Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Higher levels of albuminuria associate with increased risk for adverse outcomes independent of estimated GFR (eGFR), but whether albuminuria also associates with concurrent complications specific to chronic kidney disease (CKD) is unknown. Here, we assessed the association of spot albumin-to-creatinine ratio with anemia, acidosis, hyperphosphatemia, hypoalbuminemia, hyperparathyroidism, and hypertension among 30,528 adult participants in NHANES 1988-1994 and 1999-2006. After multivariable adjustment including eGFR, higher albumin-to-creatinine ratios associated with anemia, acidosis, hypoalbuminemia, hyperparathyroidism, and hypertension but only weakly associated with acidosis and anemia. Furthermore, the associations between albumin-to-creatinine ratio and both anemia and acidosis were not consistent across eGFR strata. Higher albumin-to-creatinine ratio levels did not associate with hyperphosphatemia. Lower eGFR associated with higher prevalence ratios for all complications, and these associations were stronger than those observed for the albumin-to-creatinine ratio; after multivariable adjustment, however, the associations between eGFR and both hypoalbuminemia and hypertension were NS. In conclusion, albuminuria and eGFR differentially associate with complications of CKD.
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PMID:Estimated GFR, albuminuria, and complications of chronic kidney disease. 2196 77

Acute kidney injury (AKI) is a rare complication of carcinoid syndrome. A 61-year-old man developed carcinoid syndrome 51 months after pneumonectomy for bronchial carcinoid, and 8 episodes of AKI 101 to 118 months after pneumonectomy. Serum chromogranin A and urine 5-hydroxyindoleacetic acid levels were elevated for more than 1 year before AKI occurred. Each episode was characterized by flushing, facial edema, mild diarrhea, necrosis of hepatic metastatic nodules, mild oliguria, hyponatremia, acidosis, hypokalemia, hypomagnesemia and hyperphosphatemia. He did not have elevated urine sodium levels or osmolality, hypotension or hypertension. Plasma levels of dopamine, epinephrine and norepinephrine, measured during a single episode, were markedly elevated. Serum creatinine levels returned to normal after most episodes. Hyponatremia persisted but was more severe during AKI. Elevated plasma levels of vasoactive substances other than 5-hydroxytryptamine, perhaps dopamine or other catecholamines, could explain recurrent AKI. The natriuretic effect of elevated plasma dopamine levels could explain chronic hyponatremia.
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PMID:Recurrent acute kidney injury associated with metastatic bronchial carcinoid. 2200 80

Hypertension is a complex disorder with high prevalence rates all over the world. We conducted the first genome-wide gene-based association scan for hypertension in a Han Chinese population. By analyzing genome-wide single-nucleotide-polymorphism data of 400 matched pairs of young-onset hypertensive patients and normotensive controls genotyped with the Illumina HumanHap550-Duo BeadChip, 100 susceptibility genes for hypertension were identified and also validated with permutation tests. Seventeen of the 100 genes exhibited differential allelic and expression distributions between patient and control groups. These genes provided a good molecular signature for classifying hypertensive patients and normotensive controls. Among the 17 genes, IGF1, SLC4A4, WWOX, and SFMBT1 were not only identified by our gene-based association scan and gene expression analysis but were also replicated by a gene-based association analysis of the Hong Kong Hypertension Study. Moreover, cis-acting expression quantitative trait loci associated with the differentially expressed genes were found and linked to hypertension. IGF1, which encodes insulin-like growth factor 1, is associated with cardiovascular disorders, metabolic syndrome, decreased body weight/size, and changes of insulin levels in mice. SLC4A4, which encodes the electrogenic sodium bicarbonate cotransporter 1, is associated with decreased body weight/size and abnormal ion homeostasis in mice. WWOX, which encodes the WW domain-containing protein, is related to hypoglycemia and hyperphosphatemia. SFMBT1, which encodes the scm-like with four MBT domains protein 1, is a novel hypertension gene. GRB14, TMEM56 and KIAA1797 exhibited highly significant differential allelic and expressed distributions between hypertensive patients and normotensive controls. GRB14 was also found relevant to blood pressure in a previous genetic association study in East Asian populations. TMEM56 and KIAA1797 may be specific to Taiwanese populations, because they were not validated by the two replication studies. Identification of these genes enriches the collection of hypertension susceptibility genes, thereby shedding light on the etiology of hypertension in Han Chinese populations.
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PMID:Identification of IGF1, SLC4A4, WWOX, and SFMBT1 as hypertension susceptibility genes in Han Chinese with a genome-wide gene-based association study. 2247 46

Vitamin D and its metabolites have wide-spread physiological roles far beyond the well described effects in skeletal biology. Many physiological processes are directly or indirectly regulated by vitamin D and in consequence, vitamin D deficiency is implicated in numerous disease conditions. Summarizing previous assumptions on the optimal vitamin D levels in humans these data point towards calcidiol levels of approximately 30 ng/ml as being sufficient. The role of vitamin D deficiency in cardiovascular disease is a relatively novel field of interest. Well substantiated experimental data describe convincingly regulatory effects of vitamin D regarding various cardiovascular risk factors such as hypertension and diabetes mellitus. Activation of the vitamin D receptor suppresses e.g. the renin-angiotensin system. These experimental data are strongly supported by epidemiological and observational human data that link vitamin D deficiency to the incidence, degree and prevalence of cardiovascular risk factors and disease conditions. In contrast to the in vivo data and to the homogenous non-interventional observations, we know much less about controlled prospectively evaluated supplementation of vitamin D as a potentially therapeutic agent on cardiovascular events. High quality, large, and randomized controlled trials aiming primarily on cardiovascular end-points are absent. Speculations about the vitamin D usage in prevention or therapy of cardiovascular disease need to take potential drawbacks of vitamin D overdosing into account: Vitamin D overdosing might induce hypercalcemia, hyperphosphatemia, and increases in fibroblast growth-factor 23. The limited evidence regarding vitamin D therapy currently prevents general recommendations for vitamin D application in cardiology.
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PMID:The role of vitamin D in cardiovascular disease: from present evidence to future perspectives. 2292 24

Pseudohypoparathyroidism is an infrequently encountered disease. It is one of the causes of Fahr syndrome which also is a rare clinical entity caused by multiple diseases. A 4-year-old man hospitalized for sudden onset left hemiparesis and hypertension was diagnosed to have right thalamic and midbrain hemorrhage on plain CT scan of the head which also revealed co-existent extensive intracranial calcifications involving the basal ganglia and cerebellum bilaterally. General physical examination revealed features of Albright hereditary osteodystrophy, goitre, hypertension, left hemiparesis, and signs of cerebellar dysfunction. Laboratory findings suggested hypocalcemia, hyperphosphatemia along with high TSH, low FT(4), low FT(3), and high anti-TPO antibody. Though bilateral intracranial calcifications are usually encountered as an incidental radiological finding in the CT scan of brain, in this case, the patient admitted for thalamic and midbrain hemorrhage was on investigation for associated intracranial calcification, and goitre was also found to have coexisting pseudohypoparathyroidism and autoimmune hypothyroidism.
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PMID:Intracranial hemorrhage revealing pseudohypoparathyroidism as a cause of fahr syndrome. 2293 38

The survival rate of dialysis patients, as determined by risk factors such as hypertension, nutritional status, and chronic inflammation, is lower than that of the general population. In addition, disorders of bone mineral metabolism are independently related to mortality and morbidity associated with cardiovascular disease and fracture in dialysis patients. Hyperphosphatemia is an important risk factor of, not only secondary hyperparathyroidism, but also cardiovascular disease. On the other hand, the risk of death reportedly increases with an increase in adjusted serum calcium level, while calcium levels below the recommended target are not associated with a worsened outcome. Thus, the significance of target levels of serum calcium in dialysis patients is debatable. The consensus on determining optimal parathyroid function in dialysis patients, however, is yet to be established. Therefore, the contribution of phosphorus and calcium levels to prognosis is perhaps more significant. Elevated fibroblast growth factor 23 levels have also been shown to be associated with cardiovascular events and death. In this review, we examine the associations between mineral metabolic abnormalities including serum phosphorus, calcium, and parathyroid hormone and mortality in dialysis patients.
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PMID:Mineral metabolic abnormalities and mortality in dialysis patients. 2352 83

Disordered potassium homeostasis is a common complication of chronic kidney disease and traditional management focuses on restricting potassium intake to avoid hyperkalemia. Permissive potassium intake carries the risk of hyperkalemia and hyperphosphatemia, and possibly may contribute to the development of uremic neuropathy. Excessive potassium restriction and removal by dialysis carries the risk of worsened chronic hypertension, intradialytic hypotension, renal fibrosis and cyst formation, and ventricular arrhythmias. Cohort studies have associated both hypokalemia and hyperkalemia with increased mortality in CKD. A single study of potassium intake in hemodialysis patients found increased intake associated with increased mortality despite adjustment for serum potassium concentration. We recommend avoiding mandatory potassium restriction in early chronic kidney disease. We endorse routine potassium restriction in advanced chronic kidney disease requiring hemodialysis and close monitoring of serum potassium concentration in any patients receiving renin-angiotensin-aldosterone system blockers.
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PMID:Chronic renal disease progression: treatment strategies and potassium intake. 2395 6

Acute kidney injury predisposes patients to the development of both chronic kidney disease and end-stage renal failure, but the molecular details underlying this important clinical association remain obscure. We report that kidney injury molecule-1 (KIM-1), an epithelial phosphatidylserine receptor expressed transiently after acute injury and chronically in fibrotic renal disease, promotes kidney fibrosis. Conditional expression of KIM-1 in renal epithelial cells (Kim1(RECtg)) in the absence of an injury stimulus resulted in focal epithelial vacuolization at birth, but otherwise normal tubule histology and kidney function. By 4 weeks of age, Kim1(RECtg) mice developed spontaneous and progressive interstitial kidney inflammation with fibrosis, leading to renal failure with anemia, proteinuria, hyperphosphatemia, hypertension, cardiac hypertrophy, and death, analogous to progressive kidney disease in humans. Kim1(RECtg) kidneys had elevated expression of proinflammatory monocyte chemotactic protein-1 (MCP-1) at early time points. Heterologous expression of KIM-1 in an immortalized proximal tubule cell line triggered MCP-1 secretion and increased MCP-1-dependent macrophage chemotaxis. In mice expressing a mutant, truncated KIM-1 polypeptide, experimental kidney fibrosis was ameliorated with reduced levels of MCP-1, consistent with a profibrotic role for native KIM-1. Thus, sustained KIM-1 expression promotes kidney fibrosis and provides a link between acute and recurrent injury with progressive chronic kidney disease.
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PMID:Chronic epithelial kidney injury molecule-1 expression causes murine kidney fibrosis. 2475 24

Endothelial dysfunction underlies multiple cardiovascular consequences of chronic kidney disease (CKD) and antecedent diabetes or hypertension. Endothelial insults in CKD or end-stage renal disease (ESRD) patients include uremic toxins, serum uric acid, hyperphosphatemia, reactive oxygen species, and advanced glycation endproducts (AGEs). Sevelamer carbonate, a calcium-free intestinally nonabsorbed polymer, is approved for hyperphosphatemic dialysis patients in the US and hyperphosphatemic stage 3-5 CKD patients in many other countries. Sevelamer has been observed investigationally to reduce absorption of AGEs, bacterial toxins, and bile acids, suggesting that it may reduce inflammatory, oxidative, and atherogenic stimuli in addition to its on-label action of lowering serum phosphate. Some studies also suggest that noncalcium binders may contribute less to vascular calcification than calcium-based binders. Exploratory sevelamer carbonate use in patients with stages 2-4 diabetic CKD significantly reduced HbA1c, AGEs, fibroblast growth factor (FGF)-23, and total and low-density lipoprotein (LDL) cholesterol versus calcium carbonate; inflammatory markers decreased and defenses against AGEs increased. Sevelamer has also been observed to reduce circulating FGF-23, potentially reducing risk of left ventricular hypertrophy. Sevelamer but not calcium-based binders in exploratory studies increases flow-mediated vasodilation, a marker of improved endothelial function, in patients with CKD. In contrast, lanthanum carbonate and calcium carbonate effects on FMV did not differ in hemodialysis recipients. The recent independent-CKD randomized trial compared sevelamer versus calcium carbonate in predialysis CKD patients (investigational in the US, on-label in European participants); sevelamer reduced 36-month mortality and the composite endpoint of mortality or dialysis inception. Similarly, independent-HD in incident dialysis patients showed improved survival with 24 months of sevelamer versus calcium-based binders. This review discusses recent exploratory evidence for pleiotropic effects of sevelamer on endothelial function in CKD or ESRD. Endothelial effects of sevelamer may contribute mechanistically to the improved survival observed in some studies of CKD and ESRD patients.
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PMID:Sevelamer revisited: pleiotropic effects on endothelial and cardiovascular risk factors in chronic kidney disease and end-stage renal disease. 2432 30

The fear of malnutrition, caused by the low-protein diet, conditions in an inappropriate use of a useful nutrition therapy in Chronic Kidney Disease. Often malnutrition is due to reduced intake of energy, because a low (or very low) protein proper diet with adequate amount of calories (30-35 cal/kg bw/day). We analyze the positive aspects of the low-protein diet for optimal control of hypertension, hyperphosphatemia, anemia, and proteinuria that is the goal of pharmacological management Chronic Kidney Disease patients.
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PMID:[Phosphate control in end stage renal disease: barriers and opportunities. Malnutrition: yes or not?]. 2390 Oct 51


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