The objective of this review is to provide a synthesis of the evidence on the effect of dietary salt and potassium intake on population blood pressure, cardiovascular disease, and mortality. Dietary guidelines and recommendations are outlined, current controversies regarding the evidence are discussed, and recommendations are made based on the evidence. Designed search strategies were used to search various databases for available studies. Randomized trials of the effect of dietary salt reduction and/or increased potassium intake on blood pressure, target organ damage, cardiovascular disease, and mortality were included. Fifty-two publications from January 1, 1990 to January 31, 2013 were identified for inclusion. Evidence from these studies demonstrate that a high salt intake not only increases blood pressure but also plays a role in endothelial dysfunction, cardiovascular structure and function, albuminuria and kidney disease progression, and cardiovascular morbidity and mortality in the general population. Conversely, dietary potassium attenuates these effects showing a linkage to reduction in stroke rates and cardiovascular disease risk. Various sub-populations, such as overweight and obese individuals and the aging adult, exhibit a greater sensitivity to the effects of reduced salt intake and may gain the most benefits. A diet that includes modest salt restriction while increasing potassium intake serves as a strategy to prevent and/or control hypertension and decrease cardiovascular morbidity and mortality. Thus, the body of evidence supports population-wide sodium reduction and recommended increases in dietary potassium as outlined by current guidelines as an essential public health effort to prevent kidney disease, stroke, and cardiovascular disease.

G. vaginalis, P. bivia, A. vaginae, and Megasphaera type I may play significant roles in iBV.

We tested for Mycoplasma genitalium in 157 HIV-infected men. Urogenital and rectal prevalence were 10.8% and 6.4%. Macrolide resistance mutations were detected in 70.6% and 80% of urogenital and rectal samples, and fluoroquinolone resistance mutations in 26.7% and 40%, respectively.

A common renal complication of multiple myeloma is "myeloma kidney," a condition also known as cast nephropathy. The renal lesions (casts) are directly related to the production of monoclonal immunoglobulin free light chains (FLCs), which coprecipitate with Tamm

IntroductionMultiple myeloma, a malignant plasma cell disorder, has an incidence rate of approximately 1.1% among all malignancies and constitutes 12%-13% of hematologic malignancies in the United States. 1 In a study examining newly diagnosed patients with multiple myeloma, the incidence of renal dysfunction, determined by serum creatinine elevation Ն 1.3 mg/dL, was 48%. These same investigators showed that an increase in the serum creatinine concentration to Ն 2.0 mg/dL portended a poor prognosis, with a 35% reduction in median survival compared with patients with normal serum creatinine concentrations. 2 Mortality was accentuated if patients developed end-stage kidney disease in the setting of multiple myeloma. In one study that examined outcomes in 3298 patients, the 2-year all-cause mortality was 58% compared with 31% for patients with end-stage kidney disease from other causes. 3 The immunoglobulin free light chain (FLC) is the culprit in most of these renal lesions, and the majority of patients with renal failure from monoclonal FLCs in this setting have tubulointerstitial renal disease. 4 These studies place importance on maintaining or improving renal function and emphasize the need to focus not only on the reduction of FLCs during treatment, but also on understanding the underlying renal pathophysiology.A major function of the kidney is to reclaim low-molecularweight proteins that appear in the glomerular ultrafiltrate. FLCs are low-molecular-weight proteins that readily undergo glomerular filtration and are processed by the proximal tubule epithelium. Specifically, FLCs are absorbed into the proximal tubule by a receptormediated complex that consists of megalin and cubilin. [5][6][7][8] Once endocytosed, proximal tubule epithelial cells hydrolyze the proteins and return the amino acid residues to the circulation. Under normal conditions, total serum FLC concentration is typically Ͻ 30 mg/L, and approximately 500 mg of FLCs are cleared daily by the kidney; however, in pathologic states such as multiple myeloma, serum levels exceeding 100 000 mg/L have been observed. 9,10 In addition, unlike other proteins, this renal reclamation process is complicated by intracellular oxidative stress due to the production of hydrogen peroxide, which promotes cytotoxicity and also initiates signaling cascades that produce a pro-inflammatory state with elaboration of monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6). 11,12 As is true for most progressive forms of renal disease regardless of underlying etiology, tubulointerstitial injury and fibrosis are invariant findings that contribute to a progressive loss of renal function. 13 Thus, receptor-mediated endocytosis and metabolism of monoclonal FLCs generates an intrarenal pro-inflammatory environment that exacerbates ongoing renal injury and tubulointerstitial fibrosis, promoting functional progression of the kidney disease.The intracellular signaling process is known to be mediated through oxidative activation of c-Src, the 60-kDa product of c-src, a...