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CHRONIC RENAL FAILURE
Chronic renal failure (English: chronic kidney disease, CKD) is a process of damage to the kidney with a span of more than 3 months. CKD can lead to glomerular filtration rate simtoma be under 60 mL/men/1.73 m2, or above that value, but is accompanied by abnormalities of urine sediment. The presence of kidney stones can also be indicative of CKD in patients with congenital abnormalities such as hiperoksaluria and sistinuria.
The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and having poor appetite. Often, chronic kidney disease was diagnosed as a result of screening (drug) / screening of people known to be at risk of kidney problems, such as those with hypertension / high blood pressure or diabetes and those who have blood relations with chronic kidney disease. Chronic kidney disease can also be identified when it leads to one of the recognized complications, such as cardiovascular disease, anemia or pericarditis.
Chronic kidney disease is identified by a blood test for creatinine. The high levels of creatinine indicate falling glomerular filtration rate and as a result of reduced renal ability to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and these conditions are found when the urine (urine sample testing) showed that the kidney is the possible loss of proteins or red blood cells into the urine. To investigate the causes of kidney damage, various forms of medical imaging, blood tests and frequent renal biopsy (removing a small sample of kidney tissue) is working to find out whether there is a cause reversible kidney damage. the latest professional guidelines classify the severity of chronic kidney disease in five phases, with phase one of the most mild and usually cause few symptoms and stage 5 being a severe disease with a poor life expectancy if untreated. 'Final stage renal disease (ESRD)', Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated term chronic renal failure (CKF) or chronic renal failure (CRF).
There is no specific treatment to slow the firm showed worsening of chronic kidney disease. If there is an underlying cause for CKD, such as vasculitis, can be treated directly with treatments aimed to slow the damage. In more advanced stages, treatment may be required for anemia and bone disease. Severe CKD requires one form of renal replacement therapy, it may be a form of dialysis, but ideally a kidney transplant.
Signs and symptoms
CKD initially without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As kidney function decreases:
• increased blood pressure due to fluid overload and production of vasoactive hormones created by the kidneys through the RAS (renin-angiotensin system), increases one's risk of developing hypertension and / or suffering from congestive heart failure.
• Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Urea is excreted by the sweat and crystallize on the skin ("uremic frost").
• Potassium accumulates in the blood (known as hyperkalemia with a variety of symptoms including malaise and potentially fatal cardiac arrhythmias).
• Erythropoietin synthesis decreased (potentially leading to anemia, which causes fatigue).
• Fluid volume overload - symptoms can range from mild edema to life-threatening pulmonary edema.
• hyperphosphatemia - due to reduced phosphate excretion, is associated with hypocalcemia (since 1.25 hydroxyvitamin D deficiency), which is due to stimulation of fibroblast growth factor -23 -
• Metabolic acidosis, due to the accumulation of sulfate, phosphate, uric acid, etc. This can lead to altered enzyme activity by excess acid acting on the enzyme and also increased the membrane excitability of the heart and nerves with the promotion of hyperkalemia due to excess acid (acidemia).
People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients suffering from chronic kidney disease and cardiovascular disease tend to have worse prognosis than those who suffer only from the latter.
Cause
The most common causes of CKD diabetes mellitus, hypertension, and glomerulonephritis. Together, causing about. 75% of all adult cases. Certain geographical areas have a high incidence of HIV nephropathy.
Historically, renal disease was classified according to the anatomy of the kidneys are involved, namely:
• Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic uremic syndrome and vasculitis.
• glomerulus, consists of a diverse group and subclassified into:
o The primary glomerular diseases such as focal segmental glomerulosclerosis and IgA nephritis.
o secondary glomerular diseases such as diabetic nephropathy and lupus nephritis.
• Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy.
• Obstructive such as with bilateral kidney stones and diseases of the prostate.
• In rare cases, pin worms infect the kidneys can also cause nephropathy.
Diagnosis
In many patients with CKD, previous renal disease or other underlying disease was unknown. A small number present with CKD of unknown cause. In these patients, causing sometimes identified retrospectively.
It is important to distinguish CKD from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound, in which the kidney size is measured, is generally performed. Kidneys with CKD is usually small (<9 cm) of normal kidneys, with exceptions such as in diabetic nephropathy and polycystic kidney disease. Other diagnostic clues that help distinguish CKD from ARF is the gradual rise in serum creatinine (more than a few months or years) as opposed to a sudden increase in serum creatinine (several days to weeks). If this level is not available (because the patient had been well and had no blood test), it is sometimes necessary to treat patients briefly as having ARF until it has been established that irreversible renal impairment.
Additional tests may include nuclear medicine MAG3 scan to confirm the blood stream and form a differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA are used chelated with the radioactive element Technetium-99.
In chronic renal failure treated with standard dialysis, uremic toxins accumulate a lot. These toxins show various cytotoxic activities in serum, has a different molecular weight and some of them are bound to other proteins, mainly to albumin. Toxic substances such as proteins bound to receive the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.
Stages
All individuals with a glomerular filtration rate (GFR) <60 mL/min/1.73 m 2 for 3 months were classified as having chronic kidney disease, regardless of the presence or absence of kidney damage. The reason for including the people are that kidney function declines to a lower level or a loss of half or more adult level of normal kidney function, which may be associated with a number of complications.
All individuals with kidney damage are classified as having chronic kidney disease, regardless of level of GFR. The reason for including individuals with GFR> 60 mL/min/1.73 m 2 is that GFR can be maintained at normal or increased levels despite substantial kidney damage and that patients with renal impairment are at increased risk of two major results from chronic kidney disease: loss of renal function and progression of cardiovascular disease.
The loss of protein in the urine is considered as an independent marker for worsening renal function and cardiovascular disease.
Phase 1
Slightly reduced function, kidney damage with normal or relatively high GFR (≥ 90 mL/min/1.73 m 2. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
Phase 2
Mild reduction in GFR (60-89 mL/min/1.73 m 2. With kidney damage, kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
Stage 3
Moderate decrease in GFR (30-59 mL/min/1.73 m 2. (Screening and Referral)
Stage 4
Severe decrease in GFR (15-29 mL/min/1.73 m 2. Preparation for renal replacement therapy.
Stage 5
Established renal failure (GFR <15 mL/min/1.73 m 2. Permanent renal replacement therapy (RRT).
Screening and Referral
Early identification of patients with kidney disease is recommended, as the action may be instituted to slow the progression and reduce cardiovascular risk. Among those who should be screened is a subject with hypertension or a history of cardiovascular disease, people with diabetes or marked obesity, those aged> 60 years, subjects with indigenous (native American Indians, First Nations) racial origin, people with a history of kidney disease in the past, as well as subjects who have relatives who have kidney disease requiring dialysis. Screening should include calculations GFR/1.73 m 2 estimated from serum creatinine levels, and measurement of urine albumin-to-creatinine ratio in first morning urine specimen and the screen for hematuria dipstick. Guidelines for nephrologist referral vary between different countries. Nephrology referral is useful when eGFR/1.73m 2 is less than 30 or decreased by more than 3 ml / min / year, when the urine albumin-to-creatinine ratio of more than 300 mg / g, when blood pressure is difficult to control, or when hematuria or other findings indicate either disorder or disease, especially glomerular secondary agrees to special treatment. Another benefit of early nephrology referral including appropriate patient education regarding options for renal replacement therapy as well as pre-emptive transplantation, and examination results on time and placement of arteriovenous fistulas in hemodialysis patients choose for the future.
Treatment
The goal of therapy is to slow or stop the progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, is the broad principles of management. Generally, angiotensin converting enzyme inhibitor s (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, because they have been found to slow the progression of CKD to stage 5. Although the use of ACE inhibitors and ARBs is the current standard of care for patients with CKD, patients are increasingly losing kidney function while on these medications, as seen in and renal studies, which reported a decrease from time to time glomerular filtration rate in patients treated by conventional methods.
Currently, several compounds in development for CKD. These include, but are not limited to, bardoxolone methyl, olmesartan medoxomil, sulodexide, and avosentan.
Replacement of erythropoietin and calcitriol, two hormones are processed by the kidneys, often necessary in patients with advanced CKD. Phosphate binders are also used to control serum phosphate levels, which are usually elevated in advanced chronic kidney disease.
When a person reaches stage 5 CKD, renal replacement therapy is necessary, in the form of either dialysis or transplant.
Normalization of hemoglobin has not been found to be of any benefit.
People with CKD are at real risk of cardiovascular disease, and often have other risk factors for heart disease, such as hyperlipidemia. The most common cause of death in people with CKD due to cardiovascular disease than kidney failure. Aggressive treatment of hyperlipidemia is justified.
Prognosis
Prognosis of patients with chronic kidney disease guarded as epidemiological data has shown that the cause of all deaths. (The overall death rate) increases as renal function decline. The main causes of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.
While renal replacement therapy patients can maintain indefinitely and prolong life, quality of life is greatly affected kidney transplantation improves survival of patients with stage 5 CKD significantly when compared with the treatment of choice. However, it is associated with increased short-term mortality (due to complications from surgery). Besides transplantation, high-intensity home hemodialysis appears associated with improved survival and quality of life is greater, when compared with conventional thrice weekly hemodialysis and peritoneal dialysis.
Organization
In the United States, the National Kidney Foundation is a national organization representing patients and the professionals who treat kidney disease. The American Kidney Fund (AKF) is a national nonprofit organization that provides financial aid-related treatment to 1 of every 5 dialysis patients each year. The Renal Support Network (RSN) is a nonprofit that focuses on the patient, the patient run organization that provides non-medical services for those affected by CKD. The American Association of Kidney Patients (AAKP) is a non-profit, patient-centric group focused on improving the health and well-being of CKD and dialysis patients. The Renal Physicians Association (RPA) is a professional association representing nephrology.
In the United Kingdom, the UK National Kidney Federation represents the patient, and kidneys Association represents renal physicians and works closely with the National Service Framework for renal disease.
The International Society of Nephrology is an international body representing the specialist in kidney disease.
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