Ferric citrate controls phosphorus and delivers iron in patients on dialysis.

Patients on dialysis require phosphorus binders to prevent hyperphosphatemia and are iron deficient. We studied ferric citrate as a phosphorus binder and iron source. In this sequential, randomized trial, 441 subjects on dialysis were randomized to ferric citrate or active control in a 52-week active control period followed by a 4-week placebo control period, in which subjects on ferric citrate who completed the active control period were rerandomized to ferric citrate or placebo. The primary analysis compared the mean change in phosphorus between ferric citrate and placebo during the placebo control period. A sequential gatekeeping strategy controlled study-wise type 1 error for serum ferritin, transferrin saturation, and intravenous iron and erythropoietin-stimulating agent usage as prespecified secondary outcomes in the active control period. Ferric citrate controlled phosphorus compared with placebo, with a mean treatment difference of -2.2±0.2 mg/dl (mean±SEM) (P<0.001). Active control period phosphorus was similar between ferric citrate and active control, with comparable safety profiles. Subjects on ferric citrate achieved higher mean iron parameters (ferritin=899±488 ng/ml [mean±SD]; transferrin saturation=39%±17%) versus subjects on active control (ferritin=628±367 ng/ml [mean±SD]; transferrin saturation=30%±12%; P<0.001 for both). Subjects on ferric citrate received less intravenous elemental iron (median=12.95 mg/wk ferric citrate; 26.88 mg/wk active control; P<0.001) and less erythropoietin-stimulating agent (median epoetin-equivalent units per week: 5306 units/wk ferric citrate; 6951 units/wk active control; P=0.04). Hemoglobin levels were statistically higher on ferric citrate. Thus, ferric citrate is an efficacious and safe phosphate binder that increases iron stores and reduces intravenous iron and erythropoietin-stimulating agent use while maintaining hemoglobin.

Herbal Nephropathy.

This column is supplied by Amita Jain, MD, and Juan Jose Olivero, MD. Dr. Jain completed an internal medicine residency at Houston Methodist Hospital in Houston, Texas, and recently joined a primary care practice in Delaware. She earned a Bachelor of Medicine and Surgery (MBBS) degree, with a distinction in microbiology, from Terna Medical College at the Maharashtra University of Health Sciences in Navi Mumbai, India. Before coming to Houston, Dr. Jain completed residency training in internal medicine and allied subspecialties at the Dr. Babasaheb Ambedkar Memorial Hospital in Byculla, Mumbai. Dr. Olivero is a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Training Program. He obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.

Lipids and Renal Disease.

The column in this issue is supplied by Anita Shah, M.D., and Juan Jose Olivero, M.D. Dr. Shah is a first-year nephrology fellow at Baylor College of Medicine in Houston, Texas. She earned her medical degree from The University of Texas Medical Branch at Galveston and completed an internal medicine residency at Houston Methodist Hospital. Dr. Olivero is a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Training Program. He obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.

Continuous Venous-Venous-Hemodialysis versus Intermittent-Hemodialysis in Critically Ill Patients.

The column in this issue is supplied by Juan Jose Olivero, M.D., a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Training Program. Dr. Olivero obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.

Venous Thrombosis in Nephrotic Syndrome.

The column in this issue is supplied by Whitney Sharp, D.O., and Juan Jose Olivero, M.D. Dr. Sharp is chief medical resident in internal medicine at Houston Methodist Hospital and earned her Doctor of Osteopathic Medicine degree at Nova Southeastern University in Fort Lauderdale, Florida. Dr. Olivero is a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Training Program. He obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.

Gadolinium-Induced Nephrogenic Systemic Fibrosis.

The column in this issue is supplied by Anita H. Shah, M.D., and Juan Jose Olivero, M.D. Dr. Shah obtained her medical degree at The University of Texas Medical Branch in Galveston and is currently an internal medicine resident at Houston Methodist Hospital. Dr. Olivero is a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Fellowship Training Program. He obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.

Acute kidney injury after cardiovascular surgery: an overview.

Acute kidney injury is a complication of open-heart surgery that carries a poor prognosis. Studies have shown that postoperative renal function deterioration in cardiovascular surgery patients increases in-hospital mortality and adversely affects long-term survival. Identifying individuals at risk for developing AKI and aggressive early intervention is extremely important to optimize outcomes. This paper provides an overview of the etiology, prognostic markers, risk factors, and prevention of AKI and treatments that may favorably affect outcomes.

Nephrogenic calcific arteriopathy.

INTRODUCTION: Vascular calcification in chronic kidney disease (CKD) is extremely common and contributes to significant morbidity and mortality among these patients. The pathogenesis is complex and involves multiple factors, including elevated calcium x phosphorus product as well as deficiencies in circulating or locally produced inhibitors of calcification, parathyroid hormone, hyperlipidemia and inflammation. Similarly, valvular heart calcifications as well as myocardial and pulmonary calcifications of fatal consequences can also occur, presumably related to the same pathogenetic factors (Figures 1, 2). Other forms of extraskeletal tissue calcification of nonfatal consequences but leading to incapacity can also develop in CKD patients (Figure 3). These complications may be prevented by awareness and early intervention directed towards correcting some of the aforementioned participating mechanisms.

Chronic kidney disease: a marker of cardiovascular disease.

The risk of developing CVD is high among CKD patients and, as a result, cardiovascular-related complications account for high morbidity and mortality. Multiple factors contribute to CVD in CKD patients, including hypertension, anemia, inflammation, hyperlipidemia, calcium-phosphorus-parathyroid hormone imbalance, and hyperuricemia. Each one of these complications needs to be identified and treated in an attempt to improve survival. Early markers of CVD such as microalbuminuria and uric acid levels need to be added to the routine annual evaluation, particularly among high-risk individuals such as diabetics, hypertensives, smokers, and the elderly. Likewise, the use of eGFR is highly recommended as a screening tool in those individuals.