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Biomedical subjects

J Lemann

Publications and source records attributed to J Lemann.

At least 55 records · Page 3Linked to original sources
PubMed1982

Rapidly progressive glomerulonephritis superimposed on diabetic glomerulosclerosis. Recognition and treatment.

Two patients with long-standing diabetes mellitus and diabetic retinopathy were evaluated for declining renal function and heavy albuminuria. Initially, diabetic glomerulosclerosis was suspected as the cause of progressive glomerulopathy. However, in both patients the rate of loss of glomerular filtration rate was greater than that usually seen in diabetic glomerulosclerosis, and the urine sediment contained many RBC casts. These findings led to renal biopsy, which demonstrated crescentic glomerulonephritis superimposed on diabetic glomerulopathy. Both patients were treated with prednisone and cyclophosphamide and both experienced substantial improvement in renal function. These experiences demonstrate the importance of searching for evidence of a superimposed treatable glomerulopathy in the diabetic patient with glomerulopathy and advancing renal insufficiency.

Adult↗
PubMed1982

Habitual excessive dietary salt intake and blood pressure levels in renal transplant recipients.

We observed that renal transplant recipients with good graft function (mean serum creatinine level 1.5 mg/dl +/- 0.5 SD, N = 68) had dietary salt intakes (estimated from serial measurements of 24-hour sodium excretion rate) which averaged 43 percent higher than that of a comparable group of healthy subjects. There was no correlation between blood pressure levels and salt intake and, despite the high dietary salt intake, hypertension was present in only 29 patients and was usually mild; mean systolic and diastolic blood pressures were 132 +/- 10 mm Hg and 89 +/- 7 mm Hg, respectively while the patients were receiving antihypertensive medication (median number of standard doses of antihypertensive medication was 1.0 doses/patient patient per day). These observations suggest that high dietary salt intake does not exert a powerful blood pressure elevating effect, since any effect of high dietary salt intake to raise blood pressure should have been magnified in the renal transplant recipients because of their reduced renal mass and their chronic glucocorticoid therapy.

Adult↗
PubMed1982

Calcium-oxalate-crystal-induced bone disease.

A 13-year-old boy with primary hyperoxaluria and a successful renal allograft developed symptomatic bone disease, hypercalcemia, and hypercalciuria. Transiliac bone biopsy revealed calcium oxalate crystals in the marrow within mononuclear phagocytes and multinucleated giant cells. Deep resorption bays were seen adjacent to these crystal-cell aggregates. Serum 1,25-(OH)2-vitamin D (calcitriol) and iPTH concentrations were low or normal. We suggest that hypercalcemia results from macrophage-mediated bone resorption initiated by Ca oxalate crystal deposition.

Adolescent↗
PubMed1982

Effects of calcitriol administration on calcium metabolism healthy men.

To evaluate the relationship between daily and fasting urinary calcium excretion and serum 1,25-(OH)2-D concentrations, we studied six healthy men during control and during chronic oral calcitriol administration (0.6, 1.2, or 1.8 nmoles every 6 hours for 6 to 12 days) while they ate normal and low calcium diets (calcium content, 19.2 or 4.2 mmoles/day). Daily urinary calcium excretion was directly related to serum 1,25-(OH)2-D concentrations but increased more (P less than 0.025) while subjects ate the normal calcium diet (slope, 0.081 mmole/day/pmole/liter, r = 0.94) than when eating the low calcium diet (slope, 0.043 mmole/day/pmole/liter; r=0.83). During calcitriol and ingestion of the low calcium diet, daily urinary calcium excretion averaged 7.32 +/- 2.6 mmoles/day, exceeding the dietary calcium intake (P less than 0.02). Moreover, during calcitriol, when serum 1,25-(OH)2-D exceeded 140 pmoles/liter, fasting urinary calcium/creatinine exceeded 0.34 mmole/mmole (the upper limit of normal) on either diet. When serum 1,25-(OH)2-D concentrations are elevated, a high fasting urinary calcium/creatinine or high daily urinary calcium excretion, even on a low calcium diet, is insufficient criteria for the documentation of a renal calcium leak.

Calcitriol↗
PubMed1982

Vitamin D metabolites and parathyroid hormone in Cushing's syndrome: relationship to calcium and phosphorus homeostasis.

We studied the effects of glucocorticoid excess on calcium and phosphorus homeostasis in relation to vitamin D metabolites and parathyroid hormone (PTH) in seven patients with spontaneous ACTH-dependent Cushing's syndrome. Remission of hypercortisolism resulted in a significant increase in tubular reabsorption of phosphate [from 76 +/- 4% to 89 +/- 2% (mean +/- SEM); P less than 0.01] and serum phosphorus (from 3.1 +/- 0.1 to 4.2 +/- 0.2 mg/dl; P less than 0.005). Serum calcium did not change, although there was a reduction in daily urinary calcium excretion from 0.23 +/- 0.02 to 0.107 +/- 0.02 mg calcium/mg creatinine. Serum immunoreactive PTH (iPTH) levels were normal during Cushing's syndrome (34 +/- 5 microleq/ml), but fell significantly after remission to 22 +/- 2 microleq/ml (P less than 0.05). This small decrease in iPTH did not correlate with the improvement of phosphate homeostasis. Plasma 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH2)D] concentrations in Cushing's syndrome did not differ from measurements in 97 normal subjects. After treatment, 25OHD did not change, but 1,25-(OH)2D fell in each patient from a mean of 44 to 22 pg/ml (P less than 0.02). 1,25-(OH)2D was inversely correlated with serum phosphorus (r = 0.59; P less than 0.01), but did not correlate with iPTH. The known impairment of intestinal calcium absorption in Cushing's syndrome cannot be attributed to a decrease in the circulating levels of 1,25-(OH)2D. Endogenous hypercortisolism decreases tubular phosphate reabsorption and serum phosphorus, increase tubular phosphate reabsorption and serum phosphorus, increases iPTH, and results in an increase in 1,25-(OH)2D. These events may contribute to the severe loss of bone mass in such patients and may account for the calciuria and phosphaturia of Cushing's syndrome.

25-Hydroxyvitamin D 2↗
PubMed1982

Urinary excretion of 25-hydroxyvitamin D in health and the nephrotic syndrome.

Patients with the nephrotic syndrome may exhibit low serum 25-OH-D concentrations. We developed a method for isolation of 25-OH-D from urine, with measurement by competitive binding assay. Daily urinary 25-OH-D excretion in healthy subjects averaged 0.17 +/- 0.15 nmol/day. Among nephrotic patients, urinary 25-OH-D excretion ranged from 0.27 to 10 nmol/day, in direct relation to the severity of proteinuria (r=0.76) and averaged 3.7 +/- 3.5 nmol/day. The 25-OH-D in the urine of nephrotic patients was unconjugated, implying that it was excreted with the serum VDBG, which has been shown to have a molecular weight and isoelectric point similar to that of albumin. We conclude that low serum 25-OH-D concentrations among nephrotic patients are principally the result or urinary losses of steroid. (J Lab Clin Med 99:325, 1982.)

25-Hydroxyvitamin D 2↗
PubMed1981

Method for detecting a progressive renal disorder superimposed on a preexisting progressive renal disorder.

We describe a patient with declining renal function due to polycystic kidney disease, who then insidiously develops bilateral renal artery stenosis. The major clue which led to the discovery of the bilateral renal artery stenosis was the finding of an unexpected increase in the rate of loss of renal function. This assessment was based on analysis of the slope of a plot of the reciprocal of the patient's serum creatinine concentration vs. time (reciprocal creatinine plot). The rationale for the use of the reciprocal creatinine plot to detect a progressive renal disorder superimposed upon a preexisting progressive renal disorder, is discussed.

Creatinine↗
PubMed1981

Synthesis and metabolic clearance of 1,25-dihydroxyvitamin D as determinants of serum concentrations: a comparison of two methods.

We evaluated endogenous renal 1,25-dihydroxyvitamin D (1,25-OH)2D) synthesis by compartmental analysis of the plasma disappearance of injected [3H]1,25-dihydroxyvitamin D3 in 11 subjects with serum 1,25-(OH)2D concentrations varying from 9-154 pM (normal, 89 +/- 25 pM). Estimated renal synthesis ranged from 2-180 pmol/kg . day. Serum 1,25-(OH)2D concentrations in these subjects best fit a log function of renal synthesis: serum 1,25-(OH)2D, pM = -13 + 74 log renal 1,25-(OH)2D production, picomoles per kg/day (r = 0.91). We also evaluated serum 1,25-(OH)2D concentrations in 6 healthy subjects who had been given 0.6, 1.2, or 1.8 nmol calcitriol every 6 h during a period 6--12 days after hormone administration was begun. Steady serum 1,25-(OH)2D concentrations 2, 4, and 6 h after the last calcitriol dose were achieved in proportion to log dose: serum 1,25-(OH)2D, pM = -12 + 103 log 1,25-dihydroxyvitamin D3 dose, picomoles per kg/day (r = 0.94). Estimated 1,25-(OH)2D production rates using these two methods and assuming a normal serum 1,25-(OH)2D concentration of 89 pM range from 10--24 pmol/kg . day or, for a 70-kg subject, 0.6--1.7 nmol/day or 0.25--0.7 microgram/day. Metabolic clearance of 1,25-(OH)2D appears to be accelerated when production rates are increased.

Calcitriol↗
PubMed1981

A human parathyroid carcinoma that produces parathyroid hormone: long term maintenance in tissue culture.

Parathyroid carcinoma cells from a pulmonary metastasis of a patient with a serum Ca of 17 mg/dl and an immunoreactive parathyroid hormone (PTH) of 6.4 ng eq bovine (b) PTH/ml (normal 40--400 pg/ml) have been maintained in tissue culture for more than 2 1/2 years. The cells secrete PTH into the culture media that 1) during immunoassay dilutes in parallel to human hyperparathyroid serum, 2) has a molecular weight similar to intact highly purified bPTH, and 3) stimulates bone resorption in a manner that is equivalent and additive to synthetic bPTH-(1--34).

Adult↗
PubMed1980

Stability of renal transplant function with alternate-day corticosteroid therapy.

Fifty-three renal transplant recipients with good to excellent renal function, while receiving daily maintenance or near-maintenance doses of azathioprine and methylprednisolone, were gradually converted to alternate-day corticosteroid therapy. Stability of allograft glomerular filtration rate (GFR) in each patient was assessed by calculating the slope of a plot of the reciprocal of the serum creatinine concentration vs time. After conversion to alternate-day therapy, GFR was stable in 80% but deteriorated in 20% of patients. However, most of the patients who experienced deteriorating GFR during alternate-day therapy regained stable renal function when given the same total corticosteroid dose but on a daily basis. This suggests but does not prove that maintenance-level daily corticosteroid therapy is better than maintenance-level alternate-day therapy in stabilizing allograft function. We conclude that maintenance-level alternate-day corticosteroid therapy should be used cautiously until a long-term prospective study determines whether there is an increased risk of losing renal function with this schedule and whether this potential risk is offset by reduced corticosteroid toxicity.

Adrenal Cortex Hormones↗
PubMed1980

Is there a disorder of phosphate metabolism in idiopathic hypercalciuria?

Hypophosphatemia either as a consequence of secondary hyperparathyroidism or as a consequence of a primary defect in phosphate metabolism appears to be a well established abnormality among subsets of patients with idiopathic hypercalciuria and nephrolithiasis. The detailed biochemical events that lead to hypophosphatemia in those patients who exhibit a primary abnormality of phosphate metabolism remain to be clarified.

Calcinosis↗
PubMed1980

Calcium and phosphate metabolism in tumoral calcinosis.

We have recently seen a patient with tumoral calcinosis, a syndrome comprising hyperphosphatemia, normocalcemia, normal glomerular filtration rate (GFR), and extensive periarticular calcific masses. Parathyroid hormone (PTH) deficiency or target organ resistance was ruled out by demonstration of normal serum PTH and urinary 3'5'cyclic AMP excretion and normal response to exogenous PTH and to endogenous stimulation by ethylenediaminetetraacetate. An intrinsic proximal tubular defect allowing enhanced renal PO4 reabsorption was probably present because there was no phosphaturic response to acetazolamine and renal PO4 threshold remained abnormally elevated even after PTH infusion. We then studied the mechanism by which serum calcium level is maintained in the normal range despite hyperphosphatemia and absence of secondary hyperparathyroidism. Normal 1,25-(OH)2 vitamin D was found, suggesting normal gastrointestinal calcium absorption. This, combined with markedly reduced urinary calcium excretion, perhaps a direct effect of hyperphosphatemia, may maintain calcium balance and prevent secondary hyperparathyroidism. A rise in urinary cyclic AMP excretion after furosemide-induced calciuria supports this hypothesis.

Adult↗
PubMed1979

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.

Acids↗
PubMed1979

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.

Adult↗
PubMed1979

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.

Adenoma↗