Guidelines for CKD: Defining, Staging, and Managing Guidelines for CKD: Defining, Staging, and Managing
Get up-to-date on the most recent guidelines for identifying and managing patients with chronic kidney disease.Journal for Nurse Practitioners
Objective: We aimed to determine the factors contributing toward diffusely increased renal uptake on bone scintigraphy using technetium-99m (Tc-99m) diphosphono-propanedicarboxylic acid (DPD) in patients with end-stage renal disease. Patients and methods: One-hundred and forty-three bone scintigraphies, performed between June 2007 and July 2013, in 135 patients with chronic kidney disease were analyzed retrospectively, including 22 bone scintigraphies (15 patients; eight women; seven men) with glomerular filtration rates less than 15 ml/min/1.73 m2. Patients with nephrocalcinosis were excluded. The clinical ...
The above-mentioned article has the following corrections.
Chronic kidney disease (CKD) is a worldwide public health problem. Although the relative risk of death for most communicable and noncommunicable diseases has improved worldwide, CKD is among the few disease states that have been associated with worsening mortality since 1990, and is now the 19th leading cause of global years of life lost.1 Even in developed countries like the United States and United Kingdom, the incidence and prevalence of CKD and end-stage renal disease remain high, and are associated with very high morbidity and mortality, due primarily to complications of cardiovascular disease.
Anemia is a common complication of chronic kidney disease. Use of erythropoiesis-stimulating agents (ESA) has been a mainstay of treatment since 1990. A series of large trials demonstrated that ESAs have serious safety problems, including increasing cardiovascular and thrombotic events, and death. Analyses suggest high pharmacologic doses of ESAs, rather than the highly achieved hemoglobin, may mediate harm. Hypoxia-inducible factor (HIF) activators stimulate endogenous erythropoietin production and enhance iron availability.
Hyperkalemia is a frequently detected electrolyte abnormality that can cause life-threatening complications. Hyperkalemia is most often the result of intrinsic (decreased glomerular filtration rate; selective reduction in distal tubule secretory function; impaired mineralocorticoid activity; and metabolic disturbances, such as acidemia and hyperglycemia) and extrinsic factors (e.g., drugs, such as renin-angiotensin-aldosterone system inhibitors, and potassium intake). The frequent use of renin-angiotensin-aldosterone system inhibitors in patients who are already susceptible to hyperkalemia (e.g., patients with chronic kidn...
In the above-mentioned article, Anton Wellstein ’s name was misspelled. The authors regret the error.
We read with great interest the study by Rubinow et al.1 on kidney function in association with alteration in the proteome of high-density lipoprotein (HDL), extending previous proteomic results2,3 to earlier stages of chronic kidney disease. However, we do not agree with the presentation and interpretation of the data for the following reasons . First, no quantitative raw data have been provided for proteins identified by mass spectrometry. Therefore, it is not possible for the reader to judge the quality of HDL preparations and the abundance of the individual proteins.
Insufficient oxygenation during pregnancy negatively influences kidney development, which likely serves as a predisposing factor in chronic kidney disease at later stages in life. In this issue of Kidney International, Kobayashi et al. demonstrate that deletion of prolyl hydroxylase 2 and 3, 2 of the major oxygen sensors, in the FoxD1 lineage cells reduces kidney size and inhibits nephrogenesis in mice. Temporospatial expression pattern and studies on additional knockouts suggest the involvement of hypoxia-inducible factor 2.
A number of histologic changes are associated with the medial arterial calcification that occurs in chronic kidney disease, leading to several different hypotheses concerning the underlying mechanism. Careful timing of these changes in relation to the onset of the calcification, as reported in this issue of the journal, can shed light on which changes are pathogenic as opposed to secondary in reaction to the calcification.
Ig light chain amyloidosis is a protein misfolding disease capable of causing multiorgan failure. Organ failure can be stopped by reducing the production of Ig light chain. The current study by Rezk et al. found that even patients with advanced chronic kidney disease can benefit if the serum free light chain can be substantially reduced within the first 3 months. This, if confirmed, can have a huge impact in the management of these patients.