Dialysis & Transplantation最新文献

In 1968, I was 2 years old and living in Las Vegas. I was suffering from bloating and uncontrollable high fevers, and the doctors had no idea what was wrong with me. They suggested that my parents rush me to Children's Hospital Los Angeles.

After a battery of tests, the specialists at Children's pinpointed the problem: complete kidney failure. At the time, the cause was a mystery, but I was later diagnosed with hemolytic uremic syndrome, a disease brought on by Escherichia coli O157:H7. The doctors hooked my 22-pound body up to a dialysis machine, which looked like a modified washing machine. The treatment kept me going for several weeks—until the day the tubing burst, and I nearly bled to death. I received immediate blood transfusions.

Ironically, this mishap saved my life. As the blood drained out of me, so did the E. coli, relieving the stress on my kidneys and enabling them to function again.

Although my diseased kidneys fought off dialysis for 10 years, they wreaked havoc on my body in other ways. Mainly, they caused my blood pressure to rise uncontrollably. New medications and a low-sodium diet controlled my blood pressure until I was 12 years old. By then, my kidneys were barely functioning, and I had to go on hemodialysis right away. Shortly afterward, they removed both of my native kidneys.

I didn't do well on hemodialysis because of crashing, cramping, and seizures, so Dr. Richard Fine wanted to try a new therapy called peritoneal dialysis. I was the first child to use this therapy in California. After a couple of weeks, I started to feel better. Peritoneal dialysis gave me a new lease on life and much-needed freedom.

A couple of years later, I was offered a peritoneal dialysis cycler machine so that I could do dialysis during the night and alleviate the burden of repeated exchanges during the day. I started ice-skating a couple of times a week and enjoying more daily activities.

During the next several years, I was fortunate enough to receive a donor kidney not once, but twice—and unfortunate enough to reject both of them almost immediately.

The final blow came when my doctors told me that my chances of undergoing a successful transplant were “slim to none.” I had 98% antibodies and type O blood. During my lifetime, I had received more than 150 units of blood, plus two unsuccessful kidney transplants, and this made finding a negative cross-match almost impossible.

By this time, I was in my late teens and felt as if the rug had been pulled out from under me. Was this the way I was going to spend the rest of my life?

What does the future hold? Using stem cells to grow your own kidneys? Fooling the body's immune system into accepting a transplanted kidney? A mechanical kidney that can be implanted or worn on the body so you don't have to be hooked up to a machine? So much hope!

One day in 1990, however, I received life-changing news. I had been on the transplant

Keloids are benign overgrowths of scar tissue composed of overproduction of cellular matrix and dermal fibroblasts. As with all genetic diseases, the prevalence of keloids varies between different patient populations, ranging from 0.09% in Great Britain to 16% in the Congo.1 Patients with the genetic predisposition to keloid formation can form large overgrowths following any skin insult.2 In addition to cosmetic concerns and disfigurement, keloids can also be painful.3 Recurrence of keloids is common despite both medical therapy and surgical removal.

Patients on hemodialysis (HD) who are prone to keloid formation present a unique challenge. Multiple studies have shown that the preferred method of access for hemodialysis is via an arteriovenous fistula (AVF).4 This was further promoted by the Fistula First initiative resulting in an increased prevalence of AVF. During cannulation of the AVF, the skin overlying the fistula is traumatized, predisposing this population to keloid formation. Further K/DOQI guidelines suggest rotating the site of the needle placement along the AVF to decrease the incidence of pseudoaneurysms.5, 6 While the K/DOQI guidelines are beneficial to the HD population at large, if we generalize to include this unique population, we place them at risk for extensive scarring and keloid formation.

To our knowledge, management of HD patients prone to keloids has not been addressed in the literature. We present four cases of patients on HD who developed keloids, and how they were managed. In our centers' diverse patient population, the incidence of keloids is about 1 in 200.

As opposed to normal scar formation, which demonstrates collagen bundles oriented in an organized fashion, keloids contain collagen type I and collagen type III fibers haphazardly connected.7 In patients with a genetic predisposition to keloid formation, regulating growth factors, including transforming growth factor, platelet-derived growth factor, and vascular endothelial growth factor, are overexpressed in the fibroblasts present in keloids, suggesting pathological signaling in the normal mechanisms of wound healing.8-10

The differential diagnosis of keloids includes hypertrophic scars. In contrast to keloids, hypertrophic scars, while large, remain confined within the site of the wound, regress with time, and lack the large disorganized collagen bundles typical of keloids. In addition, keloids are often painful with hyperesthesia, features absent in hypertrophic scars.11

Treatment options for keloids include surgical excision, pressure/compression therapy, radiation, and intralesional corticosteroids. All of these options yield suboptimal results and are associated with complications. Surgical excision carries with it a high incidence of recurrence. Radiation therapy is associated with an increased risk of cance

Renal transplant recipients with secondary hyperparathyroidism often have hypophosphatemia that can persist for years. We report the case of a renal transplanted patient with normal allograft function showing persistent hypophosphoremia due to secondary hyperparathyroidism despite treatment with oral supplements of phosphorus and calcitriol. After initiation of treatment with cinacalcet, a normalization of serum phosphorus was rapidly achieved, and phosphorus supplementation was not necessary. Renal function remained stable. Dial. Transplant. © 2011 Wiley Periodicals, Inc.

This is a classic article by Hampers and Hager in 1979 commenting on the delivery of dialysis services in the United States. Looking back some 32 years later, there are several fascinating aspects of this treatise.

First, the authors make a strong and passionate case for the delivery of outpatient dialysis services by the proprietary (for-profit) business entities in the U.S. This is particularly poignant today as the discussion and arguments are similar now just as they were then, and with the looming of the new healthcare bill recently passed by Congress the supporters and opponents of that bill are just as emotional and unyielding as we sensed in this paper. The specifics of the authors' arguments may no longer be relevant, but the general philosophy they outline is just as compelling today to some thought leaders as they were three decades ago.

Additionally, as the authors correctly predicted, the for-profit sector is winning the dialysis services battle, as illustrated by the ongoing consolidation in this arena by the large for-profit companies.

I could not help but smile when I read that federal health expenditures in 1976 represented 9.7% of the federal budget ($44.5 billion). What we would give today to have such a “low” percentage? Similarly, the median age of hemodialysis patients was around 51 years of age, a number we left in the dust long ago. The article also expressed the desire to move hemodialysis patients to home care as much as possible, an effort which is again gaining momentum in our country.

Despite the age of this article and the loss of relevance of some of its content, this is a remarkable commentary on the entire dialysis industry, and still rings mostly true today. It also gives us a unique retrospective on the evolution of the ESRD Program.

Citation: Raggi P, Chertow GM, Torres PU, et al. The ADVANCE Study: a randomized study to evaluate the effects of cinacalcet plus low-dose vitamin D on vascular calcification in patients on hemodialysis. Nephrol Dial Transplant. 2011;26:1327–1339.

Analysis: Cardiovascular disease remains a significant burden in hemodialysis patients, and coronary calcification has been shown to be an independent risk factor for both cardiovascular morbidity and all-cause mortality in this group.1, 2 Furthermore, coronary calcification tends to progress rapidly once established.3 Several studies have looked at the effects of phosphate binders, calcium intake, and statins on coronary calcification progression and mortality, with some evidence that lower calcium intake along with lower phosphorus levels slows calcification and improves outcomes.2, 4, 5 This study by Raggi and colleagues looks at cinacalcet and its effect on coronary and cardiac valve calcifications in patients with secondary hyperparathyroidism.

This prospective controlled trial randomized 360 hemodialysis patients with secondary hyperparathyroidism to therapy with cinacalcet and low dose vitamin D or to conventional therapy with vitamin D sterols alone. Patients were included if they had moderate to severe hyperparathyroidism and a baseline Agatston coronary artery and valvular calcification scores at or above 30. Calcification scores were measured at 28 and 52 weeks, and all patients were treated with calcium-based phosphate binders. The results demonstrated a statistically significant slower progression of scores in the aortic valve, with consistently less of an increase (although not reaching statistical significance) in calcification scores of the coronary arteries, aorta, and mitral valves in the cinacalcet group. Patients in the cinacalcet group had a greater decrease in serum PTH, calcium, and phosphorus as well as lower vitamin D requirements. The authors concluded that in patients with moderate to severe hyperparathyroidism, cinacalcet with vitamin D may attenuate coronary and cardiac valve calcification.

Validity and threats to validity: This large multicenter trial included a diverse patient population broadly representative of the full diversity of age, race, and dialysis vintage in the prevalent dialysis population. Patients were stratified based on calcification score before randomizing, the latter in a 1:1 fashion to the two treatment arms. Stratification is often beneficial in preventing imbalance between groups for factors known to influence treatment responsiveness and overall prognosis (such as baseline calcification scores). It also prevents a type I error (rejecting the null hypothesis when it is true), and it improves power in trials with fewer than 400 patients.6 Additional strengths of the study include the validation of calcification sc