Chronic kidney disease

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Chronic kidney disease ( CKD ) is a type of kidney disease where there is a gradual decline in kidney function over several months or years. Initially there were no symptoms. Then, leg swelling, feeling tired, vomiting, loss of appetite, or confusion can develop. Complications may include heart disease, high blood pressure, bone disease, or anemia.

The causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include family history of the condition. Diagnosis is generally by blood tests to measure glomerular filtration rate and urine test to measure albumin. Further tests such as ultrasound or renal biopsy may be performed to determine the underlying cause. A number of different classification systems exist.

Checked people at risk. Initial treatment may include medications to manage blood pressure, blood sugar, and lower cholesterol. NSAIDs should be avoided. Other recommended actions include staying active and changing certain diets. Severe disease may require hemodialysis, peritoneal dialysis, or renal transplantation. Treatment for anemia and bone disease may also be needed.

Chronic kidney disease affects 753 million people globally by 2016, including 417 million women and 336 million men. By 2015 it produced 1.2 million deaths, up from 409,000 in 1990. The causes that contributed to the greatest number of deaths were high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

Video Chronic kidney disease

Signs and symptoms

CKD is initially asymptomatic and is generally only detected as an increase in serum creatinine or protein in the urine. When kidney function decreases:

• Blood pressure is increased due to excess fluid and the production of vasoactive hormones made by the kidneys through the renin-angiotensin system, raising a person's risk of developing hypertension and/or suffering from congestive heart failure.
• Urea accumulates, causes azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to high systemic circulation, urea is excreted in eccrine sweat at high concentrations and crystallizes on the skin when the sweat evaporates ("uremic frost").
• Potassium accumulates in the blood (hyperkalemia with various symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate drops to less than 20-25 ml/min/1.73 m ² , at which point the kidneys decrease the ability to remove potassium. Hyperkalemia in CKD may be exacerbated by acidemia (which causes extracellular shift of potassium) and from lack of insulin.
• The synthesis of decreased erythropoietin causes anemia.
• Symptoms of fluid overload may vary from mild edema to life-threatening pulmonary edema.
• Hyperphosphatemia, due to reduced phosphate excretion, follows a decrease in glomerular filtration. Hyperphosphatemia is associated with an increased cardiovascular risk, being a direct stimulus for vascular calcification. In addition, the concentration of fibroblast growth factor-23 (FGF-23) circulation increased progressively due to kidney capacity for decreased phosphate excretion, but this adaptative response may also contribute to left ventricular hypertrophy and increased mortality in patients with CKD.
• Hypocalcemia, due to a deficiency of 1,25 dihydroxyvitamin D ₃ (caused by FGF-23 stimulation and reduction in renal mass), and resistance to calcemic action of parathyroid hormone. Osteocytes are responsible for the increased production of FGF-23, which is a powerful enzyme inhibitor of 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol to 1,25 dihydroxyvitamin D ₃ ). Then, this develops into secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification that further impairs the functioning of the heart. The extreme consequence is the occurrence of a rare condition called calciphylaxis.

• The concept of kidney disease-a chronic mineral bone disorder (CKD-MBD) currently represents a wider clinical syndrome that develops as a systemic disorder of minerals and bone metabolism because CKD is manifested by one or a combination of: 1) calcium, phosphorus (phosphate), parathyroid hormone or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and 3) soft or vascular tissue calcification. CKD-MBD has been associated with poor results.
• Metabolic acidosis (due to accumulation of sulfate, phosphate, uric acid, etc.) can cause changes in enzyme activity by excess acids acting on the enzyme; and also increased stimulation of the heart and nerve membranes by the promotion of hyperkalemia due to excess acid (acidemia). Acidosis is also caused by a decrease in the capacity to produce sufficient ammonia from proximal tubular cells.
• Iron deficiency anemia, which increases the prevalence with decreased renal function, especially in those who require hemodialysis. It is multifactoral in causes, but includes increased inflammation, decreased erythropoietin, and hyperuricemia leading to bone marrow suppression.

People with CKD have accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients suffering from CKD and cardiovascular disease tend to have a worse prognosis than those who suffer only from the latter.

Sexual dysfunction is very common in men and women with CKD. The majority of men have diminished sex drive, difficulty getting an erection, and reaching orgasm, and the problem gets worse with age. Most women have problems with sexual arousal, and painful menstruation and problems with doing and enjoying sex are common.

Maps Chronic kidney disease

Cause

The most common cause of CKD in 2015 is diabetes mellitus followed by high blood pressure and glomerulonephritis. Other causes of CKD include idiopathic (ie unknown cause, often associated with small kidney on renal ultrasound). Together, this accounts for about 75% of all adult cases.

Historically, renal disease has been classified according to the part of the involved renal anatomy.

• Vascular disease includes major vascular diseases such as bilateral renal artery stenosis and small blood vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome, and vasculitis.
• Glomerular disease consists of various groups and is grouped into:
  • Primary glomerular disease such as segmental focal glomerulosklerosis and IgA nephropathy (or nephritis)
  • Secondary glomerular disease such as diabetic nephropathy and lupus nephritis
• Congenital disease such as polycystic kidney disease.
• Tubulointerstitial disease includes chronic tubulointerstitial nephritis caused by drugs and toxins, and reflux nephropathy.
• Obstructive nephropathy is exemplified by bilateral kidney stones and prostate diseases such as benign prostatic hyperplasia.
• In rare cases, pinworms infecting the kidneys can also cause nephropathy.
• Non-traditional causes of CKD (CKDu) are denoted if a common cause of CKD does not exist:
  • CKD an unknown cause is the subject of study by the Sri Lankan Ministry of Health and World Health Organization 2009-2012.
  • Mesoamerica nephropathy, a form of CKDu, is "a new form of kidney disease that can be called agricultural nephropathy".

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Diagnosis

The diagnosis of CKD is largely based on history, examination and urine dipstick combined with measurement of serum creatinine levels (see above). It is important to distinguish CKD from acute kidney injury (AKI) because AKI can be reversible. One of the diagnostic guidelines that helps distinguish CKD from MMR is a gradual increase in serum creatinine (over several months or years) compared with a sudden increase in serum creatinine (days to weeks). In many patients with CKD, previous kidney disease or other underlying disease is known. A significant number comes with an unknown cause CKD.

Poison

In CKD many uremic toxins accumulate in the blood. Even when ESKD (mostly synonymous with CKD5) is treated with dialysis, toxic levels do not return to normal because dialysis is not as efficient. Similarly, after a kidney transplant, these levels may not return to normal because the transplanted kidneys can not work 100%. If so, creatinine levels are often normal. Toxins show various cytotoxic activity in serum and have different molecular weights, and some are bound to other proteins, especially on albumin. Such toxic protein-bound substances receive the attention of scientists interested in improving the standard chronic dialysis procedure used today.

Screening

Screening those without symptoms or risk factors for CKD is not recommended. Those who should be examined include: those with hypertension or a history of cardiovascular disease, those with diabetes or obesity, those aged & gt; 60 years old, subjects with native origin, those with a history of kidney disease in the past and subjects who have relatives who have kidney disease requiring dialysis. Screening should include calculations of GFR estimates of serum creatinine levels, and measurement of urinary albumin-to-creatinine ratio (ACR) in early morning urine specimens (this reflects the amount of protein called albumin in urine), as well as urinary dipstick screen for hematuria. GFR (glomerular filtration rate) is derived from serum creatinine and is proportional to 1/creatinine, ie, reciprocal (higher creatinine, lower GFR). It reflects one aspect of kidney function: how efficiently the glomeruli (filtration unit) work. But because they reach & lt; 5% of kidney mass, GFR does not show all aspects of health and kidney function. This can be done by combining GFR levels with clinical assessment of patients (especially fluid state) and measuring hemoglobin, potassium, phosphate and parathyroid hormone (PTH) levels. Normal GFR is 90-120 mL/min. The creatinine unit varies from country to country.

Nephrologist

Guidelines for referrals to nephrologists vary across countries. Although most agree that nephrology referrals are required by Stage 4 CKD (when eGFR/1.73 m ² is less than 30 ml/min, or decrease more than 3 ml/min/year); and may be useful in the early stages (eg CKD3) when the albumin to urinary creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings indicate glomerular or secondary disorder of the disease receiving special care. Other benefits of early nephrology referrals include appropriate patient education regarding options for renal replacement therapy as well as pre-emptive transplantation, and timely preparation and placement of arteriovenous fistula in patients who choose hemodialysis in the future.

Test more kidney function

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

Severity based on

All individuals with glomerular filtration rate (GFR) & lt; 60 ml/min/1.73 m ² for 3 months is classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these people is the reduction of kidney function to this level or lower indicates a loss of half or more of the adult normal renal function rate, which may be associated with a number of complications such as the development of cardiovascular disease.

Protein in urine is considered an independent marker for worsening kidney function and cardiovascular disease. Therefore, English guidelines add the letter "P" to the stage of chronic kidney disease if protein loss is significant.

Stage 1 Slightly diminishes its function; Kidney damage with normal or relatively high GFR (> = 90 ml/min/1.73 m ² ) and persistent albuminuria. Kidney damage is defined as a pathological disorder or a marker of damage, including abnormalities in blood tests or urine or imaging tests.

Stage 2 Mild reduction in GFR (60-89 ml/min/1.73 m ² ) with kidney damage. Kidney damage is defined as a pathological disorder or a marker of damage, including abnormalities in blood tests or urine or imaging tests.

Stage 3 Moderate reduction in GFR (30-59 ml/min/1.73 m ² ):. The UK Guidelines differentiate between Stage 3A (GFR 45-59) and Stage 3B (GFR 30-44) for screening and referral purposes.

Stage 4 Weight loss in GFR (15-29 ml/min/1.73 m ² ) Preparation for renal replacement therapy.

Stage 5 Failed kidney failure (GFR 15 ml/min/1.73 m ² ), permanent renal replacement therapy, or end-stage renal disease.

NDD-CKD vs. ESKD

The term "chronic dialysis-free kidney disease" (NDD-CKD) is a term used to cover the status of people with established CKD who have not yet needed life-support care for kidney failure known as renal replacement therapy. (PRC, including maintenance dialysis or renal transplant). The individual condition with CKD, which requires one of two types of renal replacement therapy (dialysis or transplant), is referred to as end-stage renal disease (ESKD). Therefore, the beginning of ESKD is practically an inalienable conclusion of NDD-CKD. Although NDD-CKD status refers to the status of people with early stage CKD (stages 1 to 4), patients with advanced stage CKD (stage 5), who have not started renal replacement therapy, also known as NDD-CKD.

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Kidney ultrasonography is useful for diagnostic and prognostic purposes in chronic kidney disease. Whether the underlying pathological changes are glomerular sclerosis, tubular atrophy, interstitial fibrosis or inflammation, the result often increases the echogenicity of the cortex. Renal echogenicity should be associated with either liver or spleen echogenicity (Figures 22 and Fig. 23). In addition, decreased renal size and cortical thinning are also frequently seen and especially when the disease develops (Fig. 24 and Fig. 25). However, renal size correlates with height, and short people tend to have small kidneys; thus, the size of the kidney as the only parameter is unreliable.

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Treatment

In addition to controlling for other risk factors, the goal of therapy is to slow or stop the development of CKD. Blood pressure control and treatment of native diseases are broad management principles.

Blood pressure

Generally, angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow down progression. 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 with placebo in individuals with CKD. In addition, ACEI may be superior to ARBs for protection against development to kidney failure and death from any cause in those with CKD. An aggressive decrease in blood pressure lowers the risk of death.

Although the use of ACE inhibitors and ARBs represents the current standard of care for people with CKD, people are increasingly losing kidney function when using these drugs, as seen in IDNT and RENAL studies, which report a decrease over time in GFR estimation (accurate size development of CKD, as described in K/DOQI guidelines) in people treated with this conventional method.

More

Aggressive treatment of high blood lipids is guaranteed. A low-protein, low-salt diet can lead to slower CKD progression and proteinuria reduction and control of further CKD symptoms to delay dialysis initiation. Replacement of erythropoietin and calcitriol, two hormones that are processed by the kidneys, are often necessary in people with advanced disease. Guidelines recommend treatment with parenteral iron before treatment with erythropoietin. Target hemoglobin level of 9-12 g/dL is recommended. Normalization of hemoglobin has not been found to be useful. It is unclear whether androgens help with anemia. Phosphate binders are also used to control serum phosphate levels, which are usually increased in advanced chronic kidney disease. Although evidence for them is limited, phosphodiesterase-5 inhibitors and zinc exhibit potential to help men with sexual dysfunction.

In stage 5 CKD, renal replacement therapy is usually necessary, in the form of dialysis or transplantation.

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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 renal failure.

Chronic kidney disease results in a worse death because all the causes (overall mortality) are increased when kidney function decreases. The main cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is a development to stage 5.

While renal replacement therapy can retain people indefinitely and prolong life, the quality of life is negatively affected. Kidney transplantation improves the survival of people with stage 5 CKD when compared with other options; However, this is associated with short-term mortality due to surgical complications. In addition to transplantation, high intensity home hemodialysis appears to be associated with improved survival and better quality of life, compared to conventional triple hemodialysis and peritoneal dialysis.

Cancer risk

Patients with ESKD have an increased risk of cancer overall. The risk is very high in younger patients and gradually decreases with age. professional organizations of medical specialties recommend that doctors do not perform routine cancer screening in patients with limited life expectancy due to ESKD because evidence does not indicate that the test results in improved patient outcomes.

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Epidemiology

About one in ten people have chronic kidney disease. African Americans, American Indians, Hispanics, and South Asians, especially those from Pakistan, Sri Lanka, Bangladesh and India, have a high risk of developing CKD. African Americans have a greater risk because of the prevalence of hypertension among them. For example, 37% of ESKD cases in African Americans can be associated with high blood pressure, compared with 19% among Caucasians.

People with high blood pressure and diabetes are also at higher risk of developing CKD than people without underlying conditions. About one in five adults with hypertension and one in three adults with diabetes have CKD. Other health conditions that can cause CKD are obesity, high cholesterol, family history of the disease, lupus, and other forms of cardiovascular disease.

Chronic kidney disease is the cause of 956,000 global deaths by 2013, up from 409,000 deaths in 1990. In Canada 1.9 to 2.3 million people are estimated to have CKD in 2008. The US Centers for Disease Control and Prevention found that CKD affected the 16 estimate , 8% of US adults aged 20 years and older in the period 1999 to 2004. Estimates of the UK suggest that in 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD.

The success of treatment also differs between racial groups. The administration of antihypertensive drugs generally halts disease progression in the white population but has little effect in slowing kidney disease among blacks, and additional treatments such as bicarbonate therapy are often necessary. While lower socioeconomic status contribute to CKD prevalence, significant differences in CKD prevalence are still apparent between African Americans and whites when controlling for environmental factors.

Studies have shown the correct association between a history of chronic kidney disease in first or second-degree relatives, and disease risk. In addition, African-Americans may have higher levels of human leukocyte antigen (HLA) serum levels. High HLA concentrations may contribute to increased systemic inflammation, which can indirectly lead to high susceptibility to developing kidney disease. The lack of nocturnal reduction in blood pressure among African American groups is also offered as an explanation, which gives further confidence to the genetic cause of the differences in CKD races.

High and unexplained CKD events, referred to as Mesoamerican nephropathy, have been noted among male workers in Central America, especially in the sugarcane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long working hours of long pieces at an average high temperature of about 36 ° C (96 ° F) is suspected, as are agricultural chemicals and other factors. In Sri Lanka, another unknown CKD epidemic has become a serious public health problem.

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Society and culture

In the US, the National Kidney Foundation is a national organization that represents patients and professionals who treat kidney disease. The American Kidney Fund is a national non-profit organization that provides care-related financial support to one out of every five dialysis patients each year. The Renal Support Network is a non-profit, focused patient organization, managed by patients who provide non-medical services to those affected by CKD. The American Association of Kidney Patients is a non-profit, patient-centric group that focuses on improving the health and wellbeing of CKD patients and dialysis. The Renal Physicians Association is an association representing nephrology professionals.

In the UK, the British National Kidney Federation and the British Kidney Patient Association (BKPA) represent patients, and the Renal Association represents the kidney doctors and works closely with the National Service Framework for Kidney Disease. Australian Kidney Health serves the country.

The International Society of Nephrology is an international body representing specialist kidney disease.

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Other animals

The total CKD rate in dogs is 16 cases per 10,000 years. The CKD mortality rate is 10 deaths per 10,000. The breed with the highest level is the Bernese mountain dog, the miniature schnauzer and the boxer. Swedish Elkhound, Siberian husky, and Finnish spitz are the lowest-priced breeds.

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Research

Currently, several compounds are under development for CKD treatment. These include angiotensin receptor blockers (ARB) olmesartan medoxomil and sulodexide, low molecular weight heparin mixtures and sulfate dermatan.

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References

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External links

• Dialysis Complications of Chronic Kidney Failure in eMedicine
• Chronic Kidney Failure Information from Great Ormond Street Hospital

Source of the article : Wikipedia