Creatinine

Definitions Under Construction
Azotemia (nitrogen in blood)	One major role of a healthy kidney is to get rid of the byproducts of nitrogen metabolism (from protein). Azotemia occurs when the kidneys are damaged and can no longer efficiently get rid of these metabolites. BUN (blood urea nitrogen) and creatinine are just two easily measured markers of nitrogen accumulation. When their levels are increased one can be said to have renal dysfunction. Eight five to 90% of kidney function can be lost (if gradual) before one notices any obvious symptoms. For those who visit a doctor regularly and have blood drawn, kidney dysfunction can be detected by accident. For others, diagnosis comes when they develop symptoms at a late stage, and may require dialysis in the short term. The possible advantage of knowing early is applying the possible interventions that might slow progression and the ability to prepare psychologically (if that is possible). (reprinted from Dr. Peter Lundin) http://nephron.con/lundin/lun_def.html
Blood Pressure	Blood pressure deserves special mention. In many it is the primary cause of kidney failure, and in others it is a secondary cause. Furthermore, renal failure, despite the cause (except systemic amyloidosis) is characteristically associated with hypertension (repeated elevated blood pressure readings). An elevated blood pressure has the effect of weight lifting on the heart; it builds up the heart muscle. In the heart's case, however, this "hypertrophy" can outstrip the coronary blood supply, and can result in heart damage and weakness over several years. Elevated blood pressures also damage other tissues beside the heart, and are a common cause of strokes. It is imperative, therefore, for all patients, especially dialysis patients, to strive to keep the blood pressure under control. There are two ways to control blood pressure in kidney patients. The first is by watching ones diet, fluid and salt intake, and remaining on dialysis long enough to achieve a dry weight. A second means to control blood pressure is through the use of antihypertensive medications. Most often, it takes a combination of both medication and volume control to keep the blood pressure stable, but in the ideal patient, diet and volume control should suffice. The control of blood pressure is associated with better outcomes - less stroke and cardiovascular disease. It is related to the adequacy of dialysis, control of fluids (and salt) and taking necessary blood pressure medications. Ideally one should challenge the dry weight until the blood pressure is in target range, with the systolic less than 140 - 150, and the diastolic less than 80 - 90. Once dry weight is established and maintained, the dosages of antihypertensive medications can be reduced. Often, blood pressure medications can be discontinued, altogether. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Blood Urea Nitrogen (BUN) (yoo-REE-uh NY-truh-jen)	Blood urea nitrogen. Urea nitrogen is produced from the breakdown of food protein. A normal BUN level is between 7 and 20 mg/dL. As kidney function decreases, the BUN level increases.

Dialysis
ESRD	End Stage Renal Disease





Hematocrit	The kidney produces a hormone called erythropoietin. This hormone stimulates the production of red blood cells. Kidney failure leads to decreases synthesis of this hormone, and thus anemia (decreased red cell count) develops. This anemia is measured by the hematocrit, the ratio of red cells to plasma volume. The accepted range for dialysis patients is 33 to 36. Synthetic erythropoietin is given either intrvenously or subcutaneously. As red cells are formed, they require building blocks such as iron, without which, they will not grow. It is therefore important that either oral or intravenous iron also be given. When the red cell production is decreased due to renal failure, synthetic erythropoietin and iron supplements will bring it back to normal. Reasons for a continued low hematocrit are usually due to inadequate dialysis, inadequate dosage of erythropoietin or inadequate iron. Patients with sickle cell disease, chronic illness other than kidney failure, recent surgery, sepsis and other hematologic disorders may have anemia (low hematocrit) despite best efforts to correct with supplements and erythropoietin. In these cases, a more thorough anemia evaluation should be undertaken. The transferrin saturation ratio (ratio of serum iron to iron binding capacity) and serum ferritin level are characteristically low in iron deficient states, such as inadequate iron dosing, and iron depleted states such as a gastrointestinal bleed. In kidney patients who do not respond to erythropoietin and iron, a stool guiaic and even gastrointestinal evaluation may be indicated, particularly when there is a family history of polyps or cancer. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Hemodialysis	In hemodialysis blood is pumped from the body to a filter made of tiny plastic capillaries. The blood is purified when the waste products diffuse from the blood across the membrane of these tiny capillaries. Purified blood is then returned to the arm. Hemodialysis is performed in a dialysis center for 4 hours three times a week. Dialysis is performed through an arteriovenous access (a v access) Advantages: No patient training is required. Disadvantages: Dialysis graft failure, lack of freedom (reprinted from the Nephron website) http://nephron.com/fkg.html

Kt/V	The Kt/V is the ratio of urea clearance times dialysis duration to the volume (body water space) that the urea is distributed in. This value should be greater than 1.2 (the minimally accepted standard), but since it is directly associated with a better dialysis outcome, even higher numbers are desired. In fact, the best outcomes in the world are in dialysis patients who run as long as six hours. A high Kt/V is associated with better mortality rates, less hospital days, less anemia and better blood pressure control. In peritoneal dialysis patients, the Kt/V is calculated on a weekly basis, and should be greater than 2.0. Many who start dialysis have residual renal function, and in the beginning do not require as much dialysis as those who have no remaining kidney function. However, progressive kidney disease is inexorable, and one can expect that as the disease worsens the dialysis requirements should increase. The Kt/V is the ratio of urea clearance times dialysis duration to the volume (body water space) that that urea is distributed in. 1.2 is the minimally accepted value; and any result below this is too low. If the Kt/V is below the desired level, it could be that the dialysis time needs to be lengthened. Those who cut their dialysis hours short will have a low Kt/V. This leads to an accumulation of toxins (poisons) in the body, that over time damages body tissues. It is no small wonder that the best outcomes in the world are in dialysis patients who run as long as six hours. Those who drink excessive fluids between dialysis periods will also have a low Kt/V. That is because the excessive fluids increase the "V." When one does the simply arithmetic, it is clear that the higher the "V," the lower the Kt/V. Sometimes increasing dialyzer time, blood flow and even dialysis flow will improve the Kt/V. A low Kt/V is also associated with a poorly functioning AV graft or fistula. Hemodialysis catheters, whether permanent or temporary, are associated with a lower Kt/V, and it is advised that patients who must be on chronic dialysis have a fistula or graft placed. In peritoneal dialysis patients, the Kt/V is calculated on a weekly basis, and should be greater than 2.0. Lower Kt/Vs in this population suggest that dialysis volumes need to be increased. The integrity of the peritoneal dialysis membrane needs to be assessed, and an equilibrium test may be necessary. It is critical that patients do not cut short the number of treatments prescribed or decrease the fill volume because of the serious effect this has on reducing peritoneal dialysis adequacy. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Lupus	L upus is a type of immune system disorder known as an autoimmune disease. In autoimmune diseases, the body harms its own healthy cells and tissues. This leads to inflammation and damage of various body tissues. Lupus can affect many parts of the body, including the joints, skin, kidneys, heart, lungs, blood vessels, and brain. Although people with the disease may have many different symptoms, some of the most common ones include extreme fatigue, painful or swollen joints (arthritis), unexplained fever, skin rashes, and kidney problems. Lupus is also known as a rheumatic disease. The rheumatic diseases are a group of disorders that cause aches, pain, and stiffness in the joints, muscles, and bones. Although "lupus" is used as a broad term, there actually are several kinds of lupus: Systemic lupus erythematosus (SLE), which is the form of the disease that most people are referring to when they say "lupus." The word "systemic" means the disease can affect many parts of the body. The symptoms of SLE may be mild or serious. Although SLE usually first affects people between the ages of 15 and 45 years, it can occur in childhood or later in life as well. This booklet focuses on SLE. Discoid lupus erythematosus primarily affects the skin. A red, raised rash may appear on the face, scalp, or elsewhere. The raised areas may become thick and scaly. The rash may last for days or years and may recur. A small percentage of people with discoid lupus later develop SLE. Drug-induced lupus refers to a form of lupus caused by medication. It causes some symptoms similar to those of SLE (arthritis, rash, fever, and chest pain, but not kidney disease) that go away when the drug is stopped. Common medications that may cause drug-induced lupus include hydralazine (Apresoline), procainamide (Procan, Pronestyl), methyldopa (Aldomet), quinidine (Quinaglute), isoniazid (INH), and some anti-seizure medications such as phenytoin (Dilantin) or carbamazepine (Tegretol). Neonatal lupus can affect some newborn babies of women with SLE or certain other immune system disorders. Babies with neonatal lupus may have a serious heart defect. Other affected babies may have a skin rash, liver abnormalities, or low blood counts. Physicians can now identify most at-risk SLE patients, allowing for prompt treatment of the infant at birth. Neonatal lupus is very rare, and most infants of mothers with SLE are entirely healthy. (reprinted from the NIH website) http://www.nih.gov/niams/healthinfo/slehandout/defining.htm
Peritoneal Dialysis	In peritoneal dialysis the bodies own membrane is used as a filter, and the fluid drained in and out of the abdomen replaces the kidneys in getting rid of the body poisons. It can be done at home, but requires careful technique. Its advantage is more freedom and less needle sticks. The disadvantages are peritonitis and membrane failure. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Peritoneal Dialysis Adequacy
Serum Albumin	The serum albumin is a marker of nutrition. Renal failure suppresses dietary intake and promotes a negative nitrogen balance. There is a balance between the nitrogen (an element found in proteins) in the diet and the nitrogen eliminated. Nitrogen is used to repair muscles and help with the body's day-to-day upkeep. When the body needs for metabolism increase, dietary intake must also increase to maintain the balance. When these needs are not met, or when dietary intake decreases, the body "borrows" protein from muscles. Albumin synthesis is an indication of health, and in this negative balance situation, the serum albumin is low. The low serum albumin and its associated negative nitrogen balance correct with adequate dialysis. A normal serum albumin indicates that one is adequately dialyzing, and is getting adequate nutrition. Albumin synthesis is an indication of health, and a low serum albumin indicates poor nutrition. Chronic diseases commonly cause a low serum albumin. In addition to kidney failurem it is seen in patients with the nephrotic syndrome, chronic liver diseae, malabsorption, and cancer. The hypoalbuminemia seen in kidney patients is generally due to inadequate dialysis. Thus, by increasing dialysis time, the size of the dialyzer or increasing blood flow, renal failure related albumin problems can be reversed. Sometimes it is necessary to revise or replace the dialysis access. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Serum Creatinine (kree-AT-uh-nin)	Creatinine is a waste product in the blood created by the normal breakdown of muscle during activity. Healthy kidneys take creatinine out of the blood and put it in the urine to leave the body. When kidneys are not working well, creatinine builds up in the blood. In the lab, your blood will be tested to see how many milligrams of creatinine are in one deciliter of blood (mg/dl). Creatinine levels in the blood can vary, and each laboratory has its own normal range. In many labs, the normal creatinine range is 0.6 to 1.2 mg/dl. If your creatinine level is only slightly above this normal range, you probably will not feel sick, but the elevation is a sign that your kidneys are not working at full strength. One formula for estimating kidney function equates a creatinine level of 2.0 mg/dl to 50 percent of normal kidney function and 4.0 mg/dl to 25 percent. But, because creatinine values are so variable and can be affected by diet, you may need to have your creatinine measured regularly to see whether your kidney function is decreasing. The doctor may refer to the measure of creatinine in your blood as your serum creatinine. Do not confuse your serum creatinine number with your creatinine clearance number. (reprinted from the NIDDK) http://www.niddk.nih.gov/health/kidney/pubs/yourkids/index.htm
Serum Phosphorus	Phosphorus is normally eliminated by the kidneys, but in renal failure it accumulates. The phosphorus binds with calcium, lowering the effective levels of calcium. Calcium balance must be maintained. Any lowering in calcium levels stimulates the parathyroid glands in the neck to secrete a hormone that leads to reabsorption of calcium from bone. Over a period of time the calcium loss weakens the bones. Also the elevated calcium phosphorus product causes soft tissue depositions, leading to itching and skin lesions. The soft tissue deposition may also occur in blood vessels, the heart conduction system, heart valves and the lungs, leading to specific organ dysfunction. Dietary calcium binders can combine with phosphorus in the stomach and intestines, and lead to its elimination before it can be absorbed and can accumulate. Dietary phosphorus restriction will also help to control the serum phosphorus. Side effects of these binders, which come in both pill and liquid form, are chiefly constipation. A stoof softener, and intermittent use of a magnesium-based binder can alleviate this problem. The inconvenience of taking a large quantity of medications is greatly outweighed by the benefit of preventing serious bone and tissue consequences. Secondary hyperparathyroidism is a result of chronically elevated serum phosphorus levels, and is treatable with calcitriol. However, calcitriol cannot be given unless the calcium-phosphorus product (serum calcium multiplied by serum phosphorus) is less than 70. Thus, in those who have developed elevated serum parathyroid hormone levels, it is imperative to maintain the phosphorus within the target range. Poor nutrition or over zealous use of binders will lower the serum phosphorus level. Total parenteral nutrition, or refeeding after a period of starvation can also cause hypophosphatemia. Occasionally, transplant patients, having regained renal function, have a disproportionately high parathyroid function, and can have hypophosphatemia. When the phosphorus level is less than 1.0 mg/100cc, seizures, metabolic acidosis and cardiac arrest can occur. To avoid this, patients at high risk to develop acute and severe hypophosphatemia should be treated with phosphorus supplements. While severe hypophosphatemia is unlikely in ESRD patients under usual circumstances, phosphate binders should be held when the serum phosphorus levels are below 3.5 mg/100 cc. Phosphorus accumulates in renal failure, and binds calcium. Calcium balance is maintained by an increase in bone reabsorption. Weakened bones and increased soft tissue calcifications are the consequence of hyperphosphatemia. This can be largely avoided by keeping the serum phosphorus under control. Foods that are high in phosphorus should be eaten in moderation or avoided. Calcium carbonate or acetate can bind dietary phosphorus, leading to its elimination prior to absorption. They also serve as a source of calcium supplements, and should be taken regularly, with meals. Ever feel like cheating on your diet? An extra dose of binder can help offset the occasional soda. By breaking calcium tablets into smaller pieces, the surface area will increase, making the dose more effective. An acceptable serum phosphorus level generally requires the effort of taking medications regularly. If your phosphorus was acceptable, keep up the good work. (reprinted from the Nephron website) http://nephron.com/reportcard.html
Serum Potassium	Potassium is an element. It is easily secreted by the kidneys, and is present in much of the food we eat. It is present in body cells, and its balance is critical for cellular function, including muscle contraction to take place. The heart, being a muscle, is very sensitive to changes in potassium. In dialysis patients, an elevated potassium usually indicates that one has missed a dialysis treatment, or that dialysis was not effective. Dietary potassium intake should be restricted in kidney patients, but generally not to an extreme because of the efficiency of the dialysis procedure. Most often, patients may have acute, and severe hyperkalemia without symptoms! Elevated potassium levels lead to ventricular fibrillation with cardiac arrest. This is a medical emergency. The best way to prevent hyperkalemia is to never miss a dialysis treatment, and to never cut the time short. Therefore, there is never a good reason to miss dialysis, and take this risk of sudden death. Severe muscle cramps and muscle stiffness are sometimes symptoms of acute hyperkalemia. The presence of these findings, particularly in one who has missed a dialysis treatment, is a medical emergency requiring immediate attention. If the serum potassium is too low, it indicates poor nutritional status. This may be the result of chronic illness, poor dietary habits or inadequate dialysis. Patients with chronic lung disease may be on certain bronchodilators, and can have a relative hypokalemia. A chronically low serum potassium indicates that the total body potassium stores have been depleted. Sometimes, changing the dialysis bath potassium will restore the potassium to a normal level. Ideally, one must search for the underlying cause of this nutritional problem. Symptoms of hypokalemia are muscle cramps, muscle twitching and acute paralysis. A normal serum potassium generally indicates that nutritional intake of potassium is adequate and that dialysis is functioning well to remove excess mineral. It should also be associated with a normal serum albumin. Among those that have residual renal function, it is probable that the native kidneys are doing some of the work of removing potassium. The kidneys strive to eliminate potassium well into renal failure, and decreased potassium excretion is usually only seen in the later stages of kidney disease. The exception is the diabetic patient that has an associated renal tubular acidosis. (reprinted from the Nephron website) http://nephron.com/reportcard.html




urea reduction ratio (URR)	The urea reduction ratio is the ratio of the difference in blood urea nitrogen (BUN) at the beginning and after dialysis to the BUN at the beginning. This number corresponds to the Kt/V (see above), but is less valuable because it does not take into account the volume of urea distribution. Yet, it is a simple calculation, and an easy number to follow. The minimally accepted ratio is 65%, but higher ratios are usually attainable and desirable. The higher the ratio, the more adequate the dialysis. Dialysis adequacy is associated with good outcomes - a longer life on dialysis, less hospital time, less anemia and even better blood pressure control. When the urea reduction ratio, the ratio of the difference in blood urea nitrogen (BUN) at the beginning and after dialysis to the BUN at the beginning, is below 65, dialysis is not adequately being performed. Major reasons are inadequate dialysis times, too small a dialyzer, or a faulty dialysis access. Dialysis access problems can be related to recirculation through the graft. A recirculation time greater than 15% suggests that the graft is malfunctioning. Blood flowing back from the dialyzer is forced toward the inlet (mixing with uncleaned blood) and is also forced to go through the dialyzer again and again. This leads to inefficient dialysis. Most often this is due to a venous outflow obstruction at the area of the graft where it connects back to the vein. Early detection and correction of this problem is necessary, not only to improve dialysis adequacy, but to preserve the graft. Patients with temporary subclavian catheters, and those with permacatheters generally have less adequate dialysis, and when it is contemplated that dialysis is going to be permanent, an AV Graft or fistula should be placed. (reprinted from Dr. Peter Lundin) http://nephron.con/lundin/lun_def.html
Uremia (urine in blood)	The end stage of "kidney failure" when one begins to get symptoms of increasing severity as the kidney fails further. Such symptoms include: 1. Progressive loss of energy - decreased exercise tolerance 2. Progressive loss of interest in life and normal activities* 3. Decrease of appetite, some weight loss (may be masked by fluid retention 4. Loss of appetite with nausea and vomiting marks a serious turn for the worse 5. Uremic pericarditis (inflammation of the outside lining of the heart), lethargy, confusion, coma indicate a progression of the final stages of uremia to death. Intervention with dialysis or transplant early in the course can prevent later complications. However, some patients have to become ill before appreciating what dialysis can do. (reprinted from Dr. Peter Lundin) http://nephron.con/lundin/lun_def.html

In hemodialysis blood is pumped from the body to a filter made of tiny plastic capillaries. The blood is purified when the waste products diffuse from the blood across the membrane of these tiny capillaries. Purified blood is then returned to the arm.

In peritoneal dialysis the bodies own membrane is used as a filter, and the fluid drained in and out of the abdomen replaces the kidneys in getting rid of the body poisons.