Kidney Disorder

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Kidney Disorder Biography

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.

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.


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).

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.

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.

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.

Kidney Disorder

Kidney Disorder

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Kidney Disorder

The Kidney

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The Kidney Biography

MoreChronic Kidney Disease Medications
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.

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.


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).

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.

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.

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.

The Kidney

The Kidney

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The Kidney

Kidney Disorders

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Kidney Disorders Biography
Unfortunately, however, millions of Americans are not getting enough of this so-called "sunshine" vitamin. Now it turns out that one group in particular is almost universally lacking in vitamin D. According to a study slated for publication in an upcoming issue of the Clinical Journal of the American Society Nephrology (CJASN), kidney disease patients who have low blood protein levels and who start dialysis during the winter are at extremely high risk of being seriously deficient in vitamin D.

Ishir Bhan, MD, of Massachusetts General Hospital, and his research team studied data from 908 U.S. dialysis patients in the Accelerated Mortality on Renal Replacement (ArMORR) cohort. The scientists' goal was to investigate routinely measured clinical and demographic characteristics to see if they could figure out which patients with end-stage renal disease (ESRD) on dialysis are at increased risk for vitamin D deficiency.

The results showed that 79% of the patients in the study were vitamin D deficient. The strongest predictors of a lack of vitamin D were being African-American, female, the winter season, and low blood levels of the protein albumin. In fact, when all these factors came together, the result was that every single kidney disease patient was deficit in vitamin D.

Specifically, the researchers found that if black dialysis patients had low blood albumin levels during the winter season, the likelihood they would be vitamin D deficient increased from 90% to 100% for women and from 85% to 100% for men. Their white counterparts fared only slightly better, with their risk of vitamin D deficiency rising from 82% to 94% in women and from 66% to 92% in males.

"This research identifies risk factors for nutritional vitamin D deficiency in the dialysis population and may provide clues to its biology in this population," Dr. Bhan said in a statement to the media.

So what is going on here that makes ESRD patients on dialysis so vulnerable to vitamin D deficiency? The scientists pointed out in their media statement that although previous studies have suggested that patients on dialysis have an impaired ability to generate vitamin D when they are exposed to adequate sunlight, their study indicates that skin-based production of vitamin D is likely to be important in patients with ESRD.

Although the researchers did not discuss the issue in their paper, their findings raise a which-came-first type issue. Is it possible vitamin D is at least part of the cause of serious kidney disease, and not merely a byproduct of the illness? With a growing number of chronic and serious illnesses -- including heart disease

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Signs Of Kidney Disease

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Signs Of Kidney Disease Biography
(NaturalNews) According to the American Society of Nephrology (ASN), the number of people in the US diagnosed with kidney disease has doubled over the past 20 years. About 20 million Americans are at risk for developing kidney disease and the ASN web site states another 20 million Americans already have some evidence of chronic kidney disease. And when chronic kidney disease progresses, it often leads to kidney failure or end stage renal disease (ESRD) -- resulting in ongoing, expensive dialysis treatments or even kidney transplants.

But like countless other diseases and conditions, kidney disease doesn't just strike out of the blue. It is often the result of what people do to their own bodies. And researchers have just reported two direct ways diet appears to be associated with declining kidney function. The culprits? Eating food high in sodium (like the fast foods and processed junk snacks Americans love) and drinking artificially sweetened sodas.

Those are the findings of two new studies, both conducted by Julie Lin, MD, and Gary Curhan, MD, ScD, of Brigham and Women's Hospital, which were recently presented at the American Society of Nephrology's annual meeting held in October in San Diego, California. The first study, entitled "Associations of Diet with Kidney Function Decline," examined the impact of specific dietary components on declining kidney function over 11 years in more than 3,000 women who participated in the Nurses' Health Study. Dr. Lin and Dr. Curhan found that "in women with well-preserved kidney function, higher dietary sodium intake was associated with greater kidney function decline, which is consistent with experimental animal data that high sodium intake promotes progressive kidney decline."

In previous research, scientists using information collected from the National Health and Nutrition Examination Survey (NHANES), a long-term collection of studies designed to assess the health and nutritional status of adults and children in the US, had found a link between sugar containing sodas and urinary protein. However, they did not collect data on any kidney function changes related to drinking sweetened sodas. So, in their second study, Dr. Lin and Dr. Curhan, decided to specifically check for any kidney function decline in women who drink sodas regularly. Once again, they used data from the Nurses' Health Study.

In a statement for the media, Dr. Lin reported they found "a significant two-fold increased odds, between two or more servings per day of artificially sweetened soda and faster kidney function decline; no relation between sugar-sweetened beverages and kidney function decline was noted." Moreover, this association persisted even when the researchers accounted for age, obesity, high blood pressure, cardiovascular disease, physical activity, calorie intake, diabetes and cigarette smoking. Clearly, artificially sweetened sodas are detrimental to kidney health.

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Signs Of Kidney Disease

Kidney Disease

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Kidney Disease Biography
Erythropoiesis-Stimulating Agents
See Skali et al and Kaufman.
Despite the lack of strong evidence that treatment of moderate levels of anemia provided mortality or morbidity benefits, erythropoiesis-stimulating agents (ESAs) were a mainstay of anemia management in nondialysis CKD patients. Critically, sparse data are available about the natural history of anemia in nondialysis CKD patients and the pattern of hemoglobin levels in the absence of ESA administration. This month, Skali and colleagues analyze the placebo arm of the TREAT study to investigate hemoglobin levels over time in patients with diabetic patients with CKD stage 3-5, moderate anemia, and minimal or no ESA exposure, reporting that most patients were able to maintain a stable hemoglobin level without long-term ESA therapy. In an accompanying editorial, Kaufman discusses the study by Skali et al in the context of the US FDA recommendations for ESA use.

Frequent Dialysis and Cognitive Function
See Yaffe et al; Kurella Tamura et al and Seliger & Weiner.
Cognitive impairment is common in individuals with CKD, particularly among those treated with dialysis. Cognitive impairment carries substantial risk, including depression and worse perceived quality of life as well as a marked increase in mortality; therefore, understanding the pathogenesis and exploring possible preventive treatments for cognitive impairment in CKD are critical to improving dialysis patient care. In this issue of AJKD, Kurella Tamura and colleagues report the effects of frequent dialysis on cognitive function in individuals participating in the Frequent Hemodialysis Network Trials and conclude that more frequent hemodialysis did not improve executive function or global cognition. Editorialists Seliger and Weiner argue that a reasonable interpretation of these results is that impaired cognitive function in dialysis patients is determined largely by factors other than uremic solute clearance; therefore, given the robust relationship between microvascular disease and cognitive function in earlier stages of CKD, treatments to address cognitive impairment should target microvascular disease and cardiovascular disease risk.

Validating the New CKD-EPI Cystatin C Equation for Estimating GFR
See Horio et al and Masson et al.
The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently developed GFR-estimating equations based on standardized serum cystatin C and standardized serum creatinine plus standardized serum cystatin C. In this issue of AJKD, these new equations are put to the test in 2 different patient populations. Horio et al studied the accuracy of these equations among Japanese individuals and report that the formulas perform well; accordingly, the authors suggest that equations based on serum cystatin C could be used in patients of different races without modification. In the study by Masson et al, the authors compared the performances of serum cystatin C and serum creatinine as endogenous markers of GFR in a large cohort of transplant recipients and report data that validates using serum cystatin C–based equations to estimate GFR in these patients.

Posttransplantation Bone Disease
See Alshayeb et al.
Kidney transplant, the most effective treatment for the metabolic abnormalities of CKD, only partially corrects CKD–mineral and bone disorders. Posttransplantation bone disease is markedly different from the mineral and bone disorders often seen in patients with native CKD and is influenced by factors such as immunosuppressive therapy, kidney graft function, hypophosphatemia, and disturbances in the fibroblastic growth factor 23–parathyroid hormone–vitamin D axis. Alshayeb and colleagues review the pathogenesis, diagnosis, and management of posttransplantation bone disease and conclude that, with the lack of sufficient prospective studies evaluating currently available therapies, clinical judgment must serve as the guiding principle to evaluate the risk-benefit of specific therapies for preventing bone loss and fractures in this setting.

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