Sunday, 28 May 2017

RICKETTSIAE


RICKETTSIAE DISEASES


INFECTIOUS AGENTS


Rickettsial infections are caused by a variety of bacteria from the genera Rickettsia, Orientia, Ehrlichia, Neorickettsia, Neoehrlichia, and Anaplasma (Table 3-18). Rickettsia spp. are classically divided into the typhus group and spotted fever group (SFG). Orientia spp. make up the scrub typhus group. The rickettsial pathogens most likely to be encountered during travel outside the United States include R. africae (African tick-bite fever), R. conorii (Mediterranean spotted fever), R. rickettsii (known as both Rocky Mountain spotted fever and Brazilian spotted fever), O. tsutsugamushi (scrub typhus), and R. typhi (murine typhus).

TRANSMISSION

Most rickettsial pathogens are transmitted by ectoparasites such as fleas, lice, mites, and ticks. Organisms can be transmitted by bites from these ectoparasites or by the inoculation of infectious fluids or feces from the ectoparasites into the skin. Inhaling or inoculating conjunctiva with infectious material may also cause infection for some of these organisms. The specific vectors that transmit each form of rickettsiae are listed in Table 3-18. Transmission of some rickettsial diseases after transfusion or organ transplantation is rare but has been reported.

EPIDEMIOLOGY

All age groups are at risk for rickettsial infections during travel to endemic areas. Both short and long-term travelers are at risk for infection. Transmission is increased during outdoor activities in the spring and summer months when ticks and fleas are most active. However, infection can occur throughout the year. Because of the 5- to 14-day incubation period for most rickettsial diseases, tourists may not necessarily experience symptoms during their trip, and onset may coincide with their return home or develop within a week after returning. Although the most commonly diagnosed rickettsial diseases in travelers are usually in the spotted fever or typhus groups, travelers may acquire a wide range of rickettsioses, including emerging and newly recognized species (Table 3-18).
Tickborne spotted fever rickettsioses are the most frequently reported travel-associated rickettsial infections. Game hunting and traveling to southern Africa from November through April are risk factors for African tick-bite fever, and this consistently remains the most commonly reported rickettsial infection acquired during travel. Mediterranean spotted fever infections are less commonly reported but occur over an even larger region, including (but not limited to) much of Europe, Africa, India, and the Middle East. Rocky Mountain spotted fever (also known as Brazilian spotted fever, as well as other local names) is reported throughout much of the Western Hemisphere, including Canada, the United States, Mexico, and various countries in Central and South America. Contact with dogs (in both rural and urban settings) and outdoor activities such as hiking, hunting, fishing, and camping increase the risk of infection.
Scrub typhus, which is transmitted by mites encountered in high grass and brush, is endemic in northern Japan, Southeast Asia, the western Pacific Islands, eastern Australia, China, maritime areas and several parts of south-central Russia, India, and Sri Lanka. More than 1 million cases occur annually. Most travel-acquired cases of scrub typhus occur during visits to rural areas in endemic countries for activities such as camping, hiking, or rafting, but urban cases have also been described.
R. typhi and R. felis, which are transmitted by fleas, are widely distributed, especially throughout the tropics and subtropics and in port cities and coastal regions with rodents. Humans exposed to flea-infested cats, dogs, and peridomestic animals while traveling in endemic regions, or who enter or sleep in areas infested with rodents, are at most risk for fleaborne rickettsioses. Murine typhus has been reported among travelers returning from Asia, Africa, and the Mediterranean Basin and has also been reported from Hawaii, California, and Texas in the United States.
R. akari, the causative agent of rickettsialpox, is transmitted by house-mouse mites, and circulates in mainly urban centers in Ukraine, South Africa, Korea, the Balkan states, and the United States. Outbreaks of rickettsialpox most often occur after contact with infected rodents and their mites, especially during natural die-offs or exterminations of infected rodents that cause the mites to seek out new hosts, including humans. The agent may spill over and occasionally be found in other wild rodent populations.
Epidemic typhus is rarely reported among tourists but can occur in communities and refugee populations where body lice are prevalent. Outbreaks often occur during the colder months when infested clothing is not laundered. Travelers at most risk for epidemic typhus include those who may work with or visit areas with large homeless populations, impoverished areas, refugee camps, and regions that have recently experienced war or natural disasters. Active foci of epidemic typhus are known in the Andes regions of South America and some parts of Africa (including but not limited to Burundi, Ethiopia, and Rwanda). Louseborne epidemic typhus does not regularly occur in the United States, but a zoonotic reservoir occurs in the southern flying squirrel, and sporadic sylvatic epidemic typhus cases are reported. Tick-associated reservoirs of R. prowazekii have been described in Ethiopia, Mexico, and Brazil, but documented human cases are rare.
Ehrlichiosis and anaplasmosis are tickborne infections most commonly reported in the United States. A variety of species are implicated in infection, but E. chaffeensis and A. phagocytophilum are most common. Infections with various Ehrlichia and Anaplasma spp. have also been reported in Europe, Asia, and South America. Neoehrlichia mikurensis is a tickborne pathogen that occurs in Europe and Asia. Sennetsu fever, caused by Neorickettsia sennetsu, occurs in Japan, Malaysia, and possibly other parts of Asia. This disease can be contracted from eating raw infected fish.

CLINICAL PRESENTATION

Rickettsioses are difficult to diagnose, even by health care providers experienced with these diseases. Most symptomatic rickettsial diseases cause moderate illness, but some Rocky Mountain and Brazilian spotted fevers, Mediterranean spotted fever, scrub typhus, and epidemic typhus may be fatal in 20%–60% of untreated cases, so prompt treatment is essential.
Clinical presentations vary with the causative agent and patient; however, common symptoms that typically develop within 1–2 weeks of infection include fever, headache, malaise, rash, nausea, and vomiting. Many rickettsioses are accompanied by a maculopapular, vesicular, or petechial rash or sometimes an eschar at the site of the tick bite. African tick-bite fever is typically milder than some other rickettsioses, but recovery is improved with treatment. It should be suspected in a patient who presents with fever, headache, myalgia, and an eschar (tache noir) after recent travel to southern Africa. Mediterranean spotted fever is a potentially life-threatening rickettsial infection and should be suspected in patients with rash, fever, and eschar after recent travel to northern Africa or the Mediterranean. Rocky Mountain and Brazilian spotted fever are characterized by fever, headache, nausea, abdominal pain, and cough; a rash is commonly reported, but eschars are not. Scrub typhus should be suspected in patients with a fever, headache, and myalgia after recent travel to Asia; eschar, lymphadenopathy, cough, and encephalitis may be present. Patients with murine or epidemic typhus usually present with a severe but nonspecific febrile illness, and approximately half will also present with a rash. Ehrlichiosis and anaplasmosis should be suspected in febrile patients with leukopenia with an exposure history.

DIAGNOSIS

Diagnosis is usually based on clinical recognition and serology; the latter requires comparison of acute- to convalescent-phase serology, so is only helpful in retrospect. Etiologic agents can generally only be identified to the genus level by serologic testing. PCR and immunohistochemical analyses may also be helpful. If ehrlichiosis or anaplasmosis is suspected, a buffy coat may be examined to identify characteristic intraleukocytic morulae. Contact the CDC Rickettsial Zoonoses Branch at 404-639-1075 for further information.


TREATMENT

Treatment of patients with possible rickettsioses should be started early and should never await confirmatory testing, which may take weeks when serology is used. Immediate empiric treatment with a tetracycline is recommended, most commonly doxycycline. Broad-spectrum antibiotics are not usually helpful. Chloramphenicol may be an alternative in some cases, but its use is associated with more deaths, particularly for R. rickettsii. Expert advice should be sought if alternative agents are being considered.


PREVENTION

No vaccine is available for preventing rickettsial infections. Antibiotics are not recommended for prophylaxis of rickettsial diseases.


Travelers should be instructed to minimize exposure to infectious arthropods during travel (including lice, fleas, ticks, mites) and animal reservoirs (particularly dogs) when traveling in endemic areas. The proper use of insect or tick repellents, self-examination after visits to vector-infested areas, and wearing protective clothing are ways to reduce risk. These precautions are especially important for people with underlying conditions that may compromise their immune systems, as these people may be more susceptible to severe disease. For more detailed information, Fallow reference below .......... 

BIBLIOGRAPHY

  1. Angelakis E, Botelho E, Socolovschi C, Sobas CR, Piketty C, Parola P, et al. Murine typhus as a cause of fever in travelers from Tunisia and Mediterranean areas. J Travel Med. 2010 Sep–Oct;17(5):310–5.
  2. Demeester R, Claus M, Hildebrand M, Vlieghe E, Bottieau E. Diversity of life-threatening complications due to Mediterranean spotted fever in returning travelers. J Travel Med. 2010 Mar–Apr;17(2):100–4.
  3. Dobler G, Wolfel R. Typhus and other rickettsioses: emerging infections in Germany. Dtsch Arztebl Int. 2009 May;106(20):348–54.
  4. Hendershot EF, Sexton DJ. Scrub typhus and rickettsial diseases in international travelers: a review. Curr Infect Dis Rep. 2009 Jan;11(1):66–72.
  5. Jensenius M, Davis X, von Sonnenburg F, Schwartz E, Keystone JS, Leder K, et al. Multicenter GeoSentinel analysis of rickettsial diseases in international travelers, 1996–2008. Emerg Infect Dis. 2009 Nov;15(11):1791–8.
  6. Leshem E, Meltzer E, Schwartz E. Travel-associated zoonotic bacterial diseases. Curr Opin Infect Dis. 2011 Oct;24(5):457–63.
  7. Nachega JB, Bottieau E, Zech F, Van Gompel A. Travel-acquired scrub typhus: emphasis on the differential diagnosis, treatment, and prevention strategies. J Travel Med. 2007 Sep–Oct;14(5):352–5.
  8. Raoult D, Parola P, editors. Rickettsial Diseases. New York: Informa Healthcare USA, Inc; 2007.
  9. Rar V, Golovljova I. Anaplasma, Ehrlichia, and “Candidatus Neoehrlichia” bacteria: pathogenicity, biodiversity, and molecular genetic characteristics, a review. Infect Genet Evol. 2011 Dec;11(8):1842–61.
  10. Roch N, Epaulard O, Pelloux I, Pavese P, Brion JP, Raoult D, et al. African tick bite fever in elderly patients: 8 cases in French tourists returning from South Africa. Clin Infect Dis. 2008 Aug 1;47(3):e28–35.

Thursday, 25 May 2017

CHRONIC KIDNEY DISEASE


CHRONIC KIDNEY DISEASE


What Is Chronic Kidney Disease?

Normal kidneys and kidney function
  • The kidneys are a pair of bean-shaped organs that lie on either side of the spine in the lower middle of the back.
  • Each kidney weighs about 5 ounces and contains approximately one million filtering units called nephrons.
  • Each nephron is made of a glomerulus and a tubule. The glomerulus is a miniature filtering or sieving device while the tubule is a tiny tube like structure attached to the glomerulus.
  • The kidneys are connected to the urinary bladder by tubes called ureters. Urine is stored in the urinary bladder until the bladder is emptied by urinating. The bladder is connected to the outside of the body by another tube like structure called the urethra.
Illustration of the kidneys, urinary tract, and bladder.
Illustration of the kidneys, urinary tract, and bladder.
The main function of the kidneys is to remove waste products and excess water from the blood. The kidneys process about 200 liters of blood every day and produce about 2 liters of urine. The waste products are generated from normal metabolic processes including the breakdown of active tissues, ingested foods, and other substances. The kidneys allow consumption of a variety of foods, drugs, vitaminsdietary and herbal supplements, food additives, and excess fluids without worry that toxic by-products will build up to harmful levels. The kidney also plays a major role in regulating levels of various minerals such as calcium, sodium, and potassium in the blood.
  • As the first step in filtration, blood is delivered into the glomeruli by microscopic leaky blood vessels called capillaries. Here, blood is filtered of waste products and fluid while red blood cells, proteins, and large molecules are retained in the capillaries. In addition to wastes, some useful substances are also filtered out. The filtrate collects in a sac called Bowman's capsule.
  • The tubules are the next step in the filtration process. The tubules are lined with highly functional cells which process the filtrate, reabsorbing water and chemicals useful to the body while secreting some additional waste products into the tubule.
The kidneys also produce certain hormones that have important functions in the body, including the following:
  • Active form of vitamin D (calcitriol or 1,25 dihydroxy-vitamin D), which regulates absorption of calcium and phosphorus from foods, promoting formation of strong bone.
  • Erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells.
  • Renin, which regulates blood volume and blood pressure in association with aldosterone manufactred in the adrenal glands, located just above the kidneys. Continue Reading
Illustration of kidney and surrounding anatomy.
Illustration of kidney and surrounding anatomy.


Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function over time. This happens gradually, usually over months to years. Chronic kidney disease is divided into five stages of increasing severity (see Table 1 below). The term "renal" refers to the kidney, so another name for kidney failure is "renal failure." Mild kidney disease is often called renal insufficiency.
With loss of kidney function, there is an accumulation of water, waste, and toxic substances in the body that are normally excreted by the kidney. Loss of kidney function also causes other problems such as anemiahigh blood pressure, acidosis (excessive acidity of body fluids), disorders of cholesterol and fatty acids, and bone disease.
Stage 5 chronic kidney disease is also referred to as kidney failure, end-stage kidney disease, or end-stage renal disease, wherein there is total or near-total loss of kidney function. There is dangerous accumulation of water, waste, and toxic substances, and most individuals in this stage of kidney disease need dialysis or transplantation to stay alive.
Unlike chronic kidney disease, acute kidney failure develops rapidly, over days or weeks.
  • Acute kidney failure usually develops in response to a disorder that directly affects the kidney, its blood supply, or urine flow from it.
  • Acute kidney failure is often reversible, with complete recovery of kidney function.
  • Some patients are left with residual damage and can have a progressive decline in kidney function in the future.
  • On occasion, patients who have acute kidney failure do not recover and irreversible kidney damage requires dialysis. Continue Reading
Table 1. Stages of Chronic Kidney Disease
StageDescriptionGFR*
mL/min/1.73 m2
*GFR is glomerular filtration rate, a measure of the kidney's function.
1Slight kidney damage with normal or increased filtrationMore than 90
2Mild decrease in kidney function60 to 89
3Moderate decrease in kidney function30 to 59
4Severe decrease in kidney function15 to 29
5Kidney failureLess than 15 (or dialysis)
Although chronic kidney disease sometimes results from primary diseases of the kidneys themselves, the major causes are diabetes and high blood pressure.
  • Type 1 and type 2 diabetes mellitus cause a condition called diabetic nephropathy, which is the leading cause of kidney disease in the United States.
  • High blood pressure(hypertension), if not controlled, can damage the kidneys over time.
  • Glomerulonephritis is the inflammation and damage of the filtration system of the kidneys, which can cause kidney failure. Postinfectious conditions and lupus are among the many causes of glomerulonephritis.
  • Polycystic kidney disease is a hereditary cause of chronic kidney disease wherein both kidneys have multiple cysts.
  • Use of analgesics such as acetaminophen (Tylenol) and ibuprofen (Motrin, Advil), and naproxen (Naprosyn, Aleve) regularly over long durations of time can cause analgesic nephropathy, another cause of kidney disease. Certain other medications can also damage the kidneys.
  • Clogging and hardening of the arteries (atherosclerosis) leading to the kidneys causes a condition called ischemic nephropathy, which is another cause of progressive kidney damage.
  • Obstruction of the flow of urine by stones, an enlarged prostate, strictures (narrowings), or cancers may also cause kidney disease.
  • Other causes of chronic kidney disease include HIV infection, sickle cell diseaseheroin abuse, amyloidosis, kidney stones, chronic kidney infections, and certain cancers.
If one has any of the following conditions, they are at higher-than-normal risk of developing chronic kidney disease. One's kidney function may need to be monitored regularly.

How Common Is Chronic Kidney Disease (CKD)?

  • Chronic kidney disease affects 14% of the US population.
  • 17,600 kidney transplants occured in the US in 2013; one-third came from living donors.
  • Kidney disease is more common among Hispanic, African American, Asian or Pacific Islander, and Native American people.
  • Older age, female gender, diabeteshypertension, higher body mass index (obesity), and cardiovascular disease are associated with a higher incidence of chronic kidney disease. 

Chronic Kidney Disease Symptoms and When to Seek Medical Care

The kidneys are remarkable in their ability to compensate for problems in their function. That is why chronic kidney disease may progress without symptoms for a long time until only very minimal kidney function is left.
Because the kidneys perform so many functions for the body, kidney disease can affect the body in a large number of different ways. Symptoms vary greatly. Several different body systems may be affected. Notably, most patients have no decrease in urine output even with very advanced chronic kidney disease.
Signs and symptoms of chronic kidney disease include:

  • need to urinate frequently, especially at night (nocturia);
  • swelling of the legs and puffiness around the eyes (fluid retention);
  • high blood pressure;
  • fatigue and weakness (from anemia or accumulation of waste products in the body);
  • loss of appetite, nausea and vomiting;
  • itching, easy bruising, and pale skin (from anemia);
  • shortness of breath from fluid accumulation in the lungs;
  • headaches, numbness in the feet or hands (peripheral neuropathy), disturbed sleep, altered mental status (encephalopathy from the accumulation of waste products or uremic poisons), and restless legs syndrome;
  • chest pain due to pericarditis (inflammation around the heart);
  • bleeding (due to poor blood clotting);
  • bone pain and fractures; and
  • decreased sexual interest and erectile dysfunction.

When to Seek Emergency Treatment for Chronic Kidney Disease
Several signs and symptoms may suggest complications of chronic kidney disease. One should call a health care professional if they notice any of the following symptoms:
  • change in energy level or strength;
  • increased water retention (puffiness or swelling) in the legs, around the eyes, or in other parts of the body;
  • shortness of breath or change from normal breathing;
  • nausea or vomiting;
  • lightheadedness;
  • bone or joint pain;
  • easy bruising; or
  • itching.
If a woman has known kidney problems, she should see a health care professional right away if she knows or suspects that she is pregnant.
See a health care practitioner as recommended for monitoring and treatment of chronic conditions such as diabetes, high blood pressure, and high cholesterol.
The following signs and symptoms represent the possibility of a severe complication of chronic kidney disease and warrant a visit to the nearest hospital emergency department.
  • Change in level of consciousness -- extreme sleepiness or difficult to awaken
  • Severe fatigue
  • Chest pain
  • Difficulty breathing
  • Severe nausea and vomiting
  • Severe bleeding (from any source)
  • Muscle weakness 

Chronic Kidney Disease Diagnosis


Chronic kidney disease usually causes no symptoms in its early stages. Only lab tests can detect any developing problems. Anyone at increased risk for chronic kidney disease should be routinely tested for development of this disease.
  • Urine, blood, and imaging tests (X-rays) are used to detect kidney disease, as well as to follow its progress.
  • All of these tests have limitations. They are often used together to develop a picture of the nature and extent of the kidney disease.
  • In general, this testing can be performed on an outpatient basis.
Urine tests
Urinalysis: Analysis of the urine affords enormous insight into the function of the kidneys. The first step in urinalysis is doing a dipstick test. The dipstick has reagents that check the urine for the presence of various normal and abnormal constituents including protein. Then, the urine is examined under a microscope to look for red and white blood cells, and the presence of casts and crystals (solids).
Only minimal quantities of albumin (protein) are present in urine normally. A positive result on a dipstick test for protein is abnormal. More sensitive than a dipstick test for protein is a laboratory estimation of the urine albumin (protein) and creatinine in the urine. The ratio of albumin (protein) and creatinine in the urine provides a good estimate of albumin (protein) excretion per day.
Twenty-four hour urine tests: This test requires the patient to collect all of their urine for 24 consecutive hours. The urine may be analyzed for protein and waste products (urea nitrogen, and creatinine). The presence of protein in the urine indicates kidney damage. The amount of creatinine and urea excreted in the urine can be used to calculate the level of kidney function and the glomerular filtration rate (GFR).
Glomerular filtration rate (GFR): The GFR is a standard means of expressing overall kidney function. As kidney disease progresses, GFR falls. The normal GFR is about 100 to 140 mL/min in men and 85 to 115 mL/min in women. It decreases in most people with age. The GFR may be calculated from the amount of waste products in the 24-hour urine or by using special markers administered intravenously. An estimation of the GFR (eGFR) can be calculated from the patient's routine blood tests. It is not as accurate in patients younger than 18, pregnant patients, and those who are very muscular or who are very overweight. Patients are divided into five stages of chronic kidney disease based on their GFR (see Table 1 above).
Blood tests
Creatinine and urea (BUN) in the blood: Blood urea nitrogen and serum creatinine are the most commonly used blood tests to screen for and monitor renal disease. Creatinine is a product of normal muscle breakdown. Urea is the waste product of breakdown of protein. The level of these substances rises in the blood as kidney function worsens.
Estimated GFR (eGFR): The laboratory or physician may calculate an estimated GFR using the information from a patient's blood work. It is not as accurate in patients younger than 18, pregnant patients, and those who are very muscular and those who are very overweight. It is important to be aware of one's estimated GFR and stage of chronic kidney disease. The physician uses the patient's stage of kidney disease to recommend additional testing and provide suggestions on management.
Electrolyte levels and acid-base balance: Kidney dysfunction causes imbalances in electrolytes, especially potassium, phosphorus, and calcium. High potassium (hyperkalemia) is a particular concern. The acid-base balance of the blood is usually disrupted as well.
Decreased production of the active form of vitamin D can cause low levels of calcium in the blood. Inability of failing kidneys to excrete phosphorus causes its levels in the blood to rise. Testicular or ovarian hormone levels may also be abnormal.
Blood cell counts: Because kidney disease disrupts blood cell production and shortens the survival of red cells, the red blood cell count and hemoglobin may be low (anemia). Some patients may also have iron deficiency due to blood loss in their gastrointestinal system. Other nutritional deficiencies may also impair the production of red cells.
Other tests
Ultrasound: Ultrasound is often used in the diagnosis of kidney disease. An ultrasound is a noninvasive type of imaging test. In general, kidneys are shrunken in size in chronic kidney disease, although they may be normal or even large in size in cases caused by adult polycystic kidney disease, diabetic nephropathy, and amyloidosis. Ultrasound may also be used to diagnose the presence of urinary obstruction, kidney stones and also to assess the blood flow into the kidneys.
Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in cases in which the cause of the kidney disease is unclear. Usually, a biopsy can be collected with local anesthesia by introducing a needle through the skin into the kidney. This is usually done as an outpatient procedure, though some institutions may require an overnight hospital stay.

Chronic Kidney Disease Self-Care at Home

Chronic kidney disease is a disease that must be managed in close consultation with a health care practitioner. Self-treatment is not appropriate.
  • There are, however, several important dietary rules one can follow to help slow the progression of kidney disease and decrease the likelihood of complications.
  • This is a complex process and must be individualized, generally with the help of a health care practitioner and a registered dietitian.
The following are general dietary guidelines:
  • Protein restriction: Decreasing protein intake may slow the progression of chronic kidney disease. A dietitian can help one determine the appropriate amount of protein.
  • Salt restriction: Limit to 2 to 4grams a day to avoid fluid retention and help control high blood pressure.
  • Fluid intake: Excessive water intake does not help prevent kidney disease. In fact, the doctor may recommend restriction of water intake.
  • Potassium restriction: This is necessary in advanced kidney disease because the kidneys are unable to remove potassium. High levels of potassium can cause abnormal heart rhythms. Examples of foods high in potassium include bananas, oranges, nuts, avocados, and potatoes.
  • Phosphorus restriction: Decreasing phosphorus intake is recommended to protect bones. Eggs, beans, cola drinks, and dairy products are examples of foods high in phosphorus.
Other important measures that a patient can take include:
  • carefully follow prescribed regimens to control blood pressure and/or diabetes;
  • stop smoking; and
  • lose excess weight.
In chronic kidney disease, several medications can be toxic to the kidneys and may need to be avoided or given in adjusted doses. Among over-the-counter medications, the following need to be avoided or used with caution:
  • Certain analgesics: Aspirin; nonsteroidal antiinflammatory drugs (NSAIDs, such as ibuprofen [Motrin, Advil])
  • Fleets or Phospho-Soda enemas because of their high content of phosphorus
  • Laxatives and antacids containing magnesium and aluminum such as magnesium hydroxide (Milk of Magnesia) and magnesium and aluminum hydroxide (Mylanta)
  • Ulcer medication H2-receptor antagonists: cimetidine (Tagamet) and ranitidine (Zantac) (decreased dosage with kidney disease)
  • Decongestants such as pseudoephedrine (Sudafed) and phenylpropanolamine (Rhindecon) especially if the patient has high blood pressure
  • Alka Seltzer, since this contains large amounts of sodium
  • Herbal medications and dietary supplements, unless they have been reviewed by the health care professional and/or pharmacist
  • Some medications, including antibiotics and anticoagulants (blood thinners), may require a dosage adjustment in patients who have chronic kidney disease.
If a patient has a condition such as diabetes, high blood pressure, or high cholesterol underlying chronic kidney disease, they should take all medications as directed and see their health care practitioner as recommended for follow-up and monitoring.

Chronic Kidney Disease Treatment

There is no cure for chronic kidney disease. The four goals of therapy are to:
  1. slow the progression of disease;
  2. treat underlying causes and contributing factors;
  3. treat complications of disease; and
  4. replace lost kidney function.
Strategies for slowing progression and treating conditions underlying chronic kidney disease include the following:
  • Control of blood glucose: Maintaining good control of diabetes is critical. People with diabetes who do not control their blood glucose have a much higher risk of all complications of diabetes, including chronic kidney disease.
  • Control of high blood pressure: This also slows progression of chronic kidney disease. It is recommended to keep blood pressure below 130/80 mm Hg if one has kidney disease. It is often useful to monitor blood pressure at home. Blood pressure medications known as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) have special benefit in protecting the kidneys.
  • Diet: Diet control is essential to slowing progression of chronic kidney disease and should be done in close consultation with a health care practitioner and a dietitian. For some general guidelines, see the Chronic Kidney Disease Self-Care at Home section of this article.
The complications of chronic kidney disease may require medical treatment.
  • Fluid retention is common in kidney disease and manifests with swelling. In late phases, fluid may build up in the lungs and cause shortness of breath.
  • Anemia is common with CKD. The two most common causes of anemia with kidney disease are iron deficiency and the lack of erythropoietin. If one is anemic, the doctor will run tests to determine if the anemia is secondary to kidney disease or due to alternative causes.
  • Bone disease develops in patients with kidney disease. The kidneys are responsible for excreting phosphorus from the body and processing Vitamin D into its active form. High phosphorus levels and lack of vitamin D cause blood levels of calcium to decrease, causing activation of the parathyroid hormone (PTH). These and several complex changes cause the development of metabolic bone disease. Treatment of metabolic bone disease is aimed at managing serum levels of calcium, phosphorus, and parathyroid hormone.
  • Metabolic acidosis may develop with kidney disease. The acidosis may cause breakdown of proteins, inflammation, and bone disease. If the acidosis is significant, the doctor may use drugs such as sodium bicarbonate (baking soda) to correct the problem.

Chronic Kidney Disease Medications


Common adverse drug reactions include hypotension (low blood pressure), cough, hyperkalemia (high potassium), headachedizziness, fatigue, nausea, skin rash and a metallic taste. In some patients, the medication may cause a further decline in kidney function. Rarely, patients may develop angioedema, which is swelling of the subcutaneous and submucosal tissue and may lead to difficulty in breathing. This may be a life-threatening condition and needs immediate medical attention.

Common adverse drug reactions include dizziness, headache, and hyperkalemia. Other side effects include hypotension, rash, diarrheadyspepsia, abnormal liver functionmuscle cramps, myalgia, back paininsomnia, anemia, and worsening of kidney function. Instances of angioedema are also reported with ARBs.

Common adverse effects include frequent urinationdehydration, muscle cramps, weakness, heart rhythm abnormalities, electrolyte abnormalities, lightheadedness, and allergic reactions. Diuretics may also cause a decline in kidney function especially if fluid is removed rapidly from the body.
  • Angiotensin converting enzyme inhibitors (ACE-Is): ACE-Is are drugs commonly used in the treatment of hypertension. Some examples of these drugs include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril, Prinivil), ramipril (Altace), quinapril (Accupril), benazepril (Lotensin) and trandolapril (Mavik). These drugs decrease blood pressure by reducing production of angiotensin-II (a hormone that causes blood vessels to constrict) and aldosterone (a hormone that causes sodium retention). Besides reducing blood pressure, these drugs have additional effects that affect progression of kidney disease including reducing pressure inside the glomerulus and decreasing scarring in the kidney.
  • Angiotensin receptor blockers (ARBs): ARBs are drugs that block the action of angiotensin 2 on its receptors. These drugs, like ACE-I, have a protective effect on the kidneys and slow the progression of kidney failure. Drugs included in this category include losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), candesartan (Atacand) and olmesartan (Benicar).
  • Diuretics: The doctor may prescribe diuretics (water pills) to control edema (swelling), blood pressure and/or potassium levels. There are several classes of diuretics, including loop diuretics (furosemideethacrynic acidbumetanidetorsemide), thiazides (hydrochlorothiazidechlorthalidoneindapamide), and potassium-sparing diuretics (spironolactoneeplerenoneamiloridetriamterene). Diuretics differ in their potential to eliminate salt and water.

More Chronic Kidney Disease Medications

ESAs may have serious side effects. These include the risk of strokes, heart attacks, and blood clots. Worsening hypertension and seizures as well as serious allergic reactions are other side effects.
The calcium-based binders may cause hypercalcemia. Lanthanum and sevelamer do not contain calcium. While non-calcium based binders are much more expensive, the doctor may favor these if a patient's blood calcium levels are high. All phosphate binders may cause constipation, nausea, vomiting, bowel obstruction, and fecal impaction. Phosphate binders may interfere with the absorption of other medications if these are taken together. Always check with the doctor to confirm the suitability of taking these medications together with other drugs.
As kidney disease progresses, activated forms of vitamin D may be prescribed. These drugs include calcitriol (Rocaltrol), paricalcitol (Zemplar), or doxercalciferol (Hectorol). These drugs are prescribed to control secondary hyperparathyroidism when the correction of nutritional vitamin D deficiency, administration of calcium supplementation, and control of serum phosphate have been ineffective.
The use of activated vitamin D may cause hypercalcemia (high calcium levels). The symptoms of hypercalcemia include feeling tired, difficulty thinking clearly, loss of appetite, nausea, vomiting, constipation, increased thirst, increased urination, and weight loss. Other side effects include diarrhea, nausea, swelling, allergic reactions, viral infections, high blood pressure, inflammation of the throat and nose, and dizziness. The doctor will recommend regular blood tests to follow the patient's kidney function, calcium, phosphorus, and parathyroid hormone levels.
  • Erythropoiesis-stimulating agents (ESAs): Patients with chronic kidney disease often develop anemia due to a lack of erythropoietin produced by the kidneys. Anemia is a condition with too few red cells and is characterized by fatigue and tiredness. After excluding other causes of anemia, the doctor may prescribe erythropoiesis-stimulating agents (ESAs) such as Procrit (erythropoietin), Aranesp (darbepoetin), or Omontys (peginesatide). ESAs stimulate the bone marrow to produce red cells and reduce the need for blood transfusions.

  • Phosphate binders: The doctor may recommend a diet low in phosphorus if one's serum phosphorus levels are high. If dietary restriction of phosphorus is unable to control the phosphorus levels, the patient may be started on phosphate binders. When taken with meals, binders combine with dietary phosphate and allow for elimination without absorption into the bloodstream. Binders are divided into large classes, including calcium-based binders such as Tums (calcium carbonate) and PhosLo (calcium acetate) and non-calcium based binders like Fosrenol (lanthanum carbonate), Renagel (sevelamer hydrochloride) and Renvela (sevelamer carbonate).
  • Vitamin D: Vitamin D deficiency is very common in patients with chronic kidney disease. The first step in treating metabolic bone disease is to ensure that there are adequate reserves of vitamin D in the body. The doctor may prescribe over-the-counter vitamin D or prescription-strength vitamin D (Drisdol) based on the patient's vitamin D levels.

Renal Replacement Therapies in Chronic Kidney Disease

In end-stage kidney disease, kidney functions can be replaced only by dialysis or by kidney transplantation. The planning for dialysis and transplantation is usually started in stage 4 of chronic kidney disease. Most patients are candidates for both hemodialysis and peritoneal dialysis (see below). There are few differences in outcomes between the two procedures. The physician or an educator will discuss the appropriate options with the patient and help them make a decision that will match their personal and medical needs. It is best to choose a modality of dialysis after understanding both procedures and matching them to one's lifestyle, daily activities, schedule, distance from the dialysis unit, support system, and personal preference.
The doctor will consider multiple factors when recommending the appropriate point to start dialysis, including the patient's laboratory work and actual or estimated glomerular filtration rate, nutritional status, fluid volume status, the presence of symptoms compatible with advanced kidney failure, and risk of future complications. Dialysis is usually started before individuals are very symptomatic or at risk for life-threatening complications.
Dialysis
There are two types of dialysis 1) hemodialysis (in-center or home) and 2) peritoneal dialysis. Before dialysis can be initiated, a dialysis access has to be created.
Dialysis access
vascular access is required for hemodialysis so that blood can be moved though the dialysis filter at rapid speeds to allow clearing of the wastes, toxins, and excess fluid. There are three different types of vascular accesses: arteriovenous fistula (AVF), arteriovenous graft, and central venous catheters.
  1. Arteriovenous fistula (AVF): The preferred access for hemodialysis is an AVF, wherein an artery is directly joined to a vein. The vein takes 2 to 4 months to enlarge and mature before it can be used for dialysis. Once matured, two needles are placed into the vein for dialysis. One needle is used to draw blood and run through the dialysis machine. The second needle is to return the cleansed blood. AVFs are less likely to get infected or develop clots than any other types of dialysis access.
  2. Arteriovenous graft: An arteriovenous graft is placed in those who have small veins or in whom a fistula has failed to develop. The graft is made of artificial material and the dialysis needles are inserted into the graft directly. An arteriovenous graft can be used for dialysis within 2 to 3 weeks of placement. Compared with fistulas, grafts tend to have more problems with clotting and infection.
  3. Central venous catheter: A catheter may be either temporary or permanent. These catheters are either placed in the neck or the groin into a large blood vessel. While these catheters provide an immediate access for dialysis, they are prone to infection and may also cause blood vessels to clot or narrow.
Peritoneal access (for peritoneal dialysis): A catheter is implanted into the abdominal cavity (lined by the peritoneum) by a minor surgical procedure. This catheter is a thin tube made of a soft flexible material, usually silicone or polyurethane. The catheter usually has one or two cuffs that help hold it in place. The tip of the catheter may be straight or coiled and has multiple holes to allow egress and return of fluid. Though the catheter can be used immediately after implantation, it is usually recommended to delay peritoneal dialysis for at least 2 weeks so as to allow healing and decrease the risk of developing leaks.

More Renal Replacement Therapies in Chronic Kidney Disease

Hemodialysis
Hemodialysis involves circulation of blood through a filter or dialyzer on a dialysis machine.
  • The dialyzer has two fluid compartments and is configured with bundles of hollow fiber capillary tubes.
  • Blood in the first compartment is pumped along one side of a semipermeable membrane, while dialysate (the fluid that is used to cleanse the blood) is pumped along the other side, in a separate compartment, in the opposite direction.
  • Concentration gradients of substances between blood and dialysate lead to desired changes in the blood composition, such as a reduction in waste products (urea nitrogen and creatinine); a correction of acid levels; and equilibration of various mineral levels.
  • Excess water is also removed.
  • The blood is then returned to the body.
Hemodialysis may be done in a dialysis center or at home. In-center hemodialysis typically takes 3 to 5 hours and is performed three times a week. The patient will need to travel to a dialysis center for in-center hemodialysis.
Some centers may offer the option of nocturnal (night-time) hemodialysis wherein the therapy is delivered while the patient sleeps. Long nocturnal dialysis offers patients a better survival and an improvement in their quality of life.
Home hemodialysis is possible in some situations. A care partner is needed to assist the patient with the dialysis treatments. A family member or close friends are the usual options, though occasionally people may hire a professional to assist with dialysis. Home hemodialysis may be performed as traditional three times a week treatments, long nocturnal (overnight) hemodialysis, or short daily hemodialysis. Daily hemodialysis and long nocturnal hemodialysis offer advantages in quality of life and better control of high blood pressure, anemia, and bone disease.
Peritoneal dialysis
Peritoneal dialysis utilizes the lining membrane (peritoneum) of the abdomen as a filter to clean blood and remove excess fluid. Peritoneal dialysis may be performed manually (continuous ambulatory peritoneal dialysis) or by using a machine to perform the dialysis at night (automated peritoneal dialysis).
  • About 2 to 3 liters of dialysis fluid are infused into the abdominal cavity through the access catheter. This fluid contains substances that pull wastes and excess water out of neighboring tissues.
  • The fluid is allowed to dwell for 2 to several hours before being drained, taking the unwanted wastes and water with it.
  • The fluid typically needs to be exchanged four to five times a day.
  • Peritoneal dialysis offers much more freedom compared to hemodialysis since patients do not need to come to a dialysis center for their treatment. The patient can carry out many of their usual activities while undergoing this treatment. This may be the preferable therapy for children.
Most patients are candidates for both hemodialysis and peritoneal dialysis. There are little differences in outcomes between the two procedures. The physician may recommend one kind of dialysis over the other based on the patient's medical and surgical history. It is best to choose one's modality of dialysis after understanding both procedures and matching them to one's lifestyle, daily activities, schedule, distance from the dialysis unit, support system, and personal preference.

Kidney Transplantation and Follow-up


Kidney transplantation offers the best outcomes and the best quality of life. Successful kidney transplants occur every day in the United States. Transplanted kidneys may come from living related donors, living unrelated donors, or people who have died of other causes (deceased donors). In people with type I diabetes, a combined kidney-pancreas transplant is often a better option.
However, not everyone is a candidate for a kidney transplant. People need to undergo extensive testing to ensure their suitability for transplantation. Also, there is a shortage of organs for transplantation, requiring waiting times of months to years before getting a transplant.
A person who needs a kidney transplant undergoes several tests to identify characteristics of his or her immune system. The recipient can accept only a kidney that comes from a donor who matches certain of his or her immunologic characteristics. The more similar the donor is in these characteristics, the greater the chance of long-term success of the transplant. Transplants from a living related donor generally have the best results.
Transplant surgery is a major procedure and generally requires 4 to 7 days in the hospital. All transplant recipients require lifelong immunosuppressant medications to prevent their bodies from rejecting the new kidney. Immunosuppressant medications require careful monitoring of blood levels and increase the risk of infection as well as some types of cancer.
Chronic Kidney Disease Follow-up
If a patient has chronic kidney disease, their health care practitioner will recommend a schedule of regular follow-up visits.
  • At these visits, the patient's underlying condition and kidney status will be evaluated.
  • The patient will have regular blood and urine tests and possibly imaging studies as part of this ongoing evaluation.

Chronic Kidney Disease Prevention

Chronic kidney disease cannot be prevented in most situations. The patient may be able to protect their kidneys from damage, or slow the progression of the disease by controlling their underlying conditions such as diabetes mellitus and high blood pressure.
  • Kidney disease is usually advanced by the time symptoms appear. If a patient is at high risk of developing chronic kidney disease, they should see their health care practitioner as recommended for screening tests.
  • If a patient has a chronic condition such as diabetes, high blood pressure, or high cholesterol, they should follow the treatment recommendations of their health care practitioner. The patient should see their health care practitioner regularly for monitoring. Aggressive treatment of these diseases is essential.
The patient should avoid exposure to drugs especially NSAIDs (nonsteroidal anti-inflammatory drugs), chemicals, and other toxic substances as much as possible.
Chronic Kidney Disease Prognosis
There is no cure for chronic kidney disease. The natural course of the disease is to progress until dialysis or transplant is required.
  • Patients with chronic kidney disease are at a much higher risk than the general population to develop strokes and heart attacks.
  • The elderly and those who have diabetes have worse outcomes.
  • People undergoing dialysis have an overall 5-year survival of 40%. Those who undergo peritoneal dialysis have a 5-year survival of 50%.
  • Transplant patients who receive a live donor kidney have a 5-year survival of 87% and those who receive a kidney from a deceased donor have a 5-year survival of almost 75%.
  • Survival continue to increase for patients with chronic renal disease. Mortality has decreased by 28% for dialysis patients and 40% for transplant patients since 1996.

Support Groups and Counseling for Chronic Kidney Disease

REFERENCES:

Kasper, D., et al. Harrison’s Principles of Internal Medicine. McGraw-Hill Education/Medical. 19th edition, 2015.

"Kidney Disease: Improving Global Outcomes (KDIGO)." Kidney Disease Improving Global Outcomes (KDIGO). 2008.

"National Kidney Foundation Guidelines and Commentaries." National Kidney Foundation. 2012.

"U.S. Renal Data System, USRDS 2015 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States." National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Bethesda, MD. 2015.

Medically Reviewed by a Doctor on  26/05/2017