The evolving role of the medical director of a dialysis facility.

The medical director has been a part of the fabric of Medicare's ESRD program since entitlement was extended under Section 299I of Public Law 92-603, passed on October 30, 1972, and implemented with the Conditions for Coverage that set out rules for administration and oversight of the care provided in the dialysis facility. The role of the medical director has progressively increased over time to effectively extend to the physicians serving in this role both the responsibility and accountability for the performance and reliability related to the care provided in the dialysis facility. This commentary provides context to the nature and expected competencies and behaviors of these medical director roles that remain central to the delivery of high-quality, safe, and efficient delivery of RRT, which has become much more intensive as the dialysis industry has matured.

The role of anemia in congestive heart failure and chronic kidney insufficiency: the cardio renal anemia syndrome.

Anemia is a major problem in patients with chronic kidney insufficiency. The development of recombinant human erythropoietin has enabled physicians to correct this anemia. Although anemia has not been considered to be a common or important contributor to congestive heart failure, anemia of any cause can lead to cardiac damage and eventually congestive heart failure. Our joint renal-cardiac heart failure team found that anemia was indeed very common in congestive heart failure and was associated with severe, medication-resistant cardiac failure. Correction of the anemia with erythropoietin and intravenous iron led to a marked improvement in patients' functional status and their cardiac function, and to a marked fall in the need for hospitalization and for high-dose diuretics; renal function usually improved or at least stabilized. Subsequent investigations by others have confirmed many of our observations. We call this interrelationship between congestive heart failure, chronic kidney insufficiency, and anemia the Cardio-Renal Anemia syndrome. Treatment of the anemia in congestive heart failure may prove vital in preventing progression of both the heart failure and the associated renal disease.

Death of an Arabian Jew.

A 69-year-old Judean man presents with chronic low-grade fever, pedal edema, and abdominal pain. His condition deteriorates over several weeks with the appearance of shortness and foulness of breath, pruritus, convulsions of every limb, and gangrene of the genitalia. Just before he dies, he orders dozens of the leading men of his kingdom imprisoned and instructs his sister to kill them all after he is gone. Who is he and what is the likely cause of his death?

Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.