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Biomedical subjects

J Coresh

Publications and source records attributed to J Coresh.

At least 37 records · Page 2Linked to original sources
PubMed1998

Familial aggregation of renal disease in a population-based case-control study.

Family history of renal disease has been associated with an increased risk of end-stage renal disease (ESRD). It is uncertain whether this risk is mediated by familial aggregation of risk factors for ESRD, such as diabetes and hypertension. The association of ESRD with familial aggregation of renal disease was examined in a large, population-based case-control study conducted in Maryland, Virginia, West Virginia, and Washington, DC. The number of first-degree relatives who were affected with any type of renal disease was compared between 689 newly treated ESRD patients registered in the Medicare ESRD program (92% of all eligible incident cases presenting between January and July of 1991) and 361 control subjects without ESRD who were selected by random-digit dialing (90% response rate). Patients and control subjects were frequency matched by age; patients with ESRD caused by polycystic kidney disease and other known hereditary kidney diseases were excluded. Analysis was conducted using multiple logistic regression. After controlling for the proband's age, gender, race, family size, socioeconomic status, and personal and family histories of diabetes and hypertension, having one first-degree relative with renal disease increased the odds of ESRD by 1.3 (95% confidence interval, 0.7 to 2.6) and having two or more affected first-degree relatives increased the odds of ESRD by 10.4 (95% confidence interval, 2.7 to 40.2). These data support familial aggregation of renal disease in excess of that predicted by clustering of diabetes and hypertension within families, suggesting that either genetic susceptibility or environmental exposures shared within families increase the risk of developing ESRD. This risk is also much higher when two or more first-degree relatives have renal disease. Unraveling the molecular basis of this increase in risk may provide new avenues for treatment and prevention of ESRD.

Adult↗
PubMed1997

A comprehensive analysis of complex traits in problem 2A.

We used descriptive analysis to investigate the relationship between affection status and five quantitative traits (Q1-Q5) in Problem 2A and results suggested the five quantitative traits fall into two groups. The first group comprised three strongly correlated traits, Q1-Q3, which underlie affection status, and the second group comprised Q4 and Q5, which are not directly related to affection status. Segregation and linkage analyses of traits Q1-Q3 and affection status from the first replicate detected one of the major loci for Q1 (MG1) linked to marker 14 on chromosome 5 (D5G14). Because our segregation analysis failed to show evidence of a major locus effect on Q2, and we overlooked the interaction between MG3 and sex, we did not detect either MG2 or MG3. Using Haseman-Elston sib-pair analysis [Haseman and Elston, 1972], we also examined the statistical power of Q1 and type I error rate (using the environmental factor as an index), for the remaining 199 replicates in the context of a genome screen.

Chromosome Mapping↗
PubMed1997

Further trends in the etiology of end-stage renal disease in African-Americans.

Publications in the past year have continued to shed light on the etiology of the excess risk of end-stage renal disease end-stage renal disease among African-Americans. Prospective data now show that even mild elevations in blood pressure are associated with an increased risk of end-stage renal disease. The prevalence of hypertension among African-Americans has been declining, but remains much higher than among White people. Management of hypertension is the best avenue to prevent much of the excess burden of end-stage renal disease, but the relative merits of different agents and levels of blood pressure control are still under study. In addition, individuals with human immunodeficiency virus-related end-stage renal disease represent a small but rapidly growing number of patients that are predominantly African-American. Studies are underway to examine ethnic differences and risk factors for the earlier stages of renal disease as well as genetic mutations for non-Mendelian forms of end-stage renal disease.

AIDS-Associated Nephropathy↗
PubMed1997

Evaluation of serum creatinine for estimating glomerular filtration rate in African Americans with hypertensive nephrosclerosis: results from the African-American Study of Kidney Disease and Hypertension (AASK) Pilot Study.

Measurement of GFR is considered the standard for estimating renal function. However, standardized accurate GFR methodology is expensive and cumbersome; therefore, estimates of GFR based on serum creatinine concentration have been employed. The purpose of the study presented here was to assess the accuracy and precision of using serum creatinine measurements to estimate GFR in the screen cohort of The African-American Study of Kidney Disease and Hypertension (AASK) Pilot Study. GFR was estimated by four methods: 100/serum creatinine, Cockcroft-Gault equation, creatinine clearance from 24-h urine collection, and a new regression equation derived from the pilot study data. These methods were compared with renal clearance of 125I-iothalamate GFR (GFR1) in 193 hypertensive (diastolic blood pressure > or = 95 mm Hg) African-American screen (142 men, 51 women). A second GFR (GFR2) was performed in 98 screen who were eligible (GFR1 25-70 mL/min per 1.73 m2) for the pilot study. Accuracy was assessed by the difference of 125I-iothalamate GFR-estimated GFR (delta GFR), and precision was estimated from the combined root mean squared error (CRMSE) and the coefficient of determination (r2). The results for accuracy (+/- SD) and precision were as follows: (1) 100/Scr, delta GFR = -0.76 +/- 16.5, CRMSE = 16.5, r2 = 0.69; (2) Cockcroft-Gault, delta GFR = 9.56 +/- 14.9, CRMSE = 17.7, r2 = 0.66; 3) 24-h creatinine clearance, delta GFR = 0.79 +/- 20.7, CRMSE = 20.7, r2 = 0.49; 4) New equation delta GFR = -0.08 +/- 12.8, CRMSE 12.7, r2 = 0.75. In comparison, a second GFR (GFR2, N = 98) had delta GFR = 1.36 +/- 8.48, CRMSE 8.6, r2 = 0.75. Estimates based on 100/SCr and the new equation were the most precise. It was concluded that GFR estimated by serum creatinine is superior to outpatient 24-h urine creatinine clearance in this population. Serum creatinine values can be used to provide a reasonably accurate estimate of GFR in hypertensive African Americans.

Adult↗
PubMed1996

Adjusting survival curves for confounders: a review and a new method.

When reporting results from survival analysis, investigators often present crude Kaplan-Meier survival curves and adjusted relative hazards from the Cox proportional hazards model. Occasionally, the investigators will also provide a graphical representation of adjusted survival curves based on regression estimates and the average covariate values in the study groups. In this paper, the authors review the limitations of this approach and examine alternative approaches to obtaining adjusted survival curves that have been proposed. Furthermore, a new method to obtain multivariate adjusted survival curves is described. This method is based on direct adjustment of the observed conditional probability of survival at the time of each event. When an unexposed group is used as a standard for adjusting an exposed group, the survival curve in the exposed group is adjusted to the covariate distribution among the unexposed at the time of the event. This method has the advantage over the average covariate method of allowing for the possibility that the adjusted survival curves differ in shape. The method can handle multiple fixed or time-dependent categorical covariates as well as left truncated data, and it allows for estimation of confidence intervals. The authors have written a macro in SAS language that produces the adjusted survival estimates and graphs. This macro is available on request and can be downloaded through the World Wide Web.

Coffee↗
PubMed1996

Exercise thallium tomography predicts future clinically manifest coronary heart disease in a high-risk asymptomatic population.

BACKGROUND: Exercise testing, even when combined with radionuclide perfusion imaging, does not accurately predict future clinical coronary heart disease (CHD) in low-risk asymptomatic populations. We hypothesized that these tests would perform better in a higher-risk population with a high prevalence of occult CHD. Siblings of persons with premature CHD represent such a group in whom it would be advantageous to identify affected individuals before the occurrence of clinically manifest CHD. METHODS AND RESULTS: Exercise thallium scintigraphy was performed in 264 asymptomatic individuals less than 60 years of age who had a sibling with documented CHD before age 60. Despite an average age of only 46 years at the time of screening, 19 of 264 siblings developed clinical CHD (sudden death in 1, myocardial infarction in 10, coronary revascularization in 8) over a mean of 6.2 years (range, 1 to 9 years) of follow-up. Abnormal thallium scans were observed in 29% of men and 9% of women, while abnormal exercise ECGs occurred in 12% and 5% respectively. Of men >/= 45 years of age, 45% had an abnormal exercise ECG, thallium scan, or both. In contrast, only 3% of women < 45 years of age had an abnormal test result. Although abnormal exercise ECGs and thallium scans were both predictive of future clinical CHD, the thallium scan was associated with a higher relative risk. After adjustment for age, sex, and exercise ECG results, the relative risk of developing clinical CHD was 4.7 for an abnormal scan. Siblings with a concordant abnormal exercise ECG and thallium scan had a relative risk of 14.5. These siblings were all men > 45 years of age at the time of screening and had a strikingly high incidence of CHD (6 of 12, 50%). CONCLUSIONS: Exercise thallium scintigraphy appears to be useful in the risk assessment of asymptomatic siblings of patients with premature CHD, particularly in male siblings who are 45 years of age or older.

Adult↗
PubMed1996

Race and sex differences in the distribution of cerebral atherosclerosis.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the influence of race, sex, and other risk factors on the location of atherosclerotic occlusive lesions in cerebral vessels. Previous angiographic studies of patients with stroke or transient ischemic attack (TIA) suggest that extracranial atherosclerosis is more common in whites and intracranial disease is more common in blacks. Noninvasive techniques such as duplex ultrasound, transcranial Doppler (TCD), and magnetic resonance angiography (MRA) allow vascular assessment of a more representative proportion of patients than does conventional angiography alone. METHODS: Consecutive patients evaluated at a community hospital for stroke or TIA over a 2-year period were reviewed. Lesions were defined as a 50% or greater atherosclerotic stenosis by angiography, duplex ultrasound, or TCD, or a moderate stenosis by MRA. RESULTS: Whites were more likely than blacks to have extracranial carotid artery lesions (33% versus 15%, P = .001), but the proportion of patients with intracranial lesions was similar (24% versus 22%). Men were more likely to have intracranial lesions than women (29% versus 14%, P = .03). When multivariate logistic regression analysis was used, white race was the only predictor for extracranial carotid artery lesions, and male sex was the only predictor for intracranial lesions. The cause of stroke/TIA was extracranial carotid artery disease in 8% and intracranial disease in 8% of all patients in the study. CONCLUSIONS: The distribution of cerebral atherosclerosis is influenced by race and sex but not by other vascular risk factors. In our patient population, intracranial disease is as common a cause of cerebral ischemia as extracranial carotid disease.

Aged↗
PubMed1995

The contribution of urinary cations to the blood pressure differences associated with migration.

People living in unacculturated societies have a low average blood pressure and little rise in blood pressure with age. In a community-based survey in southwestern China, the authors assessed the contribution of urinary cation excretion to differences in blood pressure between an unacculturated group (Yi farmers) and migrants to an urban environment, as well as urban controls from a different ethnic group (Han). In March 1989, blood pressure and overnight urinary electrolyte levels were measured on 3 consecutive days in 313 Yi farmers, 265 Yi migrants, and 253 urban Han residents, all male. Of the urinary electrolytes, a higher sodium:potassium ratio best explained the higher blood pressure in the migrants. Yi farmers had lower systolic (106.7 mmHg vs. 114.8 mmHg, respectively) and diastolic (66.2 mmHg vs. 71.3 mmHg, respectively) blood pressures than Yi migrants. However, even after adjustment for age, body mass index, alcohol intake, and urinary sodium, potassium, calcium, and magnesium excretion, Yi farmers continued to have lower average blood pressures than Yi migrants. In pooled analyses of all three groups, urinary sodium and calcium were positively related and urinary potassium and magnesium were inversely related to blood pressure. Migration is associated with a higher blood pressure that is only partially explained by higher levels of adiposity and alcohol and sodium intake and lower levels of potassium and magnesium intake.

Adult↗
PubMed1995

Segregation analysis of HDL3-C levels in families of patients undergoing coronary arteriography at an early age.

HDL cholesterol (HDL-C) level is a risk factor for coronary heart disease. Studies have shown a strong genetic influence on HDL-C levels in addition to environmental influences, but no definite major gene control has been demonstrated. Since HDL subfractions may better reflect the actions of distinct metabolic alterations than total HDL2 we tested the hypothesis that the amount of cholesterol in the denser HDL3 subfraction (HDL3-C) is under the control of a major gene. The study population included 676 family members of 116 probands who underwent coronary arteriography at an early age (men < or = 50 and women < or = 60 years). HDL3-C level was measured by using enzymatic methods after preparative ultracentrifugation at a density of 1.125 g/mL. HDL3-C was adjusted for age, gender, alcohol consumption, and smoking, which combined accounted for 3% of its variance. Segregation analysis was conducted on adjusted HDL3-C by using regressive models. The familial correlations for HDL3-C levels were spouse .03 +/- .08, parent-offspring .14 +/- .05, and sibling .24 +/- .05. The data strongly supported a codominant mendelian model, with the common allele coding for lower HDL3-C levels and the rarer allele (frequency, 25%) coding for higher HDL3-C levels. This major gene explained 34% of the variation in HDL3-C levels and 9% of the variation in total HDL-C levels. These results suggest that HDL3-C levels exhibit clearer genetic control than total HDL-C and may therefore be a useful target for further genetic studies.

Adult↗
PubMed1995

Survival on dialysis among chronic renal failure patients treated with a supplemented low-protein diet before dialysis.

Concerns have been raised about the possibility of protein restriction resulting in malnutrition and poor subsequent survival on dialysis. However, no studies have examined patients treated with protein restriction to determine their subsequent survival on dialysis. This study prospectively monitored 67 patients with established chronic renal failure (mean initial serum creatinine of 4.3 mg/dL) who were treated with a very low-protein diet (0.3 g/kg per day) supplemented with either essential amino acids or a ketoacid-amino acid mixture and observed closely for clinical complications. Forty-four patients required dialysis. Once dialysis was started, dietary treatment was no longer prescribed. The cumulative mortality rate during the first 2 yr after starting dialysis was 7% (95% confidence interval, 0 to 16%). During this period, only two deaths occurred compared with 11.5 deaths expected on the basis of national mortality rates adjusted for age, sex, race, and cause of renal disease (P = 0.002). However, the protective effect was limited to the first 2 yr on dialysis. Thereafter, mortality rates increased, resulting in a total of 10 deaths during 96.4 person-years of follow-up, which was not significantly lower than the 14.9 deaths expected (P = 0.25). Extrapolation of sequential serum creatinine measurements made before dietary treatment suggests that the improved survival cannot be due to the early initiation of dialysis. Although the lack of an internal control group and data on dialysis lends uncertainty, the large difference in mortality rate between these patients and the nationwide experience indicates that protein restriction and close clinical monitoring predialysis does not worsen and may substantially improve survival during the first 2 yr on dialysis. These findings point out the importance of studying predialysis treatments as a means for lowering mortality on dialysis.

Adult↗
PubMed1994

Minimum sample size estimation to detect gene-environment interaction in case-control designs.

As genetic markers become more available, case-control studies will be increasingly important in defining the role of genetic factors in disease causality. The authors estimate the minimum sample size needed to assure adequate statistical power to detect gene-environment interaction. One assumption is made: the prevalence of exposure is independent of marker genotypes among controls. Given the assumption, six parameters (three odds ratios, the prevalence of exposure, the proportion of those with the susceptible genotype, and the ratio of controls to cases) dictate the expected cell sizes in a 2 x 2 x 2 table contrasting genetic susceptibility, exposure, and disease. The three odds ratios reflect the association between disease and 1) exposure among non-susceptibles; 2) susceptible genotypes among nonexposed individuals; and 3) the gene-environment interaction itself, respectively. Given these parameters, the number of cases and controls needed to assure any particular Type I and Type II error rates can be estimated. Results presented here demonstrate that case-control designs can be used to detect gene-environment interaction when there is both a common exposure and a highly polymorphic marker of susceptibility.

Case-Control Studies↗
PubMed1994

Coffee intake and coronary heart disease.

We examined the risk of coronary heart disease (CHD) associated with coffee intake in 1040 male medical students followed for 28 to 44 years. During the follow-up, CHD developed in 111 men. The relative risks (95% confidence interval) associated with drinking 5 cups of coffee/d were 2.94 (1.27, 6.81) for baseline, 5.52 (1.31, 23.18) for average, and 1.95 (0.86, 4.40) for most recent intake after adjustment for baseline age, serum cholesterol levels, calendar time, and the time-dependent covariates number of cigarettes, body mass index, and incident hypertension and diabetes. Risks were elevated in both smokers and nonsmokers and were stronger for myocardial infarction. Most of the excess risk was associated with coffee drinking prior to 1975. The diagnosis of hypertension was associated with a subsequent reduction in coffee intake. Negative results in some studies may be due to the assessment of coffee intake later in life or to differences in methods of coffee preparation between study populations or over calendar time.

Adult↗
PubMed1993

Agreement between overnight and 24-hour urinary cation excretions in southern Chinese men.

Agreement between overnight and 24-hour urinary sodium, potassium, calcium, and magnesium excretion was studied in a sample of 63 normotensive Southwestern Chinese men: 30 Yi farmers and 33 urban residents in April 1989. Overnight (8-hour) and 24-hour urine specimens were collected on 3 consecutive days. Estimated correlation coefficients between 24-hour and overnight mean true values were 0.863 and 0.906 for sodium, 0.736 and 0.816 for potassium, 0.902 and 0.725 for calcium, and 0.733 and 0.703 for magnesium in Yi farmers and urban residents, respectively. Hourly overnight urinary sodium and potassium excretion rates were significantly lower than the corresponding hourly 24-hour urinary excretion rates: -0.60 and -1.99 mmol/hour for sodium, -1.24 and -0.48 mmol/hour for potassium (all p < 0.05) in Yi farmers and urban residents, respectively. In multiple regression analyses, the differences between 24-hour and overnight urinary sodium and potassium excretion rates were significantly and positively related to differences between 24-hour and overnight creatinine excretion rates. The ratios of intraindividual to interindividual variance were lower for 24-hour collections than for overnight collections for sodium and calcium, but the differences in these ratios for potassium and magnesium were small. For sodium and calcium, twice as many overnight as 24-hour collections were required to estimate the correlation between cations and blood pressure with the same accuracy; for potassium and magnesium, overnight and 24-hour collections were equally accurate. These results indicate that in normotensive populations such as the one studied, overnight urine collections may be used to estimate 24-hour cation excretion. The underestimate of cation excretion by assessments based on collection of overnight specimens may be due to either a lower creatinine clearance or a lower intake of cations at night.

Adult↗
PubMed1993

Prevalence of hyperapobetalipoproteinemia and other lipoprotein phenotypes in men (aged < or = 50 years) and women (< or = 60 years) with coronary artery disease.

The prevalence and clinical characteristics of hyperapobetalipoproteinemia (hyperapoB) and other phenotypes of dyslipoproteinemia were examined in 99 men (aged < or = 50 years) and 104 women (< or = 60 years) undergoing elective diagnostic coronary arteriography. HyperapoB was the most common phenotype (34%) associated with premature coronary artery disease (CAD). Only 20.2% of patients with CAD had a normal lipoprotein phenotype. The significant odds ratios for CAD were as follows: hypertriglyceridemic hyperapoB 17.45 (p < 0.0001), type IV 6.54 (p = 0.0001), type IIa 4.73 (p = 0.008), normotriglyceridemic hyperapoB 2.54 (p = 0.03) and type IIb 8.73 (p = 0.05). The strong association of hypertriglyceridemic hyperapoB with CAD reflected the multiplicative effect of increased low-density lipoprotein apolipoprotein B and endogenous hypertriglyceridemia, and was independent of the effects of age, sex, diabetes mellitus, systemic hypertension, body mass index and cigarette smoking. The ratio of apolipoprotein B to A-1 was better than those of low-density to high-density lipoprotein cholesterol and total to high-density lipoprotein cholesterol at discriminating dyslipidemic phenotypes from normal. Obesity was increased approximately 1.5 to two-fold in the hypertriglyceridemic phenotypes, diabetes was more prevalent in hypertriglyceridemic hyperapoB (6.8-fold; p < 0.001) and type IV (4.4-fold; p = 0.02), and hypertension was increased 1.5- to twofold in most dyslipidemic groups. The data indicate that hyperapoB and endogenous hypertriglyceridemia both contribute to the risk of premature CAD.

Apolipoproteins B↗
PubMed1993

Inheritance of plasma apolipoprotein B levels in families of patients undergoing coronary arteriography at an early age.

An elevated plasma level of apolipoprotein B (apoB), the major protein of low density lipoproteins, is a risk factor for coronary artery disease. This study tested the hypothesis, suggested by previous studies, that the apoB level is strongly influenced by a major gene. The study population included 832 family members of 116 subjects who had undergone elective coronary arteriography at an early age. The apoB level was adjusted for age, gender, body mass index, alcohol consumption, and cigarette smoking (R2 = 20%). ApoB levels revealed strong familial aggregation with correlations among spouses of 0.23, parent-offspring of 0.16, and siblings of 0.21. Regressive models were used to examine inter-individual variation in adjusted apoB levels. In the total sample, familial aggregation of the apoB level was consistent with two models: (1) a major gene model and (2) a polygenic model with a mixture of non-transmitted "types". Comparison of these two models in each family showed that 57 families supported the first model over the second. Segregation analysis in these 57 families conclusively favored a major gene model with codominant transmission. Genotypic means were 124, 164, and 208 mg/dl with relative frequencies of 45%, 44%, and 11%. Linkage studies in these families can be used to clarify the molecular basis of apoB regulation. However, in the whole population the genetic control of apoB levels may be quite complex.

Apolipoproteins B↗
PubMed1993

Two-locus and bivariate segregation analysis of HDL-C and apo AI.

Two-locus and bivariate segregation analyses of HDL-C and apo AI were carried out using the GAW8 Berkeley data set. For HDL-C, results are ambiguous. Both the mixed environmental model and the mixed Mendelian model fit the data equally well. For apo AI, however, univariate one-locus segregation analysis suggests a Mendelian major gene controlling its levels. Moreover, two-locus analysis suggests a second major gene is involved. Bivariate segregation analysis indicates these data cannot resolve the question as to whether a single Mendelian major gene with pleiotropic effects controls levels of both HDL-C and apo AI in humans.

Apolipoprotein A-I↗
PubMed1993

Association of plasma triglyceride concentration and LDL particle diameter, density, and chemical composition with premature coronary artery disease in men and women.

Low density lipoprotein (LDL) physical-chemical characteristics were studied as nontraditional risk factors of coronary artery disease (CAD) in a well-characterized population of 98 men aged < or = 50 and 100 women aged < or = 60 who underwent elective diagnostic coronary arteriography. The average LDL diameter was determined by gradient gel electrophoresis, chemical composition (%w/w) was measured, and the density of the major LDL peak was determined by equilibrium density gradient ultracentrifugation. Logistic regression was used to examine the association of various LDL characteristics with CAD before and after adjustment for other covariates. Smaller, cholesterol-poor LDL particles were associated with CAD independently of traditional risk factors (age, sex, smoking, diabetes, LDL and HDL cholesterol concentrations), other than the plasma triglyceride concentration. These characteristics were generally more strongly associated with CAD when measured on the major LDL subfraction (defined as the density gradient ultracentrifugation fraction with the highest LDL concentration) than the average characteristics of the more heterogeneous parent LDL (d 1.019-1.063 g/ml). The associations with CAD among men and women were generally similar. These data show that a broad range of LDL characteristics are associated with CAD before, but not after, adjustment for the plasma triglyceride concentration. These data further indicate the importance of hypertriglyceridemia and LDL heterogeneity in premature CAD.

Apolipoproteins B↗