Reviews recent experimental and clinical data pertaining to the role of abnormal lipid metabolism in patients with hypertension and renal disease. Amongst the areas covered are hypercholesterolemia, hyperglycemia and hypertension and lipid abnormalities after renal transplantation.

During the past decade, experimental and clinical studies have suggested that dyslipidemia may be an important risk factor for the progression of renal disease. This volume explores in great detail recent advances in our understanding of the pathogenesis and treatment of this common complication of progressive renal injury. In the experimental investigations presented, emphasis is placed on specific disturbances of lipids that are seen in progressive renal disease including the effects of oxidatively modified lipoproteins and Lp(a) on various functions of the glomerular cells. Clinical studies have identified dyslipidemia as a risk factor for progressive renal disease in diabetes mellitus, various non-diabetic renal diseases, and most recently in patients with progressive renal allograft loss. An emerging interest in the genetics of dyslipidemia has recently arisen and this topic as it specifically relates to progressive renal disease is discussed. The final section of the book offers new insights into the mechanisms of action of antilipemic therapy used in the treatment of dyslipidemia. This volume should be read by all nephrologists caring for patients with progressive renal disease and by physicians interested in the biology of lipids, diabetes and essential hypertension.

Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various metabolic processes in adulthood. Such FGFs, collectively called endocrine FGFs, are comprised of three members (FGF15/19, FGF21, and FGF23: FGF15 is the mouse ortholog of human FGF19). These endocrine FGFs share a common structural feature that enables the endocrine mode of action at the expense of the affinity to FGF receptors. To restore the affinity to FGF receptors in their target organs, the endocrine FGFs have designated the Klotho family of transmembrane proteins as obligate co-receptors. By expressing Klothos in a tissue-specific manner, this unique co-receptor system also enables the endocrine FGFs to specify their target organs among many tissues that express FGF receptors.

Dyslipidemia is a major risk factor for cardiovascular events, cardiovascular mortality, and all-cause mortality. The earlier in life dyslipidemia is treated, the better the prognosis. The current book is an excellent one on dyslipidemia written by experts on this topic. This book includes 12 chapters including 5 on lipids, 4 on hypercholesterolemia in children, and 3 on the treatment of dyslipidemia. This book should be read by all health care professionals taking care of patients, including pediatricians since atherosclerotic cardiovascular disease begins in childhood.

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a highly prevalent hereditary renal disorder in which fluid-filled cysts are appeared in both kidneys. Main causative genes of ADPKD are PKD1 and PKD2, encoding for polycystin-1 (PC1) and polycystin-2 (PC2) respectively. Those proteins are localized on primary cilia and function as mechanosensor in response to the fluid flow, translating mechanistic stimuli into calcium signaling. With mutations either of PKD1 or PKD2, hyper-activated renal tubular epithelial cell proliferation is observed, followed by disrupted calcium homeostasis and aberrant intracellular cyclic AMP (cAMP) accumulation. Increased cell proliferation with fluid secretion leads to the development of thousands of epithelial-lined, fluid-filled cysts in kidneys. It is also accompanied by interstitial inflammation, fibrosis, and finally reaching end-stage renal disease (ESRD). In human ADPKD, the age at which renal failure typically occurs is later in life, however no specific targeted medications are available to cure ADPKD. Recently, potential therapeutic targets or surrogate diagnostic biomarkers for ADPKD are proposed with the advances in the understanding of ADPKD pathogenesis, and some of them were attempted for clinical trials. Herein, we will summarize genetic and epi-genetic molecular mechanisms in ADPKD progression, and overview the currently available biomarkers or potential therapeutic reagents suggested.