Identifying and slowing progressive chronic renal failure.
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OBJECTIVE: To help inform primary care physicians about how to identify and slow progressive chronic renal failure. QUALITY OF EVIDENCE: The National Library of Medicine (1996 to 2000) was searched using PubMed with search terms pertinent to studies on identification, course, and management of chronic renal failure. References in retrieved papers and older literature known to the authors supplemented the searches. In general, sufficient high-quality studies, systematic reviews, or guidelines based on such evidence were available to support our main points. MAIN MESSAGE: End-stage renal disease (ESRD) poses a large and growing morbidity, mortality, and financial burden. Almost all patients reach ESRD as a result of chronic progressive conditions, particularly diabetic nephropathy, hypertensive-vascular renal disease, and glomerular disorders. Patients at risk merit regular renal assessment with serum creatinine tests and urinalysis. Persistent high blood pressure and heavy proteinuria are the strongest predictors of progression of chronic renal failure. Patients with renal disease should be examined and treated for vascular disease and vice versa. Blood pressure lowering, ACE inhibition, and avoidance of further renal insults (such as use of nephrotoxins) can slow the decline of renal function. Restricting dietary protein has a weak effect on slowing renal failure and is not easy to apply in primary care. Timely involvement of specialized nephrology teams is important. CONCLUSION: Family physicians play an important role in recognizing patients with potential for renal failure, in demonstrating progressive chronic renal failure, and in initiating therapy early to improve outcomes. (+info)
A simple method to estimate populational 24-h urinary sodium and potassium excretion using a casual urine specimen.
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In order to estimate the salt and potassium intake in a population and to compare their annual trends, we developed a simple method to estimate population mean levels of 24-h urinary sodium (24HUNaV) and potassium (24HUKV) excretion from spot urine specimens collected at any time. Using 591 Japanese data items from the INTERSALT study as a gold standard, we developed formulas to estimate 24-h urinary creatinine (24HUCrV), 24HUNaV and 24HUKV using both spot and 24-h urine collection samples. To examine the accuracy of the formulas, we applied these equations to 513 external manual workers. The obtained formulas were as follows: (1) PRCr (mg/day) = -2.04 x age + 14.89 x weight (kg) + 16.14 x height (cm) -2244.45; (2) estimated 24HUNaV (mEq/day) = 21.98 x XNa (0.392); (3) estimated 24HUKV (mEq/day) = 7.59 x XK(0.431); where PRCr = predicted value of 24HUCr, SUNa = Na concentration in the spot voiding urine, SUK = K concentration in the spot voiding urine, SUCr = creatinine concentration in the spot voiding urine, XNa (or XK) = SUNa (or SUK)/SUCr x PRCr. In the external group, there was a significant but small difference between the estimated and measured values in sodium (24.0 mmol/day) and potassium (3.8 mmol/day) excretion. In every quintile divided by the estimated 24HUNaV or 24HUKV, the measured values were parallel to the estimated values. In conclusion, although this method is not suitable for estimating individual Na and K excretion, these formulas are considered useful for estimating population mean levels of 24-h Na and K excretion, and are available for comparing different populations, as well as indicating annual trends of a particular population. (+info)
A cross-sectional study on association of calcium intake with blood pressure in Japanese population.
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To investigate the association of calcium intake independently of other nutrients already known as predictors of hypertension, a cross-sectional study was carried out on the same population in Japan as used for the INTERSALT study. Dietary calcium intake was estimated from a 1-day 24-h recall. Sodium and potassium intakes were evaluated by 24-h urinary excretion. Data from 476 subjects aged 20-59 years, 230 men and 246 women, were analysed. The mean dietary calcium intake ranged from 557 to 608 mg/day among men, and from 528 to 639 mg/day among women. Among men, the pooled estimate of the regression coefficients of blood pressure (mm Hg) per 100 mg increase of calcium intake, adjusted for age and body mass index (BMI), were -0.42 mm Hg for systolic blood pressure (SBP) and -0.35 mm Hg for diastolic blood pressure (DBP), but there was no statistical significance. Among women, the pooled estimates of regression coefficients adjusted for age and BMI were -0.92 mm Hg for SBP and -0.83 mm Hg for DBP with statistical significance. After adjustment for age, BMI, alcohol intake and urinary excretion of sodium and potassium, the pooled estimate of calcium intake was -0.66 mm Hg for DBP with statistical significance and -0.70 mm Hg for SBP. A significant negative association of calcium intake with blood pressure was observed among the subjects in Osaka. Our study suggests that increased calcium intake may provide a benefit of lowering blood pressure independently of other minerals such as sodium and potassium. (+info)
Rapid spot tests for detecting the presence of adulterants in urine specimens submitted for drug testing.
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Several adulterants are used to mask tests for abused drugs in urine. Adulterants such as "Klear" and "Whizzies" contain potassium nitrite, and "Urine Luck" contains pyridinium chlorochromate (PCC). The presence of these adulterants cannot be detected by routine specimen integrity checks (pH, specific gravity, and temperature). We developed rapid spot tests for detecting these adulterants in urine. Addition of 3% hydrogen peroxide in urine adulterated with PCC caused rapid formation of a dark brown color. In contrast, unadulterated urine turned colorless when hydrogen peroxide was added. When urine contaminated with nitrite and 2 to 3 drops of 2N hydrochloric acid were added to 2% aqueous potassium permanganate solution, the dark pink permanganate solution turned colorless immediately with effervescence. Urine contaminated with nitrite liberated iodine from potassium iodide solution in the presence of 2N hydrochloric acid. Urine adulterated with PCC also liberated iodine from potassium iodide in acid medium but did not turn potassium permanganate solution colorless. Urine specimens from volunteers and random urine samples that tested negative for drugs did not cause false-positive results. These rapid spot tests are useful for detecting adulterated urine to avoid false-negative drug tests. (+info)
Anthropometry-based reference values for 24-h urinary creatinine excretion during growth and their use in endocrine and nutritional research.
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BACKGROUND: Urinary creatinine reference values that take anthropometric data into account, which is mandatory during growth, are not available for healthy white children. OBJECTIVE: We sought to establish anthropometry-based reference values for 24-h urinary creatinine excretion in healthy white children aged 3-18 y. DESIGN: Anthropometric variables and 24-h urinary creatinine excretion rates were determined cross-sectionally (225 boys and 229 girls). Age and sex dependency of 24-h creatinine excretion (crude and related to individual anthropometric variables) were assessed to derive appropriate creatinine reference values. The applicability of these creatinine reference values for estimation of daily excretion of certain analytes was assessed in 40 additional children. RESULTS: Sex-specific, body-weight-related creatinine reference values were derived for the following age groups: 3, 4-5, 6-8, 9-13, and 14-18 y. The 5th percentile exceeded 0.1 mmol x kg(-1) x d(-1) in all age groups >3 y. The use of these creatinine reference values for estimating average 24-h excretion rates of certain analytes (determined as the ratio of analyte to creatinine in spot urine samples) yielded reasonable estimates of mean 24-h urinary excretion rates actually analyzed (spot and 24-h urine samples from the same children). Ideal 24-h creatinine excretion values for height were also derived for a potential determination of the creatinine height index. CONCLUSIONS: Established anthropometry-based creatinine reference values are recommended as a convenient, simple tool to 1) identify severe 24-h urine collection errors, 2) calculate average 24-h excretion rates of certain analytes (from respective ratios of analyte to creatinine) determined in spot urine samples, and 3) assess somatic protein status by determining the creatinine height index. (+info)
Disposition of inhaled mercury vapor in pregnant rats: maternal toxicity and effects on developmental outcome.
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The disposition and toxicity of inhaled elemental mercury (Hg0) vapor for pregnant Long-Evans rats, and potential adverse effects on reproductive outcome were investigated. Rats were exposed to 0, 1, 2, 4, or 8 mg Hg0/m(3) for 2 h/day from gestation day (GD) 6 through GD 15. Maternal toxicity occurred primarily in rats exposed to 4 and 8 mg/m(3) and was manifested as a concentration-related decrease in body weight gain and mild nephrotoxicity. Control rats gained about 13% of their initial body weight during the 10-day exposure. Rats exposed to 4 mg/m(3) Hg0 gained about 7% less than controls, and rats exposed to 8 mg/m(3) Hg0 lost about 17% of their initial body weight during the 10-day exposure period. Maternal kidney weights were significantly increased in the 4 and 8 mg/m(3) concentration groups, and urinalysis revealed increased levels of protein and alkaline phosphatase activity in urine of all Hg0-exposed rats. Dams exposed to 8 mg/m(3) were euthanized in moribund condition on postnatal day (PND) 1. There was no histopathological evidence of toxicity in maternal lung, liver, or kidney of exposed rats at GD 6, GD 15, or PND 1. The incidence of resorptions was significantly increased, litter size and PND 1 neonatal body weights were significantly decreased only in the 8-mg/m(3) group. Total Hg concentrations in maternal tissues increased with increasing number of exposure days and concentration. In general, approximately 70% of Hg was eliminated from maternal tissues during the week following the last exposure (GD 15 to PND 1). Elimination of Hg from maternal brain and kidney was slower than in other tissues, possibly due to higher levels of metallothionein. Total Hg concentrations in fetal tissues increased with increasing number of exposure days and concentration, demonstrating that a significant amount of Hg crossed the placenta. One week after the last exposure, significant amounts of Hg were still present in brain, liver, and kidney of PND 1 neonates. Metallothionein levels in neonatal tissues were not significantly increased by exposure to 4 mg/m(3) Hg0. The total amount of Hg in neonatal brain (ng/brain) continued to increase after termination of inhalation exposure, suggesting a redistribution of Hg from the dam to neonatal brain. These data demonstrate that inhaled Hg0 vapor is distributed to all maternal and fetal tissues in a dose-dependent manner. Adverse effects of Hg on developmental outcome occurred only at a concentration that caused maternal toxicity. (+info)
Fetal gender and cocaine exposure as determinants of cord blood gamma-glutamyl transferase activity.
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OBJECTIVE: The serum activity of the hepatic enzyme gamma-glutamyl transferase (GGT) is elevated in the newborn relative to older age groups. Few reports to date have studied the influence of perinatal factors on neonatal serum GGT and no study has assessed the influence of maternal drug ingestion. STUDY DESIGN: Cord blood was randomly collected from 234 liveborn infants and correlated with a range of maternal and fetal perinatal variables to assess influences on cord blood GGT. RESULTS: Our study showed that the range of cord blood GGT activity in 234 randomly selected term newborns was 22 to 556 IU/l. In a subgroup of 75 newborns, GGT activity was independently influenced by only two of the variables studied - cocaine exposure and fetal gender (p=0.009, r=0.39). Females had a lower GGT than males (95+/-66 vs 130+/-90 IU/l, p<0.001) while GGT activity in cocaine-exposed newborns was lower than in cocaine-nonexposed newborns (96+/-48 vs 142+/-109, p<0.01). Birth weight, race, gestational age, and maternal serum GGT were not found to significantly influence cord blood GGT activity. Maternal GGT was uniformly normal and was not affected by any of the variables tested. CONCLUSION: Our findings demonstrate that the reference range for cord blood GGT activity is wide and appears to be influenced by fetal gender and cocaine exposure. (+info)
BG9719 (CVT-124), an A1 adenosine receptor antagonist, protects against the decline in renal function observed with diuretic therapy.
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BACKGROUND: Adenosine may adversely affect renal function via its effects on renal arterioles and tubuloglomerular feedback, but effects of adenosine blockade in humans receiving furosemide and ACE inhibitors is unknown. METHODS AND RESULTS: This was a randomized, double-blind, ascending-dose, crossover study evaluating 3 doses of BG9719 in 63 patients with congestive heart failure. Patients received placebo or 1 of 3 doses of BG9719 on 1 day and the same medication plus furosemide on a separate day. Renal function and electrolyte and water excretion were assessed. BG9719 alone caused an increase in urine output and sodium excretion (P<0.05). Although administration of furosemide alone caused a large diuresis, addition of BG9719 to furosemide increased diuresis, which was significant at the 0.75-microg/mL concentration. BG9719 alone improved glomerular filtration rate (GFR) at the 2 lower doses. Furosemide alone caused a decline in GFR. When BG9719 was added to furosemide, however, creatinine clearance remained at baseline at the 2 lower doses. CONCLUSIONS: In patients with congestive heart failure on standard therapy, including ACE inhibitors, BG9719 increased both urine output and GFR. In these same patients, furosemide increased urine output at the expense of decreased GFR. When BG9719 was given in addition to furosemide, urine volume additionally increased and there was no deterioration in GFR. A1 adenosine antagonism might preserve renal function while simultaneously promoting natriuresis during treatment for heart failure. (+info)