Cofilin is a actin-binding protein in eukaryotic cells. It plays a role in maintaining the steady state of the internal environment through regulating actin dynamics, which contributes to the development of various kinds of diseases. In recent 20 years, cofilin has been widely attracted due to its regulatory effect on cell phenotype, gene transcription, apoptosis and inflammation in renal tissue. Cofilin plays a regulatory role in pathological changes in proteinuria diseases such as minimal change nephropathy, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy. It could be one of the diagnosis index for glomerular podocyte injury. At the same time, cofilin plays a key role in maintaining the polarity and function of proximal tubular epithelial cells and it is involved in the regulation of kidney inflammation in a variety of kidney diseases, such as renal ischemia/reperfusion injury, diabetic nephropathy, and hypertensive nephropathy reaction. In addition, cofilin plays an important role in epithelial-to-mesenchymal transition (EMT) of tumor cells and epithelial cells in various tissues, suggesting that cofilin may be involved in the regulation of peritoneal dialysis-related EMT and fibrosis. Cofilin might turn into the new diagnosis and treatment target of kidney diseases.
Cofilin 1 ; metabolism ; Glomerulosclerosis, Focal Segmental ; physiopathology ; Humans ; Kidney ; physiopathology ; Kidney Diseases ; physiopathology ; Proteinuria ; genetics ; physiopathology

Cardiovascular Diseases ; physiopathology ; Humans ; Inflammatory Bowel Diseases ; metabolism ; Kidney Diseases ; metabolism ; Neoplasms ; Vitamin D ; pharmacology ; physiology

Bone Density ; Coronary Artery Disease ; metabolism ; physiopathology ; Diabetes Mellitus, Type 1 ; metabolism ; physiopathology ; Humans ; Hypertension ; metabolism ; physiopathology ; Kidney Diseases ; metabolism ; physiopathology ; Macrophages ; metabolism ; Neoplasms ; metabolism ; physiopathology ; Receptors, Calcitriol ; physiology ; Risk Factors ; Skin Diseases ; metabolism ; physiopathology ; Vitamin D ; metabolism ; physiology

Aging is associated with progressive functional deterioration and structural changes in the kidney. Changes in the activity or responsiveness of the renin-angiotensin system (RAS) occur with aging. RAS changes predispose the elderly to various fluid and electrolyte imbalances as well as acute kidney injury and chronic kidney disease. Among the multiple pathways involved in renal aging, the RAS plays a central role. This review summarizes the association of the RAS with structural and functional changes in the aging kidney and age-related renal injury, and describes the underlying mechanisms of RAS-related renal aging. An improved understanding of the renal aging process may lead to better individualized care of the elderly and improved renal survival in age-related diseases.
Acute Kidney Injury/etiology/metabolism/physiopathology ; Age Factors ; Aging/genetics/*metabolism ; Animals ; Glucuronidase/genetics/metabolism ; Humans ; Kidney/*metabolism/physiopathology ; Kidney Diseases/*etiology/genetics/metabolism/physiopathology ; Prognosis ; *Renin-Angiotensin System ; Risk Factors

Bone Diseases, Metabolic ; physiopathology ; Bone and Bones ; metabolism ; physiopathology ; Child ; Child Nutrition Disorders ; physiopathology ; Child Nutritional Physiological Phenomena ; physiology ; Humans ; Infection ; physiopathology ; Kidney Failure, Chronic ; physiopathology

The klotho gene was originally identified as a putative age-suppressing gene in mice that extends life span when overexpressed. It induces complex phenotypes resembling human premature aging syndromes when disrupted. The gene was named after a Greek goddess Klotho who spun the thread of life. Since then, various functional aspects of the klotho gene have been investigated, leading to the identification of multiple novel endocrine axes that regulate various metabolic processes and an unexpected link between mineral metabolism and aging. The purposes of this review were to overview recent progress on Klotho research and to discuss a novel aging mechanism.
Aging/genetics/*metabolism ; Animals ; Chronic Disease ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics/*metabolism ; Homeostasis ; Humans ; Kidney Diseases/metabolism/physiopathology ; Phenotype ; Phosphates/metabolism ; Phosphorus, Dietary/metabolism ; *Signal Transduction

OBJECTIVETo establish a kidney deficient aging model (KDAM), assess it in antioxidant capacity, HPAT axis function and bone metabolism, and compare with D-galactose aging model.

METHODAging rat model was established by injecting D-galactose solution, meanwhile dexamethasone solution was injected to establish kidney deficient aging model. Then these models were evaluated by serum MDA (malondialdehyde) and GSH-Px (glutathione peroxidase), liver SOD (superoxide dismutase), adrenal, thymus and spleen index, CD4(+), CD8(+), and serum COR (cortisol), BGP (bone Gla-protein), plasma ACTH (adrenocorticotropic hormone) and CRH (corticotropin-releasing hormone).

RESULTCompared with the normal group, the aging model group and the kidney deficient aging group showed significant decrease in liver SOD activity (P < 0.01 on average) and significant increase in serum MDA content (P < 0.01 on average) , and the kidney deficient aging group revealed remarkable decline in plasma ACTH content (P < 0.05). Compared with the normal group and the aging model group, the kidney deficient aging model group's weight, serum GSH-Px decreased (P < 0.01, P < 0.05), adrenal index decreased (P < 0.05, P < 0.01), serum COR decreased (P < 0.05 on average), plasma CRH increased (P < 0.05, P < 0.01), serum BGP content significantly decreased (P < 0.01 on average), value of CD4(+), CD8(+) decreased (P < 0.05, P < 0.01), CD4(+)/CD8(+) increased, but without significant difference.

CONCLUSIONThe kidney deficient aging model shows significant decrease in antioxidant capacity, dysfunction of HPAT axis disorder and abnormal bone metabolism. However, D-galactose aging model only shows a significant difference in antioxidant capacity.

Aging ; drug effects ; physiology ; Animals ; Antioxidants ; metabolism ; Disease Models, Animal ; Galactose ; adverse effects ; Humans ; Kidney ; physiopathology ; Kidney Diseases ; chemically induced ; metabolism ; physiopathology ; Liver ; enzymology ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism

One of the most important drug-related problems in patients with chronic kidney disease (CKD) is medication dosing errors. Many medications and their metabolites are eliminated through the kidney. Thus, adequate renal function is important to avoid toxicity. Patients with renal impairment often have alterations in their pharmacokinetic and pharmacodynamic parameters. The clearance of drugs eliminated primarily by renal filtration is decreased by renal disease. Therefore, special consideration should be taken when these drugs are prescribed to patients with impaired renal function. Despite the importance of dosage adjustment in patients with CKD, such adjustments are sometimes ignored. Physicians and pharmacists can work together to accomplish safe drug prescribing. This task can be complex and require a stepwise approach to ensure effectiveness, minimise further damage and prevent drug nephrotoxicity.
Chronic Disease ; Decision Trees ; Drug Prescriptions ; standards ; Glomerular Filtration Rate ; Humans ; Kidney Diseases ; metabolism ; physiopathology ; Prescription Drugs ; administration & dosage ; pharmacokinetics

Diseases of the peripheral nervous system are the most prevalent in patients with end-stage renal disease (ESRD). Although increased blood levels of lead in ESRD have been reported, the role of lead remains to be elucidated. The purpose of this study was to determine the connection of blood lead concentration with peripheral nerve conduction velocity. One hundred ninety-eight healthy subjects (control group) and 68 patients with ESRD undergoing hemodialysis (ESRD group) were enrolled. Nerve conduction was measured within two hours after hemodialysis. Orthodromic sensory nerve action potentials and compound muscle action potentials were recorded on the median, ulnar, and radial nerves. Hemoglobin-corrected blood lead was significantly higher in ESRD patients than in controls (9.1+/-2.8 microgram/dL vs. 5.9+/-2.3 microgram/dL, p<0.001). 32.4% of 68 ESRD patients with diabetes mellitus were significantly related to poorer motor and sensory nerve conduction velocity (p<0.001). However, blood lead was not a significant predictor of the nerve conduction velocity (p>0.05). Our result suggested that even though the blood lead levels were high in ESRD, they were not associated with the decline of peripheral nerve function. Diabetes mellitus is a primary independent risk of neuropathy in ESRD patients.
Peripheral Nervous System Diseases/blood/etiology/physiopathology ; Peripheral Nerves/physiopathology ; Neural Conduction/*physiology ; Middle Aged ; Male ; Lead/*blood/metabolism ; Kidney Failure, Chronic/*blood/complications/*physiopathology ; Humans ; Female ; Diabetic Neuropathies/blood/physiopathology ; Case-Control Studies ; Bone and Bones/metabolism ; Body Burden ; Adult

Partial nature of "promoting blood circulation and dieresis" of Salvia Miltiorrhizain was initially demonstrated by investigating the regulation effect of AQP2 expression in kidney of trauma blood stasis model rats with the Salvia Miltiorrhizain so as to provide guidance for its clinical deployment of administration. Random allocation was taken to averagely divide 30 SD rats into two groups: 10 rats in normal group and 20 rats in blood stasis syndrome group. Trauma blood stasis rat model was established by quantitatively beating. Then the rat model group was divided into model group and salvia group. After 7 days of treatment, the rat kidney AQP2 expression was detected, the content of urine AQP2 was compared and the damaged local muscle and kidney pathological changes were observed by immunohistochemical method and western blot method. Compared with that of the normal group, rats in model group had inflammatory cells infiltration, blood stasis and edema of the injured local muscles and up-regulated AQP2 expression, decreasing urinary output, and kidney tissues blood stasis and edema (P < 0.05). On the other hand, compared with that of the model group, those parameters of rats in salvia group were all decreasing except urine output (P < 0.05). Such result indicated that Salvia Miltiorrhiza can reduce trauma blood stasis rat content of urine AQP2 and down-regulated AQP2 expression in kidney tissue, so as to reduce the reabsorption of water by renal tubular and increase urine output. The promoting blood circulation effect of Salvia Miltiorrhizain can alleviate the degree of the damaged tissue edema and encourage urine drainage. This therapy is closely related to the effect of regulating AQP2 in kidney by salvia, so the purpose of this study by verifying "promoting blood circulation and diuresis" as the mechanism for the regulation effect of the salvia on AQP2 expression.
Animals ; Aquaporin 2 ; genetics ; metabolism ; Blood Circulation ; drug effects ; Diuresis ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Kidney ; blood supply ; drug effects ; metabolism ; physiopathology ; Kidney Diseases ; drug therapy ; genetics ; metabolism ; physiopathology ; Male ; Rats ; Salvia miltiorrhiza ; chemistry