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Biomedical subjects

J Lemann

Publications and source records attributed to J Lemann.

At least 73 records · Page 4Linked to original sources
PubMed1979

The effects of dihydrotachysterol therapy on the measurement of plasma 1,25-(OH)2-vitamin D in humans.

Anephric patients have undetectable plasma concentrations of 1,25-(OH)2-D, but when anephric patients are treated with DHT2 (Hytakerol), their plasma contains a substance that is co-purified with and displaces authentic 3H-1,25(OH)2-D3 from its intestinal cytoplasmic receptor. The concentration of this substance in the plasma of anephric patients taking DHT2 is proportional to the administered daily dose of DHT2 per kilogram body weight. When DHT2 therapy is discontinued, the substance disappears from plasma with an average t 1/2 of about 8 days.

Dihydrotachysterol↗
PubMed1978

Metabolism and excretion of 3H-1,25-(OH)2-vitamin D3 in healthy adults.

The synthesis of very high specific activity 25-OH-vitamin D3 (78 Ci/mmol) has made possible the study of the metabolism and plasma disappearance of 3H after a single dose of 3H-1,25-(OH)2-D3 in quantities that are only 10-20% of the endogenous plasma pool. We studied seven healthy adults who were given doses of 1,25-(OH)2-D3 ranging from 30-2300 pmol. Plasma disappearance was rapid with only 14 +/- 2% of administered 3H remaining in the plasma pool 4 h after labeling. Plasma metabolite profiles during the first 4 h showed only 1,25-(OH)2-D3. Thereafter, significant amounts of other metabolites were detected. The 6-day cumulative excretion of 3H in urine and feces (virtually all associated with metabolites of 1,25-(OH)2-D3) averaged 16 +/- 3% and 49 +/- 11% of the dose, respectively. Compartmental analysis of the isotope data for two subjects who received the smallest doses of 1,25-(OH)2-D3 indicated that endogenous renal 1,25-(OH)2-D3 synthesis rates approximate 0.8-2.4 nmol/day (0.3-1.0 microgram/day).

Adult↗
PubMed1978

Effect of glucocorticoids on WBC counts in splenectomized renal transplant recipients.

Change in peripheral blood WBC and differential cell count in response to oral glucocorticoids (steroids) was examined in 36 stable renal transplant patients receiving their usual steroid dose on a daily or alternate-day steroid schedule. Three hours following steroid therapy mean WBC count had increased significantly. Mean change in WBC count was +2,400 cells/cu mm with individual values ranging from -600 to +8,000/cu mm. No differences were observed between patients receiving daily or alternate-day regimens. Changes in WBC count were due almost entirely to an increase in segmented granulocytes and a decrease in lymphocytes. there was no correlation between dose of steroid and WBC responses. However, when retested, a given patient's WBC response to a given dose of steroid was reproducible. Differences between patients, with respect to WBC response to steroids, could not be explained by differences in azathioprine dose and was not related to initial WBC count hematocrit value, age, duration of transplant, or levels of serum creatinine, BUM, or serum phosphorus. Because of the clinical importance of the WBC count in the renal transplant recipient and the potential for large and unpredictable changes in WBC count in response to steroids, WBC and differential cell count should be obtained before the morning steroid dose.

Azathioprine↗
PubMed1978

A model for planning health care in patients with end-stage renal disease.

Treatment modalities of end-stage renal disease (ESRD) patients include in-center dialysis, home dialysis, and kidney transplant. We present a model to account for all aspects of modality use to aid in planning regional facilities. Five years of data for 979 patients on dialysis in Wisconsin between 1970 and 1975 are used. The model shows movement (transit probabilities) from one modality to another, eg, transition from in-center dialysis to transplantation, and data were used to derive all transitional probabilities characterizing patient movement from one modality to another. Model and probabilities were used to predict number of patients in each modality in 1976, and the model was used to predict number of patients in each treatment modality through 1990. These figures may be used for planning regional facilities. Extrapolation of this model and derived probabilities for nationwide projections may be possible.

Adolescent↗
PubMed1977

The importance of phosphate in regulating plasma 1,25-(OH)2-vitamin D levels in humans: studies in healthy subjects in calcium-stone formers and in patients with primary hyperparathyroidism.

We observed that plasma 1,25-(OH)2-D concentrations average 87 +/- 30 SD pmol/l in 48 healthy adults without a personal or family history of kidney stones. Plasma 1,25-(OH)2-D concentrations were significantly elevated among 26 patients with recurrent calcium-containing renal stones and hypophosphatemia: 150 +/- 74 pmol/l; P less than 0.001, and among 9 patients with proven parathyroid adenoma and hypophosphatemia: 200 +/- 54 pmol/l; P less than 0.001. Plasma 1,25-(OH)2-D levels in these 3 groups were inversely correlated with serum phosphate concentration: plasma 1,25-(OH)2-D, pmol/l = 282 - 141 X serum PO4, mmol/l; r = 0.51; P less than 0.001. During dietary PO4 deprivation lasting 11 to 16 days in 10 healthy women, serum PO4 fell and plasma 1,25-(OH)2-D concentrations rose whereas in 8 healthy men neither serum PO4 nor 1,25-(OH)2-D concentrations changed. The change from control in plasma 1,25-(OH)2-D levels were correlated with the change from control in serum PO4 concentrations: delta1,25-(OH)2-D, pmol/l = 1 - 82 X delta serum PO4 mmol/l; r = 0.59; P less than 0.01. We conclude that reductions in serum PO4 concentrations, either directly or indirectly, stimulate renal synthesis of 1,25-(OH)2-D in humans.

Adult↗
PubMed1977

Infantile polycystic kidney disease in the adult.

We evaluated an adult with polycystic kidney disease that had been present since birth. Our evidence indicates that this patient is a unique example of survival into adult life of the recessively inherited, infantile form of polycystic kidney disease.

Adult↗
PubMed1976

A simple method of estimating progression of chronic renal failure.

In 31 of 34 patients with chronic renal insufficiency caused by various diseaes, reciprocal serum-creatinine concentration declined linearly as creatinine concentration rose from a mean of 2-6 mg/dl to 14-8 mg/dl over an average of 71 months. These results indicate that in most cases reciprocal serum-creatinine declines linearly with time as chronic renal failure progresses. Analysis of this relation in individual patients gives an estimate of the progression of the disease, may help to determine the effects of therapy, and could be used to predict when dialysis will become necessary.

Creatinine↗
PubMed1976

Interaction of rifampin and glucocorticoids. Adverse effect on renal allograft function.

Three renal transplant patients experienced progressive loss of renal allograft function during rifampin treatment for Mycobacterium tuberculosis. Previous studies have shown that rifampin causes induction of enzymes in hepatic microsomes that increase the catabolism of glucocorticoids. Evidence is presented that in our patients, the loss of renal allograft function during rifampin therapy was the result of decreased glucocorticoid effect presumably related to increased catabolism of the glucocorticoid drug they received. Thus, the adverse effects of rifampin on renal transplant function might be overcome by increasing the dose of glucocorticoid drug.

Adult↗
PubMed1976

The lack of effect of chronic metabolic acidosis on 25-OH-vitamin D metabolism and serum parathyroid hormone in humans.

We evaluated the turnover of the plasma 25-OH-vitamin D pool, acid, and mineral balances in paired balance studies of 6 normal subjects during normal acid base conditions and during stable chronic metabolic acidosis induced by NH4Cl. Positive acid balances and negative Ca balances due to hypercalciuria were observed as previously reported. Plasma 25-OH-D pool turnover averaged 6.1+/-0.4 nmol/day during control and did not change during acidosis (6.5 +/- 0.5 nmol/day) nor were any significant increments in net intestinal absorption of Ca, PO4, or Mg, the physiological expression of vitamin D action, observed during acidosis. In 3 other subjects, repetitive measurements of serum iPTH during 7 control days and 24 days of stable NH4Cl acidosis showed no changes. We interpret the data to support the hypothesis that neither PTH nor vitamin D and its metabolites mediates the increase in net bone resorption that must accompany chronic metabolic acidosis.

Acidosis↗
PubMed1976

Dietary phosphate deprivation in women and men: effects on mineral and acid balances, parathyroid hormone and the metabolism of 25-OH-vitamin D.

We evaluated the effects of dietary PO4 restriction on 25-OH-Vitamin D3 metabolism, serum iPTH levels, and mineral balances in healthy women and men. PO4 balances were progressively negative because of fecal losses without sex difference. Turnover of the plasma 25-OH-D pool was increased from 5.8 +/- 0.4 to 12 +/- 1.2 nmol/day; P less than 0.001, despite a fall in serum iPTH of -1.1 +/- 0.3 mulEq/ml; P less than 0.01. In both sexes, net intestinal calcium and magnesium absorption increased in proportion to a more rapid turnover of the plasma 25-OH-D pool, implying increased renal 1,25-(OH)2-D3 production. By contrast, there was a striking sex difference in the response of serum PO4 to dietary PO4 deprivation; the levels falling progressively in women, but remaining at control levels in men. Women demonstrated progressive hypercalciuria and negative Ca balances while in men the increments in intestinal Ca absorption were approximately matched by the increments in urinary Ca excretion so that Ca balances were not different from zero.

Adolescent↗
PubMed1976

Error introduced by specimen handling before determination of inorganic phosphate concentrations in plasma and serum.

Values for serum inorganic phosphate (Pi) concentrations in groups of healthy adults vary widely, the coefficient of variation ranging from 10 to 15%. We undertook to determine in 23 healthy adults whether part of this variation could be accounted for by (a) drawing blood in syringes vs. evacuated tubes (b) the time between blood sampling and separation of serum or plasma, and (c) the prevention of clotting. Values were unaffected by a, decreased significantly with time at room temperature between blood sampling and separation of cells in both serum and plasma, and were significantly lower in plasma than in serum. The group coefficient of variation for Pi averaged 13% and was uninfluenced by the blood-processing technique.

Blood Specimen Collection↗
PubMed1974

The effect of glucose on urinary cation excretion during chronic extracellular volume expansion in normal man.

Both glucose administration and extracellular volume expansion augment urinary calcium and magnesium excretion. While volume expansion also augments sodium excretion, glucose induces an antinatriuresis. To examine the interrelationships of volume expansion and of glucose administration on sodium, calcium, and magnesium excretion, the effects of glucose were evaluated during clearance studies in the same subjects before and after chronic extracellular volume expansion produced by desoxycorticosterone acetate (DOCA) and a normal dietary sodium intake. The augmentation of U(Ca)V and U(Mg)V by glucose was simply additive to the increments in divalent cation excretion caused by "escape" from the sodium-retaining effects of DOCA. Glucose administration reduced U(Na)V, an effect exaggerated after DOCA escape and associated with reductions in volume/glomerular filtration rate (V/GFR) and C(Na) + C(H2O)/GFR, suggesting augmented proximal tubular reabsorption. Before glucose, U(Na) was inversely correlated with U(G), and after glucose administration C(Na)/GFR was inversely correlated with T(G)/GFR. We propose that the availability of glucose in the proximal tubule stimulates Na reabsorption while delaying development of a chloride diffusion potential, thereby inhibiting tubular reabsorption of Ca and Mg.

Bicarbonates↗