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)

Ginseng is consumed by 10% to 20% of adults in Asia and by up to 5% in Western countries. Despite observational evidence suggesting a link between its intake and the development of hypertension, there remains no long-term scrutiny for its effect on blood pressure (BP). We therefore undertook a randomized, placebo-controlled, double-blinded, crossover trial in 52 hypertensive individuals to determine the effect of 12-week North American ginseng intake on 24-hour BP; we also measured serum cystatin C as a marker of renal function. After a 4-week placebo run-in, we randomly assigned 52 participants to 3 g/day of ginseng or placebo for 12 weeks. This was followed by an 8-week washout and a subsequent 12-week period in which the opposite treatment was administered. At run-in and at weeks 0 and 12 of each treatment period, participants were fitted with an ambulatory BP monitor to assess 24-hour BP. The primary outcome was the treatment difference at week 12 in mean 24-hour systolic BP. Secondary outcomes were treatment differences at week 12 in other ambulatory BP parameters and serum cystatin C. Forty participants (77%) completed the trial, with 3 removed from main analysis (n=2, antihypertensive drug changes; n=1, incomplete ambulatory monitoring). In the remaining 37, 12-week ginseng treatment was associated with a neutral effect on all ambulatory BP parameters compared with placebo; an intention-to-treat analysis supported this. Ginseng did not affect serum cystatin C level. Overall, long-term ginseng use had no effect on 24-hour BP and renal function in hypertensive individuals.
Hypertension 2006 Apr
PMID:Long-term intake of North American ginseng has no effect on 24-hour blood pressure and renal function. 1652 Apr 10

The Kidney Disease Outcome and Quality Initiative (KDOQI) Group recommended guidelines for the monitoring and treatment of chronic kidney disease (CKD) in 2002. These recommendations were based on the prevalence of known complications as seen in adults. In children, the exact prevalence of these complications is unknown. We therefore conducted a cross-sectional study of 366 patients with CKD in a single center to analyze the prevalence of these complications across all stages of kidney disease. Patients were categorized to their KDOQI stage of CKD according to their estimated renal function as determined from serum cystatin C. Fifty seven percent of patients had CKD stage 1, 29.0% stage 2, 10.4% stage 3 and 4.1% stages 4+5. Uropathies (31%) were the most prevalent causes of CKD. Glomerular disease accounted for 27%. The overall prevalence of complications was as follows: hypertension 70.2%, anemia 36.6%, proteinuria 11.5%, and metabolic bone disease 16.9%. Metabolic bone disease and anemia occurred frequently, even with a glomerular filtration rate >60 ml/min/1.73 m2. Growth failure (11.5%) was also common and is not a component of the KDOQI guidelines for CKD in children. The prevalence of all complications increased with worsening stage of kidney disease (all P-values significant). In summary, this study supports the KDOQI guidelines in defining and staging CKD in children. This study also highlights the differences in the causes and complications that occur in CKD between adults and pediatrics. We recommend modification of the KDOQI guidelines for children to reflect the differences described in this paper.
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PMID:Prevalence of complications in children with chronic kidney disease according to KDOQI. 1678 89

We investigated whether or not p38 mitogen-activated protein kinase inhibition ameliorates angiotensin II-induced target organ damage. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGRs). dTGR, with or without p38 inhibitor (BIRB796; 30 mg/kg per day in the diet), and nontransgenic Sprague-Dawley rats were studied in 2 protocols. In protocol 1 (week 7), systolic blood pressure of untreated dTGRs was 204+/-4 mm Hg, but partially reduced after BIRB796 treatment (166+/-7 mm Hg), whereas Sprague-Dawley rats were normotensive. The cardiac hypertrophy index was unchanged in untreated and BIRB796-treated dTGRs. The beta-myosin heavy chain expression of BIRB796-treated hearts was significantly lower in BIRB796 compared with dTGRs, indicating a delayed switch to the fetal isoform. BIRB796 treatment significantly reduced cardiac fibrosis, connective tissue growth factor, tumor necrosis factor-alpha, interleukin-6, and macrophage infiltration. Albuminuria was not reduced in BIRB796-treated dTGRs. Tubular and glomerular damage with tumor necrosis factor-alpha expression was unaltered, although serum creatinine and cystatin C were normalized. Renal macrophage infiltration, fibrosis, and vessel damage were reduced. In protocol 2 (week 8), we focused on mortality and arrhythmogenic electrical remodeling. Mortality of untreated dTGRs was 100% but was reduced to 10% in the BIRB796 group. Cardiac magnetic field mapping showed prolongation of depolarization and repolarization in untreated dTGRs compared with Sprague-Dawley rats with a partial reduction by BIRB796. Programmed electrical stimulation elicited ventricular tachycardias in 81% of untreated dTGRs but only in 48% of BIRB796-treated dTGRs. In conclusion, BIRB796 improved survival, target organ damage, and arrhythmogenic potential in angiotensin II-induced target organ damage.
Hypertension 2007 Mar
PMID:p38 mitogen-activated protein kinase inhibition ameliorates angiotensin II-induced target organ damage. 1722 70

Cerebral amyloid angiopathy (CAA) is characterized by deposition of cerebrovascular amyloid protein in the media of leptomeningeal vessels. (amyloid B protein, cystatin C, transthyretin, gelsolin, and prion protein). It is a cause of cerebrovascular disorders including cerebral hemorrhage, cognitive impairment and unusually transient neurological symptoms. It is the main contributing factor to cerebral hemorrhage after hypertension in the elderly. We aimed to review epidemiological, pathophysiological and clinical and MRI imaging data in CAA.
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PMID:[Cerebral amyloid angiopathy]. 1730 82

This study investigates the association between serum cystatin C, serum creatinine concentrations, N-acetyl-beta-D-glucosaminidase (NAG enzymuria), urine alpha1-microglobulin (alpha1-MG) and beta2-microglobulin (beta2-MG) levels in subjects with type 2 diabetes (n=40, 20M/20F, age range 25-65 years; duration of diabetes 8-10 years) and age- and gender-matched healthy controls (n= 20). Exclusion criteria were absence of gross proteinuria, hypertension, dyslipidaemia or cardiovascular disease. Fasting blood samples and mid-stream specimen of urine (MSSU) were collected and serum creatinine, cystatin C, urine creatinine, NAG enzymuria, alpha1-MG and beta2-MG were measured. Diabetic subjects were separated into two groups based on albumin:creatinine concentration ratio. Group A: <3.5 (mg/mmol creatinine), group B: 3.5-35 (mg/mmol creatinine). While serum creatinine concentrations remained within the laboratory reference range for all groups, serum cystatin C concentration (mg/L) was significantly increased in group B (1.79 +/- 0.42 [mean +/- SD] compared to both control [0.81 +/- 0.10] and group A values [0.95 +/- 0.10]; both P<0.001). NAG enzymuria (units/mmol creatinine) was increased in both diabetic groups compared to control values (group B: 122 +/- 7, group A: 70 +/- 5, controls 27 +/- 2, all P<0.001). alpha1-microglobulin (microg/mmol creatinine) concentrations, similar in both the control group and group A diabetics at 1.10 +/- 0.10 and 1.11 +/- 0.21, respectively, were significantly elevated in group B at 2.10 +/- 0.41 (both P<0.01). Similarly, elevated beta2-MG (microg/mmol creatinine) levels were also observed in group B compared to both group A and control values (3.20 +/- 0.21 vs. 1.80 +/- 0.51 and 0.91 +/- 0.11, respectively; both P<0.001). In addition, group B levels were significantly higher than group A (P<0.001). These observations suggest that serum cystatin C is a more appropriate and effective biomarker for the overall estimation of GFR than serum creatinine values. In addition, increased serum cystatin C values were also associated with early renal tubular insult in subjects with type 2 diabetes, as characterised by increased NAG enzymuria, alpha1- and beta2-microglobulin excretion.
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PMID:Serum cystatin C, enzymuria, tubular proteinuria and early renal insult in type 2 diabetes. 1791 Feb 81

The aim is to review the tools for early detection of renal dysfunction after pediatric solid organ transplantation. Currently, the most widely used marker for detection of renal dysfunction involves measurement of GFR. Inulin clearance forms the "gold standard" method for measuring GFR; however, nuclear medicine methods ((51)Cr EDTA and (99)Tc DTPA isotope clearance studies) have replaced inulin clearance. The measurement of serum creatinine has a low sensitivity for the early detection of renal damage. The Schwartz formula using patient height and serum creatinine requires center-specific constants and has limitations associated with creatinine determination. These limitations may be overcome using a cystatin C-based GFR estimation. In diabetic nephropathy, and more recently in hemolytic uremic syndrome, microalbuminuria has been established as a useful screening tool for renal damage, while its predictive value in the transplantation setting needs to be established. All transplant recipients should be screened for hypertension. Early referral for ambulatory 24-h blood pressure monitoring and involvement of pediatric nephrologists should be considered. All pediatric solid organ transplant recipients receiving CNI should be screened regularly for high blood pressure and early evidence of renal damage using either GFR scans or cystatin C-based GFR estimations.
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PMID:How to monitor renal function in pediatric solid organ transplant recipients. 1817 36

Similar to adults, CKD may persist after pediatric RTx. Clinical and laboratory parameters were analyzed retrospectively in 23 RTx recipients (13 males, age 11.9 +/- 5.2 yr), initially treated with prednisone, calcineurin inhibitor (TAC = 18, cyclosporine neoral = 5), and MMF at four months post-RTx (T1) and at 3.4 +/- 2.8 yr post-RTx (T2). Mean (+/-s.d.) cystatin C GFR (mL/min/1.73 m(2)) was 72 +/- 19 at T1 and 70 +/- 22 at T2 (NS). At T2, CKD stage I was present in five patients (22%), stage II in eight patients (35%), and stage III in 10 patients (43%). At T2, calcineurin inhibitors were utilized in 19, MMF in 13, and SIR in 13 patients. The prevalence of hypertension was 69% at T1 and 87% at T2 (p = NS). Anemia was diagnosed in 61% at T1 and 69% at T2 with average therapeutic MMF (2.78 +/- 1.3 mg/mL) and SIR (7.62 +/- 2.3 mg/mL) trough levels. Hypercholesterolemia was detected in 44.0% at T1 and 47% at T2. Bone disease was diagnosed in 26.0% at T1 and 21.7% at T2. Mean height Z-scores were -1.0 +/- 1.2 (T1) and -1.0 +/- 1.59 (T2, NS), with 21% at T1 and 30% at T2 below two SDS. We observed suboptimal growth, hypertension, hypercholesterolemia, bone disease, and anemia in a significant proportion of transplanted children.
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PMID:Complications of chronic kidney disease in children post-renal transplantation - a single center experience. 1818 92

Pregnancy increases plasma cystatin C, but levels are much higher in preeclampsia. Previous studies have not quantified preeclampsia risk with varying cystatin C concentrations or adjusted for confounders. We performed a case-control study of 100 preeclampsia cases and 100 random pregnancies uncomplicated by hypertension (controls). All women were free of pre-existing hypertension, diabetes, and renal disease, and gave birth to singletons. Plasma cystatin C was measured at delivery. Adjusted odds ratios (OR) and 95% confidence intervals (CI) of preeclampsia by quartiles (based on control distribution) of maternal plasma cystatin C were estimated using multivariable logistic regression models. Mean cystatin C levels were elevated in preeclampsia cases compared with controls (1.38 +/- 0.04 vs. 1.22 +/- 0.03 mg/L, p < 0.01). Compared to the first quartile, the estimated risk of preeclampsia was increased by approximately 12-fold for the fourth quartile, after adjusting for maternal age, body mass index, physical inactivity, smoking, and gestational age. Increased plasma levels of cystatin C were independently associated with preeclampsia. Further studies are required to assess the role of cystatin C levels in preeclampsia severity and maternal and fetal outcomes.
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PMID:Cystatin C and preeclampsia: a case control study. 1819 49

Coronary artery calcification (CAC) is prevalent and predicts mortality among patients with ESRD, but whether less severe kidney dysfunction is associated with CAC is uncertain. To address this question, 6749 participants of the Multi-Ethnic Study of Atherosclerosis, who were middle-aged and without known cardiovascular disease, were evaluated. Renal function was categorized by cystatin C quartiles and estimated GFR (eGFR; < to >60 ml/min per 1.73 m(2)), and CAC was evaluated by computed tomography (CT). Fifty percent of participants had CAC, mean cystatin C was 0.90 mg/L, and 10% had eGFR <60 ml/min per 1.73 m(2). In unadjusted analysis, kidney dysfunction by either measure was strongly associated with CAC; however, the associations were lost after adjustment for age, gender, race, hypertension, and IL-6 (relative risk 1.04 [95% confidence interval 0.97 to 1.11] for the highest cystatin C quartile compared with the lowest, and relative risk 1.03 [95% confidence interval 0.98 to 1.08] for eGFR below compared with above 60 m/min per 1.73 m(2)). Similarly, neither higher cystatin C nor eGFR <60 was associated with severity of CAC. These results suggest that a higher burden of CAC is unlikely to explain the association between mild to moderate kidney dysfunction and cardiovascular mortality.
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PMID:Association of mild to moderate kidney dysfunction and coronary calcification. 1823 89

Acute and especially chronic renal failure (CRF) are relatively common and important risk factor for morbidity and mortality in patients after heart, lung, liver or intestine transplantation. Numerous factors contribute to the development of CRF in this group of patients, like treatment with calcineurin inhibitors and other nephrotoxic drugs in the perioperative period, hemodynamical changes during and after the surgery, preexistent renal disease, hypertension, diabetes mellitus, dyslipidemia and anemia. Pretransplant evaluation of renal function is mandatory to predict which patients have increased risk for development of CRF. In the posttransplantation course it is necessary to timely diagnose and treat renal failure, while patients with insufficient renal function have 4.55-fold increased risk of death compared to patients with normal renal function. Special problem is diagnostic approach to patients with suspected chronic renal disease who are candidates for transplantation of other parenhimatose organs. Diagnostic value of serum creatinine and estimation of renal function based on its value is very limited. Gold diagnostic standard is radioisotope estimation of glomerular filtration, but this method is not widely available. It seems that this problem may be solved with the use of cystatin C, but this approach needs to be validated in large studies. Numerous different immunosuppressive drugs available on the market enable individualization of immunosuppression. Different drugs combinations may have less nephrotoxic potential, but one must be careful because of the possible risk of organ rejection with the change of immunosuppression. Use of angiotensin convertase enzyme inhibitors and/or angiotensin receptor blockers, statins with drugs for control of hyperglycemia, may prevent or postpone development of CRF. Although technical advances of contemporary hemodialysis machines and peritoneal dialysis equipment enable well tolerated dialysis even in critically ill patients, renal transplantation remains the method of choice for treatment of patients with transplanted parenhimatous organ that developed CRF.
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PMID:[Chronic renal failure after heart, lung, liver, or intestine transplantation]. 1857 34


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