Biomedical subjects
J Lemann
Publications and source records attributed to J Lemann.
The calciuria of increased fixed acid production in humans: evidence against a role for parathyroid hormone and 1,25(OH)2-vitamin D.
We measured mineral and acid balances, serum iPTH, urinary cAMP/creatinine, and plasma concentrations of 25OHD and 1,25(OH)2D in 7 healthy adults during control conditions and during increased fixed acid production achieved either by the administration of NH4Cl (N = 3) or by increased dietary protein intake (N = 4). When acid production was increased, the subjects were in positive acid balance and negative Ca balance because of increased urinary Ca excretion. Serum iPTH fell slightly but urinary cAMP and the plasma levels of vitamin D metabolites did not change. W conclude that the accelerated skeletal and urinary losses of Ca that occur when fixed acid production is increased are not contributed to nor compensated for by the parathyroid-vitamin D endocrine systems.
Urinary calcium excretion in human beings.
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Plasma 1,25-(OH)2-vitamin D concentrations and net intestinal calcium, phosphate, and magnesium absorption in humans.
We evaluated the relationship between plasma concentrations of the renal hormone 1,25-(OH)2-vitamin D and net intestinal absorption of Ca, PO4, and Mg in vitamin D-replete patients eating similar diets, who had undetectable, normal or elevated plasma 1,25-(OH)2-D levels, Net intestinal Ca absorption was positively correlated to plasma 1,25-(OH)2-D concentrations: percentage dietary Ca absorbed = 10 + 0.17 x plasma total 1,25-(OH)2-3, pmole/liter, r = + 0.58; P less than 0.001. By contrast, there was no significant correlation between PO4 or Mg absorption and plasma 1,25-(OH)2-D concentrations. Moreover, significant quantities of PO4 and Mg were absorbed in the absence of detectable plasma 1,25-(OH)2-D. We conclude that net intestinal Ca absorption is critically dependent upon the availability of the renal hormone 1,25-(OH)2-D in vitamin D-replete humans when dietary Ca intake is normal. By contrast, other factors must play a dominant role in regulating net intestinal PO4 and Mg absorption.
The effects of oral CaCO3 loading and dietary calcium deprivation on plasma 1,25-dihydroxyvitamin D concentrations in healthy adults.
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The interrelationships among prolactin, 1,25-dihydroxyvitamin D, and parathyroid hormone in humans.
Serum PRL, parathyroid hormone (PTH), and plasma 1,25-dihydroxyvitamin D [1,25(OH)2D]concentrations were measured in 6 women and 2 men with hyperprolactinemia, 6 normal men and 7 normal women, 4 men and 4 women with primary hyperparathyroidism, and 16 men and 4 women with Ca nephrolithiasis. Plasma 1,25(OH)2D and serum parathyroid hormone (PTH) concentrations were normal in the women and men with hyperprolactinemia. In patients with primary hyperparathyroidism and elevated serum PTH, plasma 1,25(OH)2D concentrations were elevated but serum PRL levels were normal. Likewise, serum PRL levels were normal in patients with Ca nephrolithiasis who had significantly elevated plasma, 1,25(OH)2D concentrations and normal serum PTH concentrations. Thus, hyperprolactinemia due to pituitary adenoma or idiopathic hypersecretion is not accompanied but elevated plasma concentrations of 1,25(OH)2D.
Reversal of chronic end-stage renal failure due to myeloma kidney.
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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.
Evidence for a renal PO4 leak in patients with calcium nephrolithiasis.
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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).
The simultaneous measurement of vitamin D metabolites in plasma: studies in healthy adults and in patients with calcium nephrolithiasis.
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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.
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.
Acute renal failure.
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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.
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.
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.
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.