Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persistent hyperparathyroidism is observed in 17% to 50% of patients at 1 year after renal transplantation. In 10% of these patients, hypercalcemia is also present. This condition increases the risk of vascular calcification, correlating with inferior graft function among patients with interstitial calcification in the renal allograft. Hypertension is appears in 60% to 90% of patients after transplantation, favoring progressive graft dysfunction. Hypercalcemia per se causes hypertension. Parathyroid hormone can potentiate the pressor effects of hypercalcemia. Fourteen renal transplant recipients were included based upon: total serum calcium > 10.0 mg/dL, intact parathyroid hormone levels > 70 pg/mL, graft function > 6 months, creatinine clearance > 50 mL/min, and stable immunosuppressive therapy. We also examined blood pressure and antihypertensive treatment. Initially patients received 30 mg of cinacalcet once a day. The follow-up was up to 6 months. The mean cinacalcet dose was 40 mg/24 h. Five patients received 60 mg/24 h. Both serum calcium and iPTH decreased significantly from 10.6 (DE 0.4) to 9.8 (DE Both serum calcium and iPTH decreased significantly from 10.6 (DE 0.4)to 9.8 (DE 0.6) mg/dL (P < .001) and from 195.0 (DE 140.0) to 118.62 (DE 102.2; P < .0001). There were no significant changes in renal function, proteinuria, or tacrolimus levels. Mean blood pressure diminished from 94.1 (DE 12.0) to 88.0 (DE 7.5) mm Hg (P < .019) with no changes in antihypertensive treatment. Cinacalcet was suspended in one patient because of gastrointestinal discomfort and in another one because the iPTH was reduced to 51 pg/mL. Cinacalcet is an effective treatment for persistent hyperparathyroidism associated with hypercalcemia among renal transplant patients and may be helpful for hypertension control.
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PMID:Treatment of persistent hyperparathyroidism in renal transplant patients with cinacalcet improves control of blood pressure. 1971 27

Chronic kidney disease (CKD) is a strong risk factor for cardiovascular events and death. Hypertension, dyslipidemia, anemia, vascular calcification, and secondary hyperparathyroidism have all been implicated in the pathogenesis of cardiovascular disease associated with CKD. Numerous trials have been performed assessing the effects of modifying these risk factors on cardiovascular events and on the progression to end-stage renal disease. Many guidelines have been issued. In this article we review the guidelines and the strength of evidence supporting them. Specifically, we discuss blood pressure goals for patients with CKD, the role of renin-angiotensin system blocking agents for blood pressure control and proteinuria reduction, and the evidence for treatment recommendations of dyslipidemia. We review the trials addressing risks and benefits of different hemoglobin targets for treatment of anemia with erythropoietin. The use of phosphate-binding drugs to prevent and treat secondary hyperparathyroidism is likely beneficial, but few data support the use of vitamin D compounds. Supplementation with sodium bicarbonate may be an inexpensive treatment to retard progression to end-stage renal disease. The article concludes with a discussion of the case vignette presented in the previous article.
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PMID:Management of chronic kidney disease: what is the evidence? 2013 75

There is increasing emphasis on chronic kidney disease (CKD), owing to its prevalence and its association with cardiovascular risk. Important issues concerning treatment of CKD are delaying its progression, improving patients' quality of life, and decreasing related mortality. These issues can be addressed with certain therapeutic options, targeting proteinuria, anemia, and secondary hyperparathyroidism. The management options and possible benefits related to treatment of these complications of CKD are reviewed.
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PMID:Outpatient management of chronic kidney disease: proteinuria, anemia and bone disease as therapeutic targets. 2035 Jun 54

Chronic kidney disease has been increasingly recognized as a risk factor for incident heart failure. Despite advances in chronic heart failure treatment, the prognosis remains poor. The annual mortality from all cardiovascular causes in the end stage renal disease population is significantly higher than the general population, accounting for more than half of all deaths in this group. The mechanisms underlying the enhanced susceptibility to myocardial ischemia in chronic kidney disease are not well defined. Traditional cardiovascular risk factors, although common in chronic kidney disease, do not exert the same impact as in the general population. The presence of "renal-specific" non-traditional risk factors including endothelial dysfunction, inflammation, oxidative stress, anaemia, proteinuria and changes in vitamin D metabolism (encompassing the complex interactions of calcium and phosphate metabolism, hyperparathyroidism and vascular calcification) play an important role in cardiovascular disease progression. An increased understanding of the array of metabolic changes/adaptations occurring in uraemic heart disease have allowed one to consider optimal management strategies and to develop new strategies for future management of uraemic heart disease.
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PMID:Risk factors and metabolic mechanisms in the pathogenesis of uraemic cardiac disease. 2119 37

A 35-year-old woman was admitted to the Nephrology and Dialysis Unit of Pisa University for hypertension, hypokalaemia, renal impairment, proteinuria and hyperglycaemia. plasma renin activity (PRA) and plasma aldosterone were elevated, but Doppler ultrasound and angio-computed tomography (CT) of renal arteries were normal. Abdomen CT revealed only a left adrenal mass, and measurement of catecholamines suggested the diagnosis of pheochromocytoma. Biochemical findings suggestive of hyperparathyroidism were also detected, but a multiple endocrine disorder was excluded by genetic analysis. Pathology examination confirmed the pheochromocytoma and immunohistochemistry also showed positivity for parathyroid hormone. After surgery, disappearance of the symptoms and normalization of all haemodynamic and humoral parameters was observed. This is a rare case of pheochromocytoma responsible for secondary hyperaldosteronism, hyperparathyroidism, proteinuric renal disease and diabetes mellitus.
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PMID:A case of pheochromocytoma presenting as secondary hyperaldosteronism, hyperparathyroidism, diabetes and proteinuric renal disease. 2121 67

Calcimimetics increase the sensitivity of the parathyroid calcium-sensing receptor to extracellular calcium for efficient control of hyperparathyroidism. Recent studies suggest that there are beneficial effects of calcimimetics beyond the control of bone and mineral homeostasis. Here, we tested whether the calcium-sensing receptor is also expressed and functionally relevant in podocytes. Analysis of microarray data using Gene Set Enrichment Analysis found that the calcimimetic R-568 influenced various pathways related to oxidative stress, cytoskeletal regulation, cell proliferation, and survival in cultured podocytes. R-568 induced a dose- and time-dependent phosphorylation of the ERK1/2-P90RSK-CREB signaling cascade, and induced pro-survival phosphorylation of BAD and Bcl-xl, thus reducing puromycin aminonucleoside (PAN)-induced podocyte apoptosis by half. Moreover, R-568 preserved the actin cytoskeleton in podocytes exposed to PAN and improved recovery from exposure to cytochalasin D, a reversible inhibitor of actin polymerization. In rats, co-administration of R-568 prevented the proteinuria caused by a single dose of PAN and attenuated the glomerulosclerosis and loss of GFR caused by repetitive puromycin treatment. Hence, calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton-stabilizing effects and may constitute a new approach in the prevention and treatment of glomerular disease.
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PMID:Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis. 2184 33

Secondary hyperparathyroidism is a characteristic feature of chronic kidney disease, which develops early in the course of chronic kidney disease, often in a progressive way. It occurs as the renal function continues to decline and is encountered following a series of biochemical abnormalities, which are responsible for initiation and maintenance of increased parathyroid hormone (PTH) secretion. Several agents are used in the management of secondary hyperparathyroidism. Paricalcitol is a new generation selective vitamin D receptor activator that lowers PTH levels by exerting a less hypercalcaemic and hyperphosphataemic effect. In addition, there is emerging evidence of the benefit of paricalcitol in preventing intravascular calcification and proteinuria.
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PMID:Paricalcitol in secondary hyperparathyroidism and the survival benefit in patients with chronic kidney disease. 2156 42

No study has reported the current status of the management of chronic kidney disease mineral bone disorder (CKD-MBD) in Japan. Using the Osaka Vitamin D Study in CKD (OVIDS-CKD), we examined the prevalence of patients with serum calcium, phosphate, parathyroid hormone (PTH), or 25-hydroxyvitamin D levels outside the target of KDOQI guidelines. Eighty-four percent of the patients had 25-hydroxyvitamin D <30 ng/mL. Significant determinants of poor vitamin D status were female gender, diabetes, high PTH, and high urinary protein (2+ or greater). The percentage of patients with intact PTH higher than the target was 8% in CKD stage 3a, while between 20-22% in stages 3b to 5. The patients indicated for ergocalciferol were 7, 18, and 19% in stages 3a, 3b, and 4, respectively, and those indicated for active vitamin D were 21% in stage 5. Since neither ergocalciferol nor cholecalciferol is available in 2011 in Japan, we have no choice but to prescribe alfacalcidol or calcitriol; however, the percent of patients receiving these drugs was only 1, 4, 8, and 14% in stages 3a, 3b, 4, and 5, respectively, indicating that PTH and vitamin D status are not well controlled in Japan. In contrast, more than 80% of the patients met the target of serum calcium and phosphate. Contrary to expectations, nearly 20% of the patients had hypophosphatemia in stage 3 and 5, possibly because of strict protein restriction. Given these results, nephrologists should consider prescribing active vitamin D, especially for females and patients with diabetes, massive proteinuria, or secondary hyperparathyroidism.
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PMID:Guideline-practice gap in the management of predialysis chronic kidney disease mineral bone disorder in Japan. 2159 44

Vitamin D deficiency is common in adult renal transplant recipients, but data in children are scarce. Vitamin D is shown to have multiple effects on the cardiovascular system, renal function, and maintenance of bone health. We hypothesized that 25(OH)D deficiency is common in pediatric renal transplant recipients, and may be associated with hyperparathyroidism, short stature, renal function, and blood pressure control. We recruited 106 children during the winter/spring season who had a functioning renal transplant for at least 3 months. Twenty-five hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] were measured and correlated with clinical and biochemical parameters. Of the renal transplant patients, 38% were 25(OH)D deficient, 54% had insufficient levels, and only 8% had adequate 25(OH)D levels. Despite alfacalcidol supplementation in 59 (56%) patients, parathyroid hormone was increased in 58 (55%) and showed an inverse correlation with 25(OH)D (p = 0.0003, r = 0.61) but not with 1,25(OH)(2)D levels. Height standard deviation score (SDS) correlated with 25(OH)D (p = 0.007, r = 0.42) and time post transplantation (p = 0.02, r = 0.23); both were significant and independent predictors of height SDS. 25(OH)D inversely correlated with systolic BP SDS (p = 0.02, r =-0.26); this association was lost on multiple regression analysis, but 25(OH)D was the only modifiable risk factor for hypertension. There was no correlation with estimated GFR or proteinuria. In conclusion, 25(OH)D deficiency is common in pediatric renal transplant recipients and correlates with hyperparathyroidism and short stature. 25(OH)D deficiency may be a modifiable risk factor for hypertension in transplant recipients. Further studies are required to test if routine supplementation with ergo or cholecalciferol is safe and effective in children after renal transplantation.
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PMID:Vitamin D deficiency is associated with short stature and may influence blood pressure control in paediatric renal transplant recipients. 2164 44

Because secondary hyperparathyroidism is associated with morbidity and mortality in patients with chronic kidney disease, suppression of parathyroid hormone (PTH) and minimization of associated derangements in mineral metabolism are cardinal therapeutic goals. There is an ongoing debate regarding the proper treatment strategy for PTH suppression in this population. While some practitioners believe that calcitriol analogues should be the primary therapy in this setting, others contend that calcimimetics offer unique treatment benefits. Recent advancements in the understanding of the pathophysiology of secondary hyperparathyroidism and the secondary effects of these agents may help clarify this debate. Here, we review the classical actions of calcitriol analogues and calcimimetics on mineral metabolism. We also examine the potential nonclassical effects of these therapies on the renin-angiotensin-aldosterone system, proteinuria, vascular calcification, fibroblast growth factor-23, inflammation, and overall survival.
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PMID:Does it matter how parathyroid hormone levels are suppressed in secondary hyperparathyroidism? 2168 72


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