PubMed Health⌕ Search

Biomedical subjects

R D Lindeman

Publications and source records attributed to R D Lindeman.

At least 19 recordsLinked to original sources
PubMed1992

Low blood glutathione levels in healthy aging adults.

The objective of this investigation was to test the hypothesis that blood glutathione levels are lower in aging human subjects as previously found in blood and tissues of standard rodent models of aging. Thus a study was conducted with 39 men and 130 women, 20 to 94 years old, who were selected by the criteria of being ambulatory, healthy, and free from diabetes mellitus, thyroid disease, anemias, and cancer. The reference group was comprised of the 20- to 39-year-old subjects, whose blood glutathione levels were 547 +/- 53.5 micrograms/10(10) erythrocytes (mean +/- SD) for 40 individuals and defined the reference range (95% confidence limits) of 440 to 654. Based on the 440 micrograms/10(10) erythrocyte cutoff, the incidence of low blood glutathione content in the older subjects increased significantly, particularly in the 60- to 79-year-old group. Their glutathione levels were 452 +/- 86.8 micrograms/10(10) erythrocytes, 17% lower than the reference group (p < 0.001). These findings demonstrate an increased incidence of low glutathione levels in apparently healthy elderly subjects, who thus may be at risk because of a decreased capacity to maintain many metabolic and detoxification reactions mediated by glutathione.

Adult↗
PubMed1990

Overview: renal physiology and pathophysiology of aging.

Cross-sectional studies in humans have suggested that there is a progressive decline of renal function with age after 40 years. The decline in various functions (eg, tubular maximums, concentrating and diluting abilities, and acidification) tend to parallel the decreases in glomerular filtration rate (GFR) and renal blood (plasma) flow (RPF). Recent observations from the Baltimore Longitudinal Study of Aging suggest that not all individuals follow this pattern, and that, indeed, many show no decline and some even an increase in their renal function over time. Whether the observed decreases in renal function with aging are the results of intervening pathologic processes, eg, immunologic, infectious, and toxic injury and ischemia, or can be related to hyperperfusion and hyperfiltration with resultant glomerulosclerosis, or to some other relentless involutional process, remains unclear. The purpose of this report is to review the descriptive studies documenting the changes in renal morphology and physiology with age and to discuss what is known about mechanisms involved in these losses of renal substance and function.

Aging↗
PubMed1989

Trace minerals and the kidney: an overview.

The deviations from normal health produced by abnormalities in trace mineral metabolism in patients with renal disease and renal disorders produced by deficiencies or excesses of these trace minerals serve as the focus for this symposium on trace minerals and the kidney. Zinc, the trace mineral of most interest of the nephrologist, and aluminum, the nonessential (toxic) trace element of most interest, are treated in separate reviews. Iron, copper, selenium, and silicon (essential trace elements) and cadmium, lead, mercury, and lithium (nonessential or toxic elements) are covered in this review.

Humans↗
PubMed1987

Hypertension and the kidney.

The purpose of this study was to confirm, using longitudinal observations in a normal population, that the rate of decline in renal function (creatinine clearance) is inversely correlated with blood pressure. The negative regression coefficients plotting individual rates of decline over time (Bcr) against mean blood pressures (MBP) were highly significant (p less than 0.001) for all subjects and subjects in category 3 (normals). Although the Bcr also decreases significantly with age and MBP increases with age suggesting this might be an age effect, a multiple regression analysis shows that both MBP and age as independent variables exert statistically significant effects on Bcr, the dependent variable.

Adult↗
PubMed1986

Anatomic and physiologic age changes in the kidney.

Cross-sectional studies of renal function in man indicate there is a progressive decline with age after the age of 40 years. The blood vessels, glomeruli, tubules and interstitium are all potential sites of primary involvement in the aging process as well as for renal disease. Regardless of the anatomic structure initially affected, most chronic renal conditions evolve with destruction of the entire nephron. Whether the observed decrease in renal function associated with aging is the result of intervening pathologic processes, e.g. ischemia (vascular obliteration) or infection, or is the result of a more insidious involutional process, it has generated much discussion but few answers. The purpose of this report is to review the descriptive studies documenting the changes in renal morphology and physiology with age and to focus on what is known about the mechanisms involved in these losses of renal substances and function.

Adolescent↗
PubMed1986

Magnesium deficiency inhibits biosynthesis of blood glutathione and tumor growth in the rat.

Previously we found that blood glutathione (GSH) levels increase in response to tumor growth in the rat and that this increase is not prevented with zinc deficiency. We also found that zinc deficiency which inhibited tumor growth did not prevent this increase in blood GSH. Therefore, the objectives of this study were to determine the effects of another nutritional modification, namely magnesium deficiency, on blood GSH status and on tumor growth. Magnesium was selected because it is an obligatory cofactor in GSH synthesis and in all biosynthetic reactions involving ATP. To this end, magnesium- and zinc-deficient rats with and without tumors were compared to pair-fed control rats with and without tumors. After 32 days of depletion, the rats were killed, and blood samples were analyzed for nonprotein sulfhydryls (SH) and specifically for GSH. The key finding was that in magnesium-deficient rats with or without tumors, blood GSH levels were low and SH levels were normal indicating a decrease in GSH biosynthesis. In contrast, zinc deficiency affected SH and GSH in parallel. Thus, these two deficiencies must act by different mechanisms. The zinc data verified our earlier results obtained with a different tumor type and rat strain, for blood GSH levels increased in tumor-bearing rats fed control diets, and zinc deficiency did not prevent this increase. Depletion of magnesium or zinc was equally effective in inhibiting tumor growth. These results provide in vivo evidence of a magnesium requirement for GSH biosynthesis in rat erythrocytes. Further, the results suggest that magnesium deficiency may inhibit tumor growth by limiting GSH synthesis from SH precursors.

Animals↗
PubMed1986

The aging kidney.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMed1986

Chronic renal failure and magnesium metabolism.

A number of factors affect the concentration and distribution of magnesium in patients with chronic renal failure (CRF). Poor nutritional intake, impaired absorption from the intestine, vomiting, diarrhea, the use of diuretics and acidosis may result in a negative balance. More commonly, accumulation of magnesium may be the consequence of reduced renal excretion. Magnesium concentrations are increased in serum and red cells in CRF patients. Bone concentrations and total body magnesium also appear to be increased; muscle magnesium does not appear to be increased. Use of magnesium hydroxide-containing antacids as phosphate binders in patients with CRF was largely discontinued 2 decades ago after reports described increases in serum magnesium concentrations to toxic levels. More recently, the undesirable effects of aluminum-containing phosphate binders (encephalopathy, osteomalacia) have led several investigators to report favorable experiences using low concentrations of magnesium in dialysate and a combination of magnesium and aluminum-containing antacids, as phosphate binders, while closely monitoring serum magnesium concentrations.

Antacids↗
PubMed1985

Longitudinal studies on the rate of decline in renal function with age.

Serial creatinine clearances (5 to 14 studies) were obtained for 446 normal volunteers in the Baltimore Longitudinal Study of Aging followed between 1958 and 1981. When those subjects with possible renal or urinary tract disease and subjects on diuretics and antihypertensives were removed from the study, leaving a group of 254 "normal" subjects, the mean decrease in creatinine clearance was 0.75 ml/min/year. The slopes of the creatinine clearance vs. time fell into a normal (Gaussian) distribution around this mean. One third of all subjects followed had no absolute decrease in renal function (positive slope of creatinine clearance vs. time) and there was a small group of patients who showed a statistically significant increase (P less than 0.05) in creatinine clearance with age.

Adult↗
PubMed1978

Urinary zinc excretion following infusions of zinc sulfate, cysteine, histidine, or glycine.

Zinc sulfate (40 mg elemental zinc) or one of three amino acids (5 or 10 g cysteine, 10 g histidine, or 10 g glycine) was infused into anesthetized dogs over a 60-min period. Plasma concentrations and urine excretions of zinc and five other cations, and glomerular filtration rates were determined before, during, and after these infusions. Infusions of zinc sufficient to produce a 20-fold increase in total plasma zinc concentrations had little effect on urinary zinc excretions (threefold increase) or plasma ultrafilterable zinc concentrations. Ten grams of cysteine urinary zinc excretions more than 100-fold, 5 g of cysteine increased zinc excretions more than 30-fold, 10 g of histidine increased zinc excretions sixfold, and 10 g of glycine had no effect. Cysteine infusions appeared to produce a net tubular secretion of zinc. Only histidine appeared to increase serum ultrafilterable zinc concentrations significantly. It would appear that plasma and urine concentrations of certain amino acids, specifically cysteine and histidine, along with polypeptides and other metabolites containing these amino acids, may be major determinants of urinary zinc excretion.

Animals↗
PubMed1978

Effects of acute and chronic splenectomy on experimental acute renal tubular lesions.

The first half of this study describes the effects of acute splenectomy on epinephrine-induced ATL in the dog. Renal morphology and hematocrit were compared in 12 dogs without splenectomy (group I), six dogs with antecedent splenectomy (group II), and seven dogs with antecedent splenectomy after splenic contraction was induced by topical application of epinephrine (group III). Splenectomy was performed in groups II and III 20 to 30 min prior to epinephrine infusion; all three groups received equal infusions (4 microgram/kg/min) for 6 hr before the kidneys were harvested. ATL and renal congestion were consistently severe in group I but infrequent and less severe in groups II and III. The second half of this study describes the apparent protective effect of chronic (2-week) splenectomy on epinephrine-induced ATL. Renal morphology and hematocrits were compared in 13 intact dogs (group IV) and 10 dogs splenectomized 2 weeks before the epinephrine infusion (group V). The severity of the ATL and the degree of renal congestion were significantly less in the chronically splenectomized dogs. This chronic protection afforded by acute and chronic splenectomy observed after epinephrine infusion remains unclear.

Animals↗
PubMed1977

Hereditary (familial) renal disease: clinical and genetic studies.

Four or more generations of three Oklahoma-Kansas families in which multiple members have been found to have glomerulonephritis or interstitial nephritis have been studied. Twenty-five of 146 members in kindred A, 16 of 50 members in kindred B, and 33 of 156 members in kindred C were identified as probably to definitely afflicted. Renal tissue from members of the first two families showed an acute or chronic glomerulonephritis. Renal failure often appeared by the third decade. The lesions were less frequent but more rapidly lethal in the male members. Renal tissue from members of the third kindred showed an interstitial nephritis. This appeared later in life and followed a more chronic course. Hearing loss was common in both groups. The hereditary studies are consistent with the hypothesis that the disease is transmitted by an autosomal dominant gene with imcomplete penetrance (not all members carrying the gene develop renal disease) and variable expressivity. Male-to-male transmission was present in all three families but less frequently than would be predicted, suggesting a reduced clinical expression of the disease in males who receive the mutant gene from their father.

Adult↗