losartan-potassium and Chronic-Kidney-Disease-Mineral-and-Bone-Disorder

Topics: Aged; Anemia; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Trials as Topic; Disease Progression; Electrolytes; Epidemiologic Methods; Erythropoietin; Hemodialysis Solutions; Humans; Hypertension; Kidney Failure, Chronic; Male; Models, Biological; Nutrition Disorders; Quality of Life; Renal Dialysis; Toxins, Biological; Uremia

Studies in rats with renal ablation indicate that anemia lessens, whereas its vigorous correction with recombinant human erythropoietin (r-HuEPO) worsens systemic and glomerular hypertension, factors known to promote progression of chronic renal failure (CRF). However, in human studies, use of r-HuEPO in predialysis patients has not been associated with worsening renal function, provided blood pressure control is achieved. Histological evidence of bone disease is common in early renal failure, and deficits in calcitriol synthesis seem to be an important factor in the pathogenesis of secondary hyperparathyroidism (HPTH) in early CRF. Reports to data, on the use of low dose active vitamin D metabolites in predialysis patients, indicate either a reversible decline or no decline in renal function. Adynamic bone disease, however, may ensure during such therapy if excessive reductions in serum intact parathyroid hormone concentrations occur. Recent data suggest that chronic metabolic acidosis decreases albumin synthesis, increases muscle proteolysis, and induces negative nitrogen balance in patients with CRF. Despite these experimental data, the clinical relevance of correction of metabolic acidosis in end-stage renal disease (ESRD) is still not defined. Even though therapy of metabolic acidosis in the adult patient with CRF remains conjectural at this time, reports indicate that its correction might lead to healing of osteomalacia and osteopenia, and possibly may decrease protein degradation and improve growth in children with CRF.

Topics: Acidosis; Adult; Anemia; Animals; Calcitriol; Calcium Compounds; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Erythropoietin; Humans; Kidney Failure, Chronic; Rats; Recombinant Proteins; Renal Dialysis

Topics: Anemia; Cardiovascular Diseases; Chronic Kidney Disease-Mineral and Bone Disorder; Erythropoiesis; Erythropoietin; Glutathione; Hemolysis; Humans; Kidney Failure, Chronic; Nutrition Disorders; Oxidation-Reduction

Topics: Aluminum; Angiotensin II; Chronic Kidney Disease-Mineral and Bone Disorder; Communicable Diseases; Erythropoietin; History, 20th Century; Humans; Insulin; Kidney Failure, Chronic; Renal Dialysis; Renin; Uremia; Vitamin D

The effects of removal of all renal tissue on hematopoiesis, osteodystrophy, blood pressure regulation and metabolic functions are reviewed; and, the indications for, and results of, bilateral nephrectomy are discussed. Nephrectomy results in a more severe anemia in dialysis patients which is poorly responsive to androgen therapy. No differences were detected in the severity of osteodystrophy between nephric and anephric patients. However, bilateral nephrectomy can occasionally result in the acute onset of hypocalcemia. Blood pressure regulation must be accomplished in the absence of a functioning renin-angiotensin system. This is largely on the basis of volume, but changes in vascular tone may also be significant. Little is known about the metabolic consequences of nephrectomies. The effect on substances metabolized by the kidney is an area for further investigation. Kidney tissue should be preserved, if at all possible, and nephrectomy performed only for specific indications.

Topics: Adult; Anemia; Angiotensin II; Blood Pressure; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Erythropoietin; Female; Hematocrit; Hematopoiesis; Humans; Hypocalcemia; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Nandrolone; Nephrectomy; Renal Dialysis; Renin; Testosterone; Vitamin D

Progressive renal failure occurs in a large number of patients even in the absence of the original cause of injury. It is suggested that the initial reduction in nephron number progressively damages the remaining ones. Various mechanisms underlie the pathogenesis of progressive glomerular injury. Several studies have extensively shown that both dietary protein restriction and pharmacologic intervention with ACE-inhibitiors and angiotensin receptor antagonists effectively slow the progression of chronic renal diseases. This article will present treatment recommendations designed to delay the progression of chronic renal disease, to optimize its medical management and to reduce complications induced by renal insufficiency including hypertension, renal osteodystrophy and anemia. Ten steps in the management of patients with chronic renal failure recommended by an international panel of experts based on existing guidelines are presented.

Topics: Anemia; Angiotensin-Converting Enzyme Inhibitors; Calcitriol; Calcium Channel Agonists; Chronic Kidney Disease-Mineral and Bone Disorder; Diuretics; Erythropoietin; Glomerular Filtration Rate; Humans; Hypertension, Renal; Kidney Failure, Chronic; Kidney Function Tests; Proteinuria; Renal Replacement Therapy

Adynamic bone disease (ABD) has an increasing prevalence in the dialysis population, more so in peritoneal dialysis patients. Anemia in patients with high turnover bone disease and high intact parathyroid hormone (iPTH) tends to be resistant to recombinant human erythropoietin (rHuEPO). The same problem may occur in patients with ABD; however, data are scarce. This study evaluates the effectiveness of rHuEPO in 32 chronic peritoneal dialysis patients, 9 with iPTH levels below 100 pg/mL for more than 6 months (group A, with ABD) and 23 with iPTH levels above 100 pg/mL (group B, without ABD). In group A and group B respectively, the dosage of rHuEPO was 141.8 +/- 59 U/kg/week and 144.8 +/- 77 U/kg/week, and hematocrit was 33.2% +/- 4.3% and 31.7% +/- 4.5% (p > 0.05). Iron indices, nutritional parameters, and bone indices were similar, except that group A had lower alkaline phosphatase and serum ferritin levels. The data suggest that patients with ABD may not be resistant to rHuEPO, but may even have a slightly better hematocrit at a similar rHuEPO dosage. Further studies in a larger number of patients are needed to confirm these findings.

Topics: Aged; Alkaline Phosphatase; Anemia; Chronic Kidney Disease-Mineral and Bone Disorder; Drug Resistance; Erythropoietin; Female; Ferritins; Hematocrit; Humans; Iron; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Peritoneal Dialysis; Recombinant Proteins

We evaluated the intraplatelet and plasma levels of transforming growth factor beta (TGF-beta) in patients with or without renal osteodystrophy (ROD) who were undergoing hemodialysis (HD). Intraplatelet and plasma levels of TGF-beta were examined before and after HD, and compared with those from healthy controls. Patients undergoing HD had significantly higher mean intraplatelet levels of TGF-beta before and after HD than did the healthy subjects (22.7 +/- 7.8 and 29.5 +/- 15.8 vs. 18.7 +/- 7.9 ng/10(5) platelets; p < .05). The mean intraplatelet and plasma levels of TGF-beta in patients after HD were significantly increased than those before HD and in healthy subjects (p < .05). Moreover, patients with ROD showed a significantly higher mean intraplatelet and plasma levels of TGF-beta than that without ROD (p < .05). To investigate the effects of TGF-beta on ROD in HD patients, we evaluated such parameters as parathyroid hormone (PTH) and alkaline phosphatase (ALP), which reflect the lesions of ROD. The mean intraplatelet level of TGF-beta was not correlated with either para-meter. Meanwhile, no correlation was observed between the intraplatelet level of TGF-beta and the hematocrit (Hct). Similarly, no correlation was observed between the intraplatelet levels of TGF-beta and the dose of erythropoietin (EPO) administered. These findings indicate that metabolism of TGF-beta occurs during HD and overproduction of TGF-beta may play an important role in the pathogenesis of ROD.

Topics: Blood Platelets; Case-Control Studies; Chronic Kidney Disease-Mineral and Bone Disorder; Enzyme-Linked Immunosorbent Assay; Erythropoietin; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Recombinant Proteins; Renal Dialysis; Transforming Growth Factor beta

Most patients with anemia caused by end-stage renal disease respond well to Epoetin alfa therapy, but in a small number the hematocrit fails to rise as expected. A potential cause of suboptimal response is osteitis fibrosa. Understanding the pathophysiology, manifestations, diagnosis, and treatment for osteitis fibrosa helps nurses to identify this condition as a cause of resistance to Epoetin alfa and to manage patients appropriately.

Topics: Adult; Anemia; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Erythropoietin; Humans; Kidney Failure, Chronic; Male; Phosphorus

Topics: Aged; Amyloidosis; Anticoagulants; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis Solutions; Erythropoietin; Heart Failure; Humans; Hypotension; Kidney Diseases; Membranes, Artificial; Middle Aged; Renal Dialysis; Survival Rate

Topics: Adult; Aged; Anemia; Bone and Bones; Chronic Kidney Disease-Mineral and Bone Disorder; Erythropoietin; Female; Humans; Male; Middle Aged; Recombinant Proteins; Renal Dialysis; Time Factors

Topics: Chronic Kidney Disease-Mineral and Bone Disorder; Erythropoietin; Glomerular Filtration Rate; Humans; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidneys, Artificial; Prostaglandins; Renal Dialysis; Vitamin D