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Chronic kidney disease

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(Redirected from End-stage renal disease)
This article is about CKD in general. For severe disease, see kidney failure.
Chronic kidney disease
Other namesChronic renal disease, kidney failure, impaired kidney function[1]
Illustration of a kidney from a person with chronic renal failure
SpecialtyNephrology
SymptomsEarly: None[2]
Later: Leg swelling, feeling tired, vomiting, loss of appetite, confusion[2]
ComplicationsHeart disease, high blood pressure, anemia[3][4]
DurationLong-term[5]
CausesDiabetes, heart failure, high blood pressure, glomerulonephritis, polycystic kidney disease[5][6]
Risk factorsSmoking, genetic predisposition,
low socioeconomic status[7]
Diagnostic methodBlood tests, urine tests[8]
TreatmentMedications to manage blood pressure, blood sugar, and lower cholesterol, renal replacement therapy, kidney transplant[9][10]
Frequency753 million (2016)[1]
Deaths1.2 million (2015)[6]

Chronic kidney disease (CKD) is a type of long-term kidney disease, in which either there is a gradual loss of kidney function which occurs over a period of months to years, or an abnormal kidney structure (with normal function).[2][5] Initially, patients are usually asymptomatic, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion.[2] Complications can relate to hormonal dysfunction of the kidneys and include (in chronological order) high blood pressure (often related to activation of the renin–angiotensin system), bone disease, and anemia.[3][4][11] Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.[12] CKD can lead to end-stage kidney disease (ESKD) requiring kidney dialysis or kidney transplantation.[9]

Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease.[5][6] Risk factors include a family history of chronic kidney disease.[2] Diagnosis is by blood tests to measure the estimated glomerular filtration rate (eGFR), and a urine test to measure albumin.[8] Ultrasound or kidney biopsy may be performed to determine the underlying cause.[5] Several severity-based classification systems are in use.[13][14]

Screening at-risk people is recommended.[8] Initial treatments may include medications to lower blood pressure, blood sugar, and cholesterol.[10] 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.[15] Loop diuretics may be used to control edema and, if needed, to further lower blood pressure.[16][10][17] NSAIDs should be avoided.[10] Other recommended measures include staying active, eating a healthy diet, and sometimes individualized dietary changes recommended by healthworkers.[10][18] The idea of a standard 'renal diet' or 'kidney diet' is outdated and is not patient-centred. Treatments for anemia and bone disease may also be required.[19][20] Severe disease requires hemodialysis, peritoneal dialysis, or a kidney transplant for survival.[9]

Chronic kidney disease affected 753 million people globally in 2016 (417 million females and 336 million males.)[1][21] In 2015, it caused 1.2 million deaths, up from 409,000 in 1990.[6][22] 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.[6]

Signs and symptoms

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Uremic frost on the head in someone with chronic kidney disease

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, more unpleasant symptoms may emerge:[23]

  • Blood pressure is increased due to fluid overload and the production of vasoactive hormones created by the kidney via the renin-angiotensin system, increasing the risk of developing hypertension and heart failure. 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.[24][unreliable medical source?] People with both CKD and cardiovascular disease have significantly worse prognoses than those with only cardiovascular disease.[25]
  • Urea accumulates, leading to azotemia (high urea concentration) and ultimately uremia (a clinical syndrome of anorexia, vomiting, fatigue, itching, pericarditis, asterixis, and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on the 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, when the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (triggering the cells to release potassium into the bloodstream to neutralize the acid) and from lack of insulin.[26]
  • Fluid overload symptoms may range from mild edema to life-threatening pulmonary edema.
  • Hyperphosphatemia results from poor phosphate elimination in the kidney, and contributes to increased cardiovascular risk by causing vascular calcification.[27] 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 .[28][29]
  • Hypocalcemia results from 1,25 dihydroxyvitamin D3 deficiency (caused by high FGF-23 and reduced kidney mass)[30] and the skeletal resistance to the calcemic action of parathyroid hormone.[31] 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).[32] 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.[33]
  • 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.[11] CKD–mineral and bone disorders have been associated with poor outcomes.[11][21]
  • Metabolic acidosis may result from decreased capacity to generate enough ammonia from the cells of the proximal tubule.[26] Acidemia affects the function of enzymes and increases the excitability of cardiac and neuronal membranes by the promotion of hyperkalemia.[34]
  • Anemia is common and is especially prevalent in those requiring hemodialysis. 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.[35]
  • At very low GFR, less than 15 mL/min/1.73m2, and usually less than 10 mL/min/1.73m2, cachexia may develop, leading to unintentional weight loss, muscle wasting, weakness, and anorexia.[36]
  • Cognitive decline in patients experiencing CKD is an emerging symptom revealed in research literature.[37][38][39][40] Research suggests that patients with CKD face a 35–40% higher likelihood of cognitive decline and or dementia, worse with more severe disease (higher G category).[37][38][40][41][38]
  • 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. Most women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.[42]

Causes

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The most common causes of CKD are diabetes mellitus, hypertension, and glomerulonephritis.[43][44] 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.[45]

By anatomical location

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Other

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Diagnosis

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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. Differentiating CKD from acute kidney injury (AKI) is important 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.[citation needed]

Screening

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Screening those who have neither symptoms nor risk factors for CKD is not recommended.[53][54] 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.[citation needed]

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.[55]

The 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. The normal GFR is >90 ml/min. The units of creatinine vary from country to country, but since the glomeruli comprise <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.[citation needed]

Ultrasound

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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 the liver or the spleen. Moreover, decreased kidney size and cortical thinning are often seen especially when the disease progresses. However, kidney size correlates to height, and short persons tend to have small kidneys; thus, kidney size as the only parameter is unreliable.[56]

  • 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.[56]
    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.[56]
  • Nephrotic syndrome. Hyperechoic kidney without demarcation of cortex and medulla.[56]
    Nephrotic syndrome. Hyperechoic kidney without demarcation of cortex and medulla.[56]
  • 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.[56]
    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.[56]
  • 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.[56]
    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.[56]

Additional imaging

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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.[57]

Categorization

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Chronic kidney disease (CKD) categories – CKD G1-5 A1-3
glomerular filtration rate (GFR) and albumin/creatinine ratio (ACR)
 
ACR
GFR
 A1 A2 A3
Normal to mildly increased Moderately increased Severely increased
<30 30–300 >300
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 indicate the risk of progression as well as the 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 [58]

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 as signs of damage seen in blood, urine, or imaging studies. Urine abnormalities include albumin/creatinine ratio (ACR) ≥ 30.[59] All people with a GFR <60 mL/min/1.73 m2 for 3 months are defined as having chronic kidney disease.[59]

Protein in the urine, or proteinuria, which can be assessed by urine albumin-creatinine ratio (UACR or ACR), urine protein-creatinine ration (PCR), dipstick proteinuria, or 24-h urine collection for protein, is an independent marker for the worsening of kidney function and cardiovascular disease. It is a risk factor for progression to higher G category, and a risk factor for cardiovascular events, at all levels of GFR (all G categories), and is included as a second dimension in the KDIGO international classification.

British guidelines and some researchers distinguish between category 3A (GFR 45–59) and category 3B (GFR 30–44) for purposes of screening and referral.[60]

Kidney disease is now categorized by G (GFR) and A (albuminuria) categories, as shown above.[61] The word 'stage' was opposed before its international adoption,[62] introduced in 2005 KDIGO CKD guidelines, and finally removed from the classification in 2012.

This outdated pre-2012 classification system should not be used. It is shown here for historical interest and to account for the continued ubiquity of the word 'stage' in discussions of severity of kidney disease:

  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.[59]
  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.[59]
  3. Stage 3: Moderate reduction in GFR (30–59 mL/min/1.73 m2).[59]
  4. Stage 4: Severe reduction in GFR (15–29 mL/min/1.73 m2)[59]
  5. Stage 5: Established kidney failure (GFR <15 mL/min/1.73 m2), or permanent kidney replacement therapy,[59] 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 meaning 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 end-stage kidney disease (ESKD). This term, using the plain-language word 'kidney' rather than the word 'renal' is preferred to the term end-stage renal disease (ESRD), and has largely replaced it. ESRD continues as an administrative term in policy and legislation, and continues to be used in those contexts, and in research derived from those databases. Some people in category G5 have NDD-CKD and others are using KRT to improve quality and length of life. No standard nomenclature exists for these situations within G4 and G5 kidney disease:

  1. Planned conservative care (PCC). People living with advanced kidney disease who have been offered but do not intend to pursue KRT (dialysis or transplant), who are not clinically at the point where it would be recommended.
  2. Conservative care (CC). People living with advanced kidney disease who have been offered but do not intend to pursue KRT, who are clinically at or beyond the point where it would have been recommended.
  3. Planned conservative care owing to lack of resources (PCCR). People living with advanced kidney disease who do not have the resources for KRT and whose state does not provide it for them, who are not clinically at the point where it would be recommended if available.
  4. Conservative care owing to lack of resources (CCR). People living with advanced kidney disease who do not have the resources for KRT and whose state does not provide it for them, who are clinically at or beyond the point where it would have been recommended, if available.

In practice, conservative care is a patient-centred continuum that does not necessarily identify the point at which KRT would have been started.

Management

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Chronic kidney disease (CKD) is a serious condition often linked to diabetes and high blood pressure. There is no cure, but a combination of lifestyle changes and medications can help slow its progression. This might include a plant-dominant diet with less protein and salt, medications to control blood pressure and sugar, and potentially newer anti-inflammatory drugs. Doctors may also focus on managing heart disease risk, preventing infections, and avoiding further kidney damage. While dialysis may eventually be needed, a gradual transition can help preserve remaining kidney function. More research is ongoing to improve CKD management and patient outcomes.[63]

Blood pressure

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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.[15] 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.[15] ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD.[15] In a 2017 meta-analysis, lower, compared with higher, blood pressure targets, in people with G3 to G5 CKD reduced the risk of death from all causes by 14%.[64]

Other measures

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  • A randomized controlled trial, conducted in people with CKD, showed cardiovascular benefits from simvastatin plus ezetimibe[65] that are thought likely to generalize to other drugs that lower cholesterol, including statins alone.
  • Though consuming excessive protein is not recommended (e.g., more than 1.5 g/kg/day) because of its effects on hyperfiltration, one of the mechanism of progression of chronic kidney disease, following a low-protien diet (e.g., less than 0.8 g/kg/day) is no longer widely recommended because of the low certainty of the evidence that it improves outcomes, the high resource costs of its safe implementation, and the risk of malnutrition even when implemented as safely as possible. 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.[66] A tailored low-protein diet, designed for low acidity, may help prevent damage to kidneys for people with CKD.[67] Additionally, avoiding high levels of salt ingestion helps to decrease the incidence of coronary heart disease, lowering blood pressure and reducing albuminuria.[68]
  • Anemia – A target hemoglobin level of 100–120 g/L is recommended;[69][70] raising hemoglobin levels to the normal range does not result in benefit and doubles the risk of stroke.[71][72]
  • 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.[42]

Lifestyle interventions

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Diet and obesity

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People living with obesity may be at increased risk of CKD, and at increased risk of disease progression to ESKD or kidney failure compared with controls with healthy weight,[75] and obesity, depending on body habitus, affects access to kidney transplantation.[76] Dietary factors may play a role, for example, the consumption of high calorie and high fructose beverages is associated with a 60% increase in the risk of developing CKD.[77][78]

In primary prevention (i.e., avoiding developing the earliest indications of CKD) there are no intervention studies, but a 2020 systematic review and meta-analysis[79] identified the following associations, at low to very low certainty. This rating relates to the quality of the studies included in the review and to the inherent problems with observational methods to answer questions of causation.

  • Higher dietary potassium intake - 22% reduction in risk (NB: increasing dietary potassium without medical advice is not safe for people with established CKD and should be discussed with a health professional before undertaking)
  • Higher vegetable intake - 21% reduction in risk
  • Higher salt intake - 21% increase in risk
  • Physical activity (compared with sedentary lifestyle) - 18% reduction in risk
  • Current and former smokers - 18% increase in risk

Weight management interventions in overweight and obese adults with CKD include lifestyle interventions (dietary changes, physical activity/exercise, or behavioural strategies), pharmacological (used to reduce absorption or suppress appetite) and surgical interventions. Any of these can help people with CKD lose weight, however, it is not known if they can also prevent death or cardiovascular events like heart complications or stroke.[80] It is recommended that weight management interventions should be individualised, according to a thorough patients' assessment regarding clinical condition, motivations, and preferences.[80] GLP-1RAs reduce weight, cardiovascular risk, and risk of kidney disease progression across a spectrum of patients with and without kidney disease and with and without diabetes[81]; their introduction constitutes a paradigm shift in risk-factor management primary prevention of CKD, in prevention of CKD progression and complications, and in improving access to transplantation. Many jurisdictions and insurance agencies currently limit their use to people with diabetes[82], but randomized trials have shown that benefits apply also to people without diabetes.

Dietary salt intake

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High dietary sodium intake may increase the risk of hypertension and cardiovascular disease. The effect of dietary restriction of salt in foods has been investigated in people with chronic kidney disease. For people with CKD, including those on dialysis, reduced salt intake may help to lower both systolic and diastolic blood pressure, as well as albuminuria.[83] Some people may experience low blood pressure and associated symptoms, such as dizziness, with lower salt intake. The effect of salt restriction on extracellular fluid, oedema, and total body weight reduction is unknown.[83]

EHealth interventions may improve dietary sodium intake and fluid management for people with CKD.[84]

Omega-3 supplementation

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These are ineffective. In people with CKD who require hemodialysis, there is a risk that vascular blockage due to clotting, may prevent dialysis therapy from being possible. Even though Omega-3 fatty acids contribute to the production of eicosanoid molecules that reduce clotting, it does not have any impact on the prevention of vascular blockage in people with CKD.[85]

Protein supplementation

[edit]

Regular consumption of oral protein-based nutritional supplements may increase serum albumin levels slightly in people with CKD, especially among those requiring hemodialysis or who are malnourished.[86] Prealbumin level and mid-arm muscle circumference may also be increased following supplementation.[86] Despite possible improvement in these indicators of nutritional status, it is not certain that protein supplements affect the quality of life, life expectancy, inflammation, or body composition.[86]

Iron supplementation

[edit]

Intravenous (IV) iron therapy may help more than oral iron supplements in reaching target hemoglobin levels. However, allergic reactions may also be more likely following IV-iron therapy.[87]

Sleep

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Individuals with CKD have an increased prevalence of sleep apnea compared to the general population (both OSA and central sleep apnea). The presence of sleep apnea in CKD has been associated with an increased risk of cardiovascular events and mortality.[88]

People with CKD also experience sleep disorders, thus unable to get quality sleep. There are several strategies that could help, such as relaxation techniques, exercise, and medication. Exercise may be helpful with sleep regulation and may decrease fatigue and depression in people with CKD. However, none of these options have been proven to be effective in the treatment of sleep disorders. This means that it is unknown what is the best guidance to improve sleep quality in this population.[89]

Referral to a nephrologist

[edit]

Guidelines for referral to a nephrologist vary between countries. Most agree that nephrology referral is required by G3 CKD (when eGFR/1.73m2 is less than 30 mL/min/1.73m2; or decreasing rapidly). The Ontario guidelines[90] reflect international practices in social democracies which provide health care free at the point of use:

Indications for referral for chronic kidney disease (CKD), including proteinuria:

  • eGFR < 30, or
  • Rapid deterioration in kidney function: eGFR < 45 and decline of > 5 within 6 months in absence of self-limited illness; eGFR must be repeated in 2-4 weeks to confirm persistent decline, or
  • ACR > 60, or
  • 5-year Kidney Failure Risk Equation (KFRE) ≥ 5%

While people and their primary care physician often want to arrange a timely appointment so that their clinical concerns can be addressed and/or alleviated quickly, most nephrologists will triage referred individuals based on level of need. Those people who are at high risk of progressing to end-stage renal disease (ESRD), and/or who may require a renal biopsy for diagnosis, should be seen more urgently.

Other indications for referral to nephrology:

  • Resistant or suspected secondary hypertension
  • Suspected glomerulonephritis/renal vasculitis, including RBC casts or hematuria (> 20 RBC/hpf)
  • Metabolic work-up for recurrent kidney stones
  • Clinically important electrolyte disorder

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.[citation needed]

In at least one social democracy, recognition and referral for kidney disease has been found to be biased against women.[91] Other sex and gender disparities are recognized.[92][93][94]

Renal replacement therapy

[edit]

Discussions of kidney replacement therapy (dialysis or kidney transplant), patient education, and planning can be based on absolute level of GFR or on estimates of the risk of progression. It is essential to recognize that access to KRT is not available to millions of people with CKD living in low- and middle-income countries where the costs are not covered by the state.[95]

In CKD numerous uremic toxins accumulate in the blood. Dialysis controls the accumulation of toxins but does not restore normal effective clearance, or quality of life. Toxin clearance and quality of life are generally higher in patients who have undergone successful kidney transplantation than in patients on dialysis. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes.[96] 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.[97]

Prognosis

[edit]

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.[98] The leading cause of death in chronic kidney disease is cardiovascular disease and not ESKD or its complications.[98][99][100]

While kidney replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected.[101][102] Kidney transplantation increases survival compared with patients eligible for transplant but remaining on the waiting list;[103][104] however, it is associated with an increased short-term mortality and morbidity owing to complications of the surgery and intense early immunosuppression. 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.[105]

People with ESKD are at increased overall risk for cancer.[106] This risk is particularly high in younger people and gradually diminishes with age.[106] Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in people with limited life expectancies due to ESKD because the evidence does not show that such tests lead to improved outcomes.[107][108]

In children, growth failure is a common complication of CKD. Children with CKD will be shorter than 97% of children the same age and sex. This can be treated with additional nutritional support or medication such as growth hormone.[109]

Survival without dialysis

[edit]

Survival in people with CKD is generally longer with dialysis than without (having only conservative kidney management). However, from the age of 80 and in elderly patients with comorbidities there is no difference in survival between the two groups. Quality of life might be better for people without dialysis.[110]

People who have decided against dialysis treatment when their CKD becomes problematically symptomatic may survive several years and experience experience fewer hospitalizations overall. However, the provision of adequate multi-disciplinary and patient-centred end-of-life care is highly variable by jurisdiction and socio-economic status.[111][112]

Epidemiology

[edit]

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.[71] CKD affected an estimated 17% of U.S. adults aged 20 years and older in the period from 1999 to 2004.[113] In 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD.[114]

Chronic kidney disease was the cause of 956,000 deaths globally in 2013, up from 409,000 deaths in 1990.[22]

Chronic kidney disease of unknown aetiology

[edit]

The cause of chronic kidney disease is sometimes unknown; 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.[48] 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.[115] CKDu also affects people in Sri Lanka where it is the eighth largest cause of in-hospital mortality.[116]

Race

[edit]

African, Hispanic, and South Asian (particularly those from Pakistan, Sri Lanka, Bangladesh, and India) populations 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.[7] 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.[7] 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.[7]

Although CKD of unknown etiology was first documented among sugar cane workers in Costa Rica in the 1970s, it may well have affected plantation laborers since the introduction of sugar cane farming to the Caribbean in the 1600s. In colonial times the death records of slaves on sugar plantations were much higher than for slaves forced into other labor.[115]

Denial of care

[edit]

Denial of care in chronic kidney disease treatment and management is a significant issue for minority populations. This can be due to healthcare provider prejudice, structural barriers, and health insurance coverage disparities. Healthcare provider biases can lead to under-treatment, misdiagnosis, or delayed diagnosis. Structural barriers, such as lack of insurance and limited healthcare facilities, hinder access to timely care. Furthermore, health insurance coverage disparities, with minority populations lacking adequate coverage, contribute to these disparities. Denial of care worsens health outcomes and perpetuates existing health inequities.[citation needed]

Race-based kidney function metric - no longer used

[edit]

Race-based kidney function metrics, particularly normalizing creatinine, were, before 2021 widespread in diagnosing and managing chronic kidney disease (CKD) and in research. Using race in calculations of GFR that are used in the determination of access to care is ethically wrong, is rejected by racialized communities, has not been shown to improve outcomes, and perpetuates health disparities: this practice has been abandoned.[117] This approach fails to account for the complex interplay of genetic, environmental, and social factors influencing kidney function. Alternative approaches that consider socioeconomic status, environmental exposures, and genetic vulnerability, are needed to accurately assess kidney function and address CKD care disparities.[citation needed]

Society and culture

[edit]

Organisations

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

United States

[edit]

United Kingdom

[edit]

CKD was reported to be costing the National Health Service about £1.5 billion a year in 2020.[118]

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

[edit]

Kidney Health Australia serves that country.

Other animals

[edit]

Dogs

[edit]

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.[119][120]

Cats

[edit]
Main article: Chronic kidney disease in cats

Cats with chronic kidney disease may have a buildup of waste products usually removed by the kidneys. They may appear lethargic, unkempt, and lose weight, and may have hypertension. The disease can prevent appropriate concentration of urine, causing cats to urinate in greater volumes and drink more water to compensate. Loss of important proteins and vitamins through urine may cause abnormal metabolism and loss of appetite. The buildup of acids within the blood can result in acidosis, which can lead to anemia (which can sometimes be indicated by pink or whitish gums, but by no means does the presence of normal colored gums guarantee that anemia is not present or developing), and lethargy.[121]

Research

[edit]

Randomized trials have shown benefits for RASi (ACEi and ARB), SLGT2i, GLP-1RA, and finerenone, an MRA, in subgroups of people with CKD.

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