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Biomedical subjects

F Llach

Publications and source records attributed to F Llach.

At least 73 records · Page 4Linked to original sources
PubMed1986

Hypercalcemia and elevated calcitriol in a maintenance dialysis patient with tuberculosis.

A patient on maintenance hemodialysis had widely disseminated tuberculosis, hypercalcemia, and elevated levels of calcitriol (1,25-dihydroxycholecalciferol). Hypercalcemia was not observed until the eighth month of hemodialysis, when persistent fevers began. At the end of a calcium-free dialysis, the plasma calcium concentration decreased to 6.6 mg/dL (1.65 mmol/L). The baseline calcitriol level was 56 pg/mL (normal, 19 to 50 pg/mL) and increased to 147 pg/mL at the end of hemodialysis. Parathyroid hormone levels by three separate assays did not appreciably increase during the hypocalcemia induced by the calcium-free hemodialysis. The serum phosphate concentration decreased from 7.3 to 4.5 mg/dL (2.36 to 1.45 mmol/L). Extrarenal production of calcitriol may occur in disseminated tuberculosis and may be stimulated by hypocalcemia and reduced serum phosphate. The expected parathyroid hormone response to hypocalcemia may have been inhibited by persistently elevated calcitriol levels or preexisting hypercalcemia.

Calcitriol↗
PubMed1985

Effect of dialysis and ultrafiltration on osmolality, colloid osmotic pressure, and vascular refilling rate.

The effect of regular dialysis and isolated ultrafiltration on plasma osmolality, plasma colloid osmotic pressure (COP), plasma volume, and vascular refilling rate was evaluated in maintenance dialysis patients. Nineteen patients underwent regular dialysis and 11 isolated ultrafiltration. Blood samples from these subjects were obtained from arterial or venous dialysis system ports and peripheral veins. For any decrease in plasma volume, there was an increment in COP with each procedure in both venous and arterial ports and the presence of a progressive decrease of plasma osmolality was observed only during regular dialysis. Second, five additional patients underwent 2 hrs of regular dialysis and isolated ultrafiltration in separate sessions removing comparable amounts of fluid (approximately 2.5 liter); after 2 hrs, there were no differences in the changes of plasma volume and COP, but again plasma osmolality decreased only during regular dialysis. These studies demonstrate that moderate changes in plasma osmolality do not affect COP. Furthermore, the ability of the plasma to recruit fluid and generate vascular refilling (as assessed by COP) is similar during regular dialysis and isolated ultrafiltration, provided the rates of ultrafiltration are the same.

Adult↗
PubMed1985

Altered divalent ion metabolism in early renal failure: role of 1,25(OH)2D.

The present study evaluates the role of 1,25(OH)2D in the pathogenesis of abnormal mineral metabolism in patients with early renal failure (ERF). This was accomplished by examining the calcemic response to PTH and the handling of an oral phosphate load both before and after 6 weeks of therapy with 1,25(OH)2D. Twelve patients with ERF and six normal volunteers were studied. Patients with ERF as compared with normal subjects have low serum phosphate, low urinary calcium, low serum 1,25(OH)2D, and high plasma PTH and urinary cyclic AMP (cAMP). With EDTA infusion, an impaired calcemic response to PTH is observed in patients with ERF. The phosphate load test shows that these patients have an increased ability to excrete phosphate. After 1,25(OH)2D therapy a significant increase in serum phosphate, urinary calcium, and a decrease in urinary cAMP is observed only in ERF patients. In addition, the impaired calcemic response to PTH improves significantly, the renal handling of phosphate becomes normal, and the low baseline level of 1,25(OH)2D increases to normal. A significant correlation between levels of 1,25(OH)2D and creatinine clearance is observed in both patients and normals. In summary, the present data suggest that a mild deficiency of 1,25(OH)2D is present in ERF patients. The pathophysiological consequence of such a deficiency in patients with ERF may be important.

Aged↗
PubMed1985

On the mechanism of secondary hyperparathyroidism in moderate renal insufficiency.

The effect of prolonged (60 days) dietary phosphate restriction on divalent ion metabolism was studied in four patients with moderate renal insufficiency in an effort to delineate the mechanisms of secondary hyperparathyroidism in renal failure. The patients had low normal serum phosphorous and normal vitamin D metabolite levels but had evidence of disturbances in target organs for vitamin D, including impaired intestinal absorption of calcium, reduced calcemic response to PTH, low serum ionized calcium levels, and, consequently, elevated PTH levels. After dietary phosphate restriction, there was marked improvement or normalization of intestinal absorption of calcium, calcemic response to PTH, and ionized calcium and PTH levels. There was also a significant rise (44%) in serum 1,25-dihydroxyvitamin D levels. The data suggest that intracellular phosphorous retention, which may develop as renal insufficiency ensues, may interfere with the action and production of 1,25-dihydroxyvitamin D. This leads to defective intestinal calcium absorption and reduced calcemic responses to PTH. As a result, hypocalcemia develops, causing secondary hyperparathyroidism. Our data assign a critical role for a disturbance(s) in vitamin D metabolism in genesis of the hyperparathyroidism of renal failure.

Calcium↗
PubMed1984

Thromboembolic complications in nephrotic syndrome. Coagulation abnormalities, renal vein thrombosis, and other conditions.

In patients with nephrotic syndrome, the presence of a hypercoagulable state is thought to give rise to a high incidence of thromboembolic phenomena. Renal vein thrombosis is a common complication in nephrotic patients, mainly in those with membranous nephropathy, and many other types of thromboembolic complications also occur. The mortality rate in nephrotic patients with thromboembolic complications may be significantly increased, with pulmonary emboli likely being the most common cause of death.

Antithrombins↗
PubMed1984

Parathyroid hormone and bone histology: response to hypocalcemia in osteitis fibrosa.

The parathyroid hormone (PTH) response to hypocalcemia was studied in 18 hemodialysis patients with osteitis fibrosa, and the relationship with PTH and bone histology in 26 hemodialysis patients. Hypocalcemia was produced during hemodialysis by the use of a dialysate devoid of calcium. Both amino (N) (P less than 0.05) and carboxy (C) (P less than 0.005) terminal PTH attained maximum levels by 15 min despite only a minimal decline in plasma calcium. Throughout the remainder of the study, C and N-PTH levels remained elevated but did not increase despite a further decline in plasma calcium. Five patients increased both C and N-PTH to maximum or near maximum levels by the first sampling, although plasma calcium remained above 9 mg/dl. Basal C and N-PTH correlated with the maximum levels of each induced by hypocalcemia (P less than 0.005). Both basal N-PTH and the maximum change in C-PTH produced by hypocalcemia correlated with osteoblastic osteoid, active resorption, osteoclasts/mm2, and endosteal fibrosis (P less than 0.005). In conclusion, (1) a minimal decline in plasma calcium produces a maximum C and N-PTH response; (2) an altered PTH set point may be present in some hemodialysis patients; (3) the correlation between basal and maximally stimulated PTH levels suggests that basal PTH levels may reflect parathyroid gland mass; and (4) a correlation with basal and stimulated PTH and bone histology is present.

Adult↗
PubMed1984

Phosphorus administration in patients with profound hypophosphatemia.

The influence of severe hypophosphatemia (less than or equal to 1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (+/- SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 +/- 1.3 vs. 17.8 +/- 1.3 ng/ml, P less than 0.001). With phosphorus administration, serum phosphorus increased from 0.59 +/- 0.07 to 2.58 +/- 0.09 mg/dl while 1,25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 +/- 4.3 to 14.3 +/- 2.9 pg/ml (P less than 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggesting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P less than 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P less than 0.005) and after (r = 0.74, P less than 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].

Adult↗
PubMed1984

Postparathyroidectomy hypocalcemia as an accurate indicator of preparathyroidectomy bone histology in the uremic patient.

19 chronic renal failure patients underwent iliac crest bone biopsy prior to total parathyroidectomy with autotransplantation. The preoperative serum calcium concentration did not correlate with the number of osteoclasts/mm2 present on the preparathyroidectomy iliac biopsy. However, the postparathyroidectomy decrement in serum calcium (mg/dl and percent change) and the osteoclasts/mm2 were strongly correlated (p less than 0.001). In addition, the postoperative fall in serum calcium also correlated with the postoperative change in serum alkaline phosphatase (p less than 0.001). The nadir in postparathyroidectomy serum calcium was attained in a mean of 4.4 +/- 2.7 days. Our results indicate that the preoperative serum calcium concentration does not necessarily reflect active bone resorption, but the postoperative decrement in serum calcium provides an accurate index of preoperative histologic activity. The available data do not provide information with respect to the mechanism of postparathyroidectomy hypocalcemia since either the cessation of bone resorption, continued bone deposition, or a combination of both may be operative.

Adult↗
PubMed1983

Parathyroid hormone response to hypocalcemia in hemodialysis patients with osteomalacia.

The parathyroid hormone response to hypocalcemia was investigated in hemodialysis patients with osteomalacia and compared to those with osteitis fibrosa. Hypocalcemia was induced during hemodialysis by employing a dialysate devoid of calcium. Patients with osteomalacia had a blunted maximum amino terminal parathyroid hormone response (+/- SD) (0.39 +/- 0.33 vs. 0.87 +/- 0.53 ng/ml, P less than 0.05) and maximum carboxy terminal parathyroid hormone response (+/- SD) (0.36 +/- 0.20 vs. 0.84 +/- 0.47, P less than 0.02) to hypocalcemia. The decline in plasma calcium was greater in patients with osteomalacia at 90 (P less than 0.05), 120 (P less than 0.01), and 150 min (P less than 0.01). In osteomalacia patients the surface density of histologically detectable trabecular bone aluminum correlated directly with the percent relative osteoid volume (P less than 0.005) and inversely with the maximum amino terminal parathyroid hormone response to hypocalcemia (P less than 0.025). These results suggest that hemodialysis patients with osteomalacia have diminished secretion of parathyroid hormone and a decreased ability to restore plasma calcium homeostasis during hypocalcemia.

Bone and Bones↗
PubMed1983

Animal model of aluminum-induced osteomalacia: role of chronic renal failure.

Both aluminum toxicity and a relative deficiency of parathyroid hormone have been implicated in the development of osteomalacia in dialysis patients. To study the effect of intraperitoneal (IP) aluminum injections on bone histology and parathyroid hormone and to determine if chronic renal failure accentuates aluminum toxicity, rats were divided into five groups: normals (N); low dose aluminum (LDA), 0.1 mg IP aluminum daily; high dose aluminum (HDA), 1.0 mg IP aluminum daily; chronic renal failure (CRF); and chronic renal failure plus high dose aluminum (CRF-HDA). At the conclusion of the study, there were no differences between N and LDA rats. Between the other groups, marked differences were observed. Compared to N rats, the relative osteoid volume (P less than 0.02) and the osteoid seam width (P less than 0.001) were increased in HDA, CRF, and CRF-HDA rats. Percent resorption and osteoclasts/mm2 were increased in CRF rats (P less than 0.02) and decreased in HDA rats (P less than 0.05). Compared to N rats, the amino terminal parathyroid hormone was decreased in HDA rats (P less than 0.02) despite the presence of hypocalcemia. These data suggest that (1) aluminum toxicity produces osteomalacia; (2) a relative parathyroid hormone deficiency may be a contributory factor; (3) chronic renal failure increases the severity of aluminum-induced osteomalacia; and (4) chronic renal failure alone does not result in osteomalacia.

Aluminum↗
PubMed1983

The effects of calciferol and its metabolites on patients with chronic renal failure. I. Calciferol, dihydrotachysterol, and calcifediol.

The available data with regard to the use of calciferol, dihydrotachysterol, and calcifediol in the management of renal insufficiency are reviewed. Very limited data are available with regard to calciferol therapy; with the advent of more active metabolites, the use of calciferol is not warranted. Dihydrotachysterol seems to be effective in the treatment of renal patients with osteitis fibrosa; its low cost makes therapy with this compound a reasonable alternative, although it should not be used in the treatment of patients with liver disease. Calcifediol seems to be effective in patients with osteitis fibrosa; however, limited data on histologic characteristics of bone are available. Detailed prospective studies are necessary to establish the therapeutic benefit of calcifediol.

Absorption↗
PubMed1983

The effects of calciferol and its metabolites on patients with chronic renal failure. II. Calcitriol, 1 alpha-hydroxyvitamin D3, and 24,25-dihydroxyvitamin D3.

The available data with regard to the use of calcitriol, 1 alpha-hydroxyvitamin D3 (1 alpha-OH D3), and 24,25-dihydroxyvitamin D3 (24,25-[OH]2D3) in the management of chronic renal insufficiency are reviewed. Patients with mild to moderate osteitis fibrosa experience substantial improvement with either calcitriol or 1 alpha-OH D3 therapy. However, few patients experience a reversal to normal in histologic characteristics of bone. The conditions of patients with osteomalacia do not respond to either calcitriol or 1 alpha-OH D3 therapy. The bone lesion appearing in these patients is most likely a toxic effect of aluminum. The prognosis is usually poor, but the conditions of some patients may respond to administration of 24,25-(OH)2D3 together with calcitriol. Preliminary data suggest that use of chelating agents may be beneficial. In this group of patients, 24,25-(OH)2D3 administration together with calcitriol may be beneficial.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Mechanisms of splenectomy protection in epinephrine-induced renal and cardiac necrosis.

This study was intended to elucidate the mechanism(s) of protection afforded by splenectomy against EPI-induced ATN and myocardial necrosis. Renal function parameters, hematocrit, circulating catecholamines (EPI and NE), serum enzymes (CPK and SGOT), and urinary PGE2 were measured before and during intravenous infusion of EPI (4 micrograms/kg/min for 6 hr) in intact and chronically splenectomized animals. All but serum enzymes were measured in another group of splenectomized animals that were implanted with small fragments of the autologous spleen (autoimplanted animals) 2 weeks prior to EPI infusion. Renal function tests and urinary PGE2 levels were monitored for several hours during the recovery period. The development of ARF in intact animals was accompanied by marked increases in circulating catecholamine levels, hematocrit, and serum enzymes and by a marked decrease in urinary PGE2 levels. These animals had diffuse ATN and hemorrhagic lesions of the heart (myocardial necrosis), and none survived. Chronically splenectomized animals were protected against the adverse effects of EPI infusion. The protected animals showed minimal elevation of circulating catecholamine levels and no changes in urinary PGE2 levels or hematocrit. Serum enzymes and renal and cardiac histopathology remained essentially normal in these animals. Implantation of autologous splenic tissue in splenectomized animals caused reversal of the protective effect of splenectomy. The response of autoimplanted animals to EPI infusion was in all respects similar to that in intact animals with the exception of hematocrit, which did not rise. All autoimplanted animals survived. They showed prompt recovery of renal function associated with significant increase of urinary PGE2 levels during the recovery period. Focal ATN was observed but no hemorrhagic lesion of the heart was found. From these observations we conclude the following: (1) high circulating NE and/or low renal (urinary) PGE2 activity are important in the pathogenesis of EPI-induced ARF, (2) the spleen may release some factor(s) that modulate plasma NE level and/or renal PGE2 activity during EPI infusion, (3) EPI-induced ARF may occur independently of myocardial necrosis, and (4) hematocrit has no major role in EPI-induced ARF.

Acute Kidney Injury↗