monitoring (number of times a year). Kidney Disease Improving Global Outcomes - KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease

A glomerular filtration rate (GFR) ≥ 60 ml/min/1.73 m² is considered normal without chronic kidney disease if there is no kidney damage present.

Kidney damage is defined signs of damage seen in blood, urine, or imaging studies which includes lab albumin/creatinine ratio (ACR) ≥ 30. All people with a GFR <60 ml/min/1.73 m² for 3 months are defined as having chronic kidney disease.

Protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant.

1. Stage 1: Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 ml/min/1.73 m²) and persistent albuminuria. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
2. Stage 2: Mild reduction in GFR (60–89 ml/min/1.73 m²) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
3. Stage 3: Moderate reduction in GFR (30–59 ml/min/1.73 m²):. British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral.
4. Stage 4: Severe reduction in GFR (15–29 ml/min/1.73 m²) Preparation for kidney replacement therapy.
5. Stage 5: Established kidney failure (GFR <15 ml/min/1.73 m²), permanent kidney replacement therapy, or end-stage kidney disease.

The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation). The condition of individuals with CKD, who require either of the two types of kidney replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), people with advanced stage of CKD (stage 5), who have not yet started kidney replacement therapy, are also referred to as NDD-CKD.

Management

Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD. Control of blood pressure and treatment of the original disease are the broad principles of management.

Blood pressure

Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are recommended as first-line agents since they have been found to slow the decline of kidney function, relative to a more rapid decline in those not on one of these agents. They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD. ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD. Aggressive blood pressure lowering decreases people's risk of death.

Other measures

• Aggressive treatment of high blood lipids is recommended.
• A low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start. A tailored low-protein diet, designed for low acidity, may help prevent damage to kidneys for people with CKD. Additionally, controlling salt ingestion helps to decrease the incidence of coronary heart disease, lowering blood pressure and reducing albuminuria.
• Anemia - A target hemoglobin level of 9–12 g/dL is recommended; raising hemoglobin levels to the normal range has not been found to be of benefit.
  • Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin.
  • Replacement of erythropoietin is often necessary in people with advanced disease.
  • It is unclear if androgens improve anemia.
• Calcitriol is recommended for vitamin D deficiency and control of metabolic bone disease.
• Phosphate binders are used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease.
• Phosphodiesterase-5 inhibitors and zinc may improve sexual dysfunction in men.

Lifestyle Interventions

Obesity may have a negative impact in CKD, increasing the risk of disease progression to ESKD or kidney failure compared to controls with healthy weight, and when in advanced stages also may hinder people's eligibility to kidney transplantation. Weight management interventions in overweight and obese adults with CKD (of various stages) have been studied to assess its safety and efficacy. A recent systematic review collected evidence from 17 studies which evaluated lifestyle (including dietary, physical activity/exercise, or behavioural strategies used in isolation or in combination), pharmacological (used to reduce absorption or suppress appetite) and surgical interventions. The review concluded that lifestyle interventions may provide some health benefits, namely improving body weight, low density lipoprotein (LDL) cholesterol and diastolic blood pressure (DBP), when compared to usual care or controls. Whether these benefits extend to help reducing cardiovascular events, kidney function and risk of death is uncertain. These conclusions were based on very low quality of evidence, so future robust studies are needed. Thus, it is recommended that weight management interventions should be individualised, according to a thorough patients' assessment regarding clinical condition, motivations and preferences.

Sleep

People with CKD suffer from sleep disorders, thus not being able to get quality sleep. There are several strategies that could help, such as relaxation techniques, exercise, acupressure and medication: 

• Exercise: weak evidence demonstrates that exercise may be helpful with sleep regulation. Nevertheless, exercise possibly decreases fatigue and depression in people with CKD.
• Acupressure: evidence suggests that this technique may have slight effects on latency and sleep duration, as well as on fatigue reduction, although these results are not reliable due to the diversity of conclusions in several articles. 

Despite all the available options studied so far, evidence shows that none of them is effective in the treatment of sleep disorders. This means that we are not able to conclude which is the best guidance to improve sleep quality in this type of population.

eHealth interventions

There is currently limited evidence suggesting that eHealth interventions may improve dietary sodium intake and fluid management for people with chronic kidney disease (CKD). The findings are based on low certainty evidence of 43 studies. So, more large and higher quality research studies are needed to understand the impact of eHealth on the health of people with CKD.

Referral to a nephrologist

Guidelines for referral to a nephrologist vary between countries. Most agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m² is less than 30 ml/min; or decreasing by more than 3 ml/min/year).

It may also be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper education regarding options for kidney replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those people with chronic kidney disease opting for future hemodialysis.

Renal replacement therapy

At stage 5 CKD, kidney replacement therapy is usually required, in the form of either dialysis or a kidney transplant.

In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes. Hemodialysis with high-flux dialysis membrane, long or frequent treatment, and increased blood/dialysate flow has improved removal of water-soluble small molecular weight uremic toxins. Middle molecular weight molecules are removed more effectively with hemodialysis using a high-flux membrane, hemodiafiltration and hemofiltration. However, conventional dialysis treatment is limited in its ability to remove protein-bound uremic toxins.

Prognosis

CKD increases the risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure.

Chronic kidney disease results in worse all-cause mortality (the overall death rate) which increases as kidney function decreases. The leading cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.

While kidney replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected. Kidney transplantation increases the survival of people with stage 5 CKD when compared to other options; however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis.

People with ESKD are at increased overall risk for cancer. This risk is particularly high in younger people and gradually diminishes with age. Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in people with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved outcomes.

Epidemiology

About one in ten people have chronic kidney disease. In Canada 1.9 to 2.3 million people were estimated to have CKD in 2008. CKD affected an estimated 16.8% of U.S. adults aged 20 years and older in the period from 1999 to 2004. In 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD.

Chronic kidney disease was the cause of 956,000 deaths globally in 2013, up from 409,000 deaths in 1990.

Chronic kidney disease of unknown aetiology

The cause of chronic kidney disease is in some cases not known; it is referred to as chronic kidney disease of unknown aetiology (CKDu). As of 2020 a rapidly progressive chronic kidney disease, unexplained by diabetes and hypertension, had increased dramatically in prevalence over a few decades in several regions in Central America and Mexico, a CKDu referred to as the Mesoamerican nephropathy (MeN). It was estimated in 2013 that at least 20,000 men had died prematurely, some in their 20s and 30s; a figure of 40,000 per year was estimated in 2020. In some affected areas CKD mortality was five times the national rate. MeN primarily affects men working as sugarcane labourers. The cause is unknown, but in 2020 the science found a clearer connection between heavy labour in high temperatures and incidence of CKDu; improvements such as regular access to water, rest and shade, can significantly decrease the potential CKDu incidence. CKDu also affects people in Sri Lanka where it is the 8th largest cause of in-hospital mortality.

Although CKDu was first documented among sugar cane workers in Costa Rica in the 1970s, it may well have affected plantation labourers since the introduction of sugar cane farming to the Caribbean in the 1600s. In colonial times the death records of slaves on sugar plantations was much higher than for slaves forced into other labour.

Race

African, Hispanics, and South Asians, particularly those from Pakistan, Sri Lanka, Bangladesh, and India, are at high risk of developing CKD. Africans are at greater risk due to the number of people affected with hypertension among them. As an example, 37% of ESKD cases in African Americans can be attributed to high blood pressure, compared with 19% among Caucasians. Treatment efficacy also differs between racial groups. Administration of antihypertensive drugs generally halts disease progression in white populations but has little effect in slowing kidney disease among black people, and additional treatment such as bicarbonate therapy is often required. While lower socioeconomic status contributes to the number of people affected with CKD, differences in the number of people affected by CKD are still evident between Africans and Whites when controlling for environmental factors.

Society and culture

The International Society of Nephrology is an international body representing specialists in kidney diseases.

United States

• The National Kidney Foundation is a national organization representing people with chronic kidney diseases and professionals who treat kidney diseases.
• The American Kidney Fund is a national nonprofit organization providing treatment-related financial assistance to one of every five people undergoing dialysis each year.
• The Renal Support Network is a nonprofit, patient-focused, patient-run organization that provides non-medical services to those affected by CKD.
• The American Association of Kidney Patients is a nonprofit, patient-centric group focused on improving the health and well-being of CKD and people undergoing dialysis .
• The Renal Physicians Association is an association representing nephrology professionals.

United Kingdom

It was said to be costing the National Health Service about £1.5 billion a year in 2020.

Kidney Care UK and The UK National Kidney Federation represent people with chronic kidney disease. The Renal Association represents Kidney physicians and works closely with the National Service Framework for kidney disease.

Australia

Kidney Health Australia serves that country.

Other animals

The incidence rate of CKD in dogs was 15.8 cases per 10,000 dog years at risk. The mortality rate of CKD was 9.7 deaths per 10,000 dog years at risk. (rates developed from a population of 600,000 insured Swedish dogs; one dog year at risk is one dog at risk for one year)The breeds with the highest rates were the Bernese mountain dog, miniature schnauzer and boxer. The Swedish elkhound, Siberian husky and Finnish spitz were the breeds with the lowest rates.

Research

Currently, several compounds are in development for the treatment of CKD. These include the angiotensin receptor blocker (ARB) olmesartan medoxomil; and sulodexide, a mixture of low molecular weight heparin and dermatan sulfate.

Unbiased research with complete reporting is required to determine the safety and effectiveness of acupuncture to treat depression, pain, sleep problems, and uraemic pruritus in people who are undergoing dialysis treatments on a regular basis.