PubMed Health⌕ Search

Biomedical subjects

F Llach

Publications and source records attributed to F Llach.

At least 37 records · Page 2Linked to original sources
PubMed1993

Parathyroid gland function in chronic renal failure.

The concept that the PTH-calcium curve is representative of parathyroid function has been discussed. Comparisons of parathyroid function have been made between normal humans and hemodialysis patients and also between hemodialysis patients with different forms of renal osteodystrophy. From these comparisons, it is apparent that the magnitude of HPT is much greater in patients with renal failure than in normal humans, and as represented by the ratio of basal to maximal PTH, the parathyroid gland appears to be stimulated at basal serum calcium levels in hemodialysis patients. Similarly, based on an analysis of the PTH-calcium curve, we were able to determine that several differences in parathyroid function were present in hemodialysis patients with different forms of renal osteodystrophy. As compared to hemodialysis patients with LTAABD and aplastic bone disease, patients with osteitis fibrosa have a greater magnitude of hyperparathyroidism, a greater sensitivity of the parathyroid cell (slope), a higher set point of calcium, and greater PTH stimulation at basal serum calcium (ratio of basal to maximal PTH). Calcitriol treatment of hemodialysis patients with osteitis fibrosa resulted in a significant decrease in PTH throughout the PTH-calcium curve and also reduced the sensitivity (slope) of the PTH-calcium curve. The concept of hysteresis has been discussed as well as the role that the ambient basal serum calcium concentration may have on the determination of the PTH-calcium curve. Finally, the effect that successful renal transplantation has on HPT has been examined. In conclusion, we believe that the PTH-calcium curve provides a reliable assessment of parathyroid function, and as such, has considerable application for the study of parathyroid disorders in the clinical setting.

Calcitriol↗
PubMed1993

Aluminum kinetics using bicarbonate dialysate with the sorbent system.

In the REDY system a sorbent cartridge is used to regenerate the spent hemodialysate so that only six liters of dialysate are required for a treatment. The manufacturer claims that the cartridge can be used to remove aluminum from the dialysate and that it does not add aluminum to the dialysate. This claim for acetate dialysate is supported by the literature, but there are few data available relative to bicarbonate dialysate. The present study evaluates the use of bicarbonate dialysate and the REDY system in regard to aluminum kinetics both in vitro and in vivo. In vitro, the sorbent cartridge removed aluminum from dialysate prepared from water containing as much as 470 micrograms/liter of aluminum, giving a dialysate containing less than 10 micrograms/liter. The first 500 ml of effluent contained 13 micrograms/liter of aluminum but after filtration decreased to below 10 micrograms/liter. Thus, it is unnecessary, as recommended, to discard the first effluent since this unfilterable aluminum will not pass through a dialysis membrane. In vivo, in a crossover study comparing the REDY with single pass, there were no significant differences between the pre- and post-plasma aluminum concentrations, and the dialysate aluminum remained below 4 micrograms/liter during the dialysis. In a second in vivo study the effect of dialysate from tap water on plasma aluminum using the predialysis purification procedure was evaluated. There was no differences between the pre- and post-plasma aluminum concentration. The aluminum levels were comparable to those of the crossover study. The dialysate remained below 4 micrograms/liter during the dialysis.

Absorption↗
PubMed1993

Methods of controlling hyperphosphatemia in patients with chronic renal failure.

The problem of hyperphosphatemia in patients with chronic renal failure is reviewed. The importance of high plasma phosphorus levels in the pathogenesis of hyperparathyroidism is concisely discussed. Basic concepts about phosphorus metabolism in normal persons and in patients with chronic renal failure are outlined. This is followed by a detailed discussion of the various therapeutic methods to control hyperphosphatemia. Dietary restriction, dialysance of phosphorus, and the use of the currently available phosphorus binders are comprehensively discussed. Finally, the various clinical situations associated with failure to control hyperphosphatemia are reviewed.

Animals↗
PubMed1991

Calcitonin, an important factor in the calcemic response to parathyroid hormone in the rat.

The role of calcitonin on the calcemic response to parathyroid hormone (PTH) in renal failure has not been evaluated previously. Often animal studies evaluating the calcemic response to PTH in renal failure are performed in thyroparathyroidectomized (TPTX) animals, and thus eliminate any potential physiologic effect of calcitonin. In addition, parathyroidectomy (PTX), presumably by reduction of high PTH levels, has corrected the calcemic response to PTH in animals with renal failure. The present study was designed to evaluate the effect of endogenous calcitonin production on the calcemic response to PTH in rats with renal failure and secondary hyperparathyroidism, and in rats with normal renal function with diet induced hyperparathyroidism. Four groups of rats were evaluated: 1) chronic renal failure plus TPTX with autotransplant of the parathyroid gland, (CT-) CRF; 2) chronic renal failure plus selective PTX with autotransplant of the parathyroid gland, (CT+) CRF; 3) normal renal function plus TPTX with autotransplant of the parathyroid gland, (CT-) NRF; and 4) normal renal function plus selective PTX with autotransplant of the parathyroid gland, (CT+) NRF. Renal failure was surgically induced by a two-stage 5/6 nephrectomy, and exogenous thyroxine was administered to the two thyroidectomized (CT-) groups. Hyperparathyroidism was induced with a high phosphate diet (1.2%), and thus at the time of PTH infusion, PTH levels were (CT-) CRF 84 +/- 16, (CT+) CRF 89 +/- 21, (CT-) NRF 37 +/- 7, and (CT+) NRF 31 +/- 4 pg/ml, respectively (normal 21 +/- 3 pg/ml). Rat 1-34 PTH (2.6 U/hr) was infused for 48 hours via a subcutaneously implanted Alzet pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Sigmoidal relationship between calcitonin and calcium: studies in normal, parathyroidectomized, and azotemic rats.

Calcitonin secretion is stimulated by acute hypercalcemia. Furthermore, in the rat, the calcemic response to parathyroid hormone (PTH) is decreased by calcitonin stimulation. However, in renal failure, it is not known if an increase in the serum calcium concentration within the physiologic range of serum calcium stimulates calcitonin and whether the increased calcitonin decreases the calcemic response to PTH. In the present study, four groups of pair-fed rats were evaluated: normals (N); parathyroidectomy (PTX); and two groups with renal failure (RF)--basal serum calcium less than 8.5 mg/dl (RFa) and basal serum calcium greater than 8.5 mg/dl (RFb). Hypocalcemia was induced by parathyroidectomy or in the RFa group, by a high phosphate diet. Increases in the serum calcium were produced by a 48 hour infusion of rat 1-34 PTH. In the RFa and PTX groups, stimulation of calcitonin was observed as the serum calcium increased from hypocalcemia to normal levels of calcium (P less than 0.01). In all four groups, increasing the serum calcium from normal levels to hypercalcemia increased the serum calcitonin level (P less than 0.05). The relationship between serum calcitonin and calcium was best expressed as a sigmoidal curve. In the two groups with basal hypocalcemia, PTX and RFa, the calcitonin-calcium curve was shifted to the left of the N and RFb groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Calcemic response to parathyroid hormone in renal failure: role of phosphorus and its effect on calcitriol.

The calcemic response to parathyroid hormone (PTH) is decreased in renal failure. The reduction of hyperphosphatemia improves the calcemic response to PTH in animals with advanced renal failure. However, since low calcitriol levels in renal failure may also contribute to the decreased calcemic response to PTH, the improved calcemic response observed during the reduction of serum phosphorus may be partially mediated by an increase in serum calcitriol levels. The present study evaluated the calcemic response to PTH in rats with moderate and advanced renal failure and how this response was modified by a high and a low phosphorus diet. In addition, the effect of a change in dietary phosphorus on calcitriol levels was also evaluated. A 48-hour continuous infusion of 1-34 rat PTH increased the serum calcium level to 18.2 +/- 0.4 mg/dl in normal rats, versus 13.7 +/- 0.9 and 12.1 +/- 0.2 mg/dl in rats with moderate and advanced renal failure, respectively. During the PTH infusion, a high phosphorus diet increased the serum phosphorus and resulted in a reduced calcemic response to PTH at each level of renal function; respective serum calcium levels were 13.8 +/- 0.6 mg/dl in normals, 11.2 +/- 0.2 mg/dl in moderate renal failure and 9.6 +/- 0.5 mg/dl in advanced renal failure. In normal rats and in rats with moderate renal failure, dietary phosphorus restriction during the PTH infusion increased serum calcitriol levels. In rats with advanced renal failure, serum calcitriol levels were lower than in the other two groups and were not affected by changes in dietary phosphorus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Calcemic response to parathyroid hormone in renal failure: role of calcitriol and the effect of parathyroidectomy.

Hyperparathyroidism due to renal failure begins in the early stages of renal insufficiency and is in part secondary to skeletal resistance to the calcemic action of parathyroid hormone (PTH). Factors which have been reported to reduce the calcemic response to PTH include: decreased calcitriol levels, hyperphosphatemia and down regulation of PTH receptors in bone. While hyperphosphatemia may directly decrease the calcemic response to PTH, it may also act indirectly by a suppression of calcitriol synthesis. In this study, the effect of calcitriol on the calcemic response to PTH was evaluated in normal rats and in rats with moderate and advanced renal failure. To determine the combined effect of calcitriol and phosphorus on the calcemic response to PTH, rats receiving calcitriol were fed either a high (1.0%) or low (0.2%) phosphorus diet during a 48-hour PTH infusion. In advanced renal failure, calcitriol administration increased the calcemic response to PTH independent of the dietary phosphorus intake. During ingestion of a low phosphorus diet, a 48 hour PTH infusion resulted in a serum calcium level of 13.7 +/- 0.5 and 12.1 +/- 0.2 mg/dl (P less than 0.02) with and without calcitriol administration, respectively. In normal rats and in rats with moderate renal failure, calcitriol administration improved the calcemic response only during a high phosphorus intake. After a 48-hour PTH infusion in normal rats, the serum calcium levels with and without calcitriol were 16.1 +/- 0.9 and 14.8 +/- 0.6 mg/dl, P less than 0.01 respectively; in rats with moderate renal failure, calcitriol administration increased serum calcium, 13.2 +/- 0.5 versus 11.2 +/- 0.4 mg/dl, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

A comparison of parathyroid-gland function in haemodialysis patients with different forms of renal osteodystrophy.

Parathyroid function was studied in three different histological forms of renal osteodystrophy: osteitis fibrosa (OF), low-turnover aluminium-associated bone disease (LTAABD), and aplastic bone disease without aluminium (ABD). Parathyroid function was determined by the evaluation of the sigmoidal parathyroid hormone-(PTH)-calcium curve, which was obtained by the performance of a reduced calcium and an increased calcium haemodialysis. Parameters of the sigmoidal PTH-calcium curve evaluated included maximally stimulated (PTHMax) and inhibited (PTHMin) PTH, the set point of calcium for PTH (ICA50), defined as the ionised calcium concentration at which PTHMax was reduced by 50%, the ratio of basal PTH to maximally stimulated PTH (PTHBase:PTHMax), the ionised calcium concentration at which basal (ICABase), maximally stimulated (ICAMax), and maximally inhibited (ICAMin) PTH values were observed, and the slope of the PTH-calcium curve. Both PTHMax and PTHMin were greater in OF than the other two groups (P less than 0.02). The ratio of basal to maximally stimulated PTH was greater (P less than 0.02) in OF (61 +/- 7%) than LTAABD (33 +/- 5%) and ABD (36 +/- 7%). The ICA50 and the ICAMax were greater (P less than 0.03) in OF than the other two groups; however, no differences were observed in the ICABase and ICAMin. The slope of the PTH-calcium curve (% maximal PTH), which should indicate the sensitivity of parathyroid cells, was greater in OF than LTAABD (P less than 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1991

Osteocalcin levels in uremic patients: influence of calcitriol treatment through two different routes and type of dialysis.

Osteocalcin, the most abundant non-collagen protein of bone, is synthesized by the osteoblast. Serum osteocalcin concentration depends primarily on new cellular synthesis, and is a sensitive marker of bone turnover reflecting osteoblastic function. In uremic and hemodialysis (HD) patients, a direct relationship between serum osteocalcin and histological parameters of bone formation has been observed. The modality of dialysis may influence serum osteocalcin levels though the available data are controversial. The aim of this study is to assess the acute and chronic effects of calcitriol and the influence of modality of dialysis on serum osteocalcin levels. Twelve patients on continuous ambulatory peritoneal dialysis (CAPD) were treated with calcitriol. For control purposes, 24 patients, 12 on CAPD and 12 on HD, not treated with calcitriol serum osteocalcin levels were included. In CAPD patients previously treated with calcitriol, serum osteocalcin levels were higher than in nontreated patients. The higher levels occur independent of serum levels of parathyroid hormone (PTH), Ca and P. Hemodialysis patients had osteocalcin levels similar to those of CAPD patients under calcitriol treatment. However, the levels of HD patients were higher than CAPD nontreated patients. Serum ionized Ca was similar in CAPD and HD nontreated patients; however, total Ca was significantly higher in HD than in CAPD patients, both with and without calcitriol. After the intravenous administration of calcitriol, serum osteocalcin levels increased from 9.2 + 2.5 to 13.5 + 5.4 ng/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

The effect of long-term intravenous calcitriol administration on parathyroid function in hemodialysis patients.

Secondary hyperparathyroidism is common in dialysis patients. Intravenous calcitriol has proven to be an effective therapy for the reduction of parathyroid hormone (PTH) levels. However, the effect of i.v. calcitriol on parathyroid function, defined as the sigmoidal PTH-calcium curve developed during hypocalcemia and hypercalcemia, has not been evaluated during the prolonged administration of i.v. calcitriol. Six hemodialysis patients with marked secondary hyperparathyroidism, PTH levels greater than 500 pg/mL (normal, 10 to 65 pg/mL), were treated for 42 wk with 2 micrograms of i.v. calcitriol after each hemodialysis. Parathyroid function was evaluated before and after 10 and 42 wk of calcitriol therapy. Between baseline and 42 wk, the basal PTH level decreased from 890 +/- 107 to 346 +/- 119 pg/mL (P less than 0.02) and the maximally stimulated PTH level decreased from 1293 +/- 188 to 600 +/- 140 pg/mL (P less than 0.01). In addition, calcitriol administration significantly decreased PTH levels throughout the hypocalcemic range of the PTH-calcium curve. Although the slope of the PTH-calcium curve (with maximal PTH as 100%) decreased between baseline and 42 wk (P less than 0.05), the set point of calcium did not change. Two patients with a decrease in both basal and maximally stimulated PTH levels after 10 wk of calcitriol, developed marked hyperphosphatemia between 10 and 42 wk; this resulted in an exacerbation of hyperparathyroidism despite continued calcitriol therapy. In conclusion, prolonged i.v. calcitriol administration is an effective treatment for secondary hyperparathyroidism in hemodialysis patients provided that reasonable control of the serum phosphate is achieved. In addition, the slope of the PTH-calcium curve may be a better indicator of parathyroid cell sensitivity than the set point of calcium.

Adult↗
PubMed1991

Current advances in the therapy of secondary hyperparathyroidism and osteitis fibrosa.

Secondary hyperparathyroidism is commonly observed in dialysic patients. Recent observations demonstrate a direct inhibitory effect of calcitriol on parathyroid hormone (PTH) synthesis and secretion. These observations may have important clinical and therapeutical implications. Thus, several studies have shown that intravenous calcitriol, in dialysis patients with severe secondary hyperparathyroidism, has a direct inhibitory effect on PTH levels. Furthermore, the sigmoidal PTH-calcium relationship is shifted toward a more normal range after intravenous calcitriol. In addition, the use of calcitriol early during the course of renal failure prior to dialysis has demonstrated therapeutic benefits. Thus, both early therapy with oral calcitriol and later during maintenance dialysis, the addition of the intravenous form may provide various therapeutical alternatives which make surgical parathyroidectomy rarely necessary. Furthermore, the course of patients undergoing surgical parathyroidectomy is not benign.

Calcitriol↗
PubMed1990

Aluminum administration in the rat separately affects the osteoblast and bone mineralization.

Aluminum administration in the experimental animal results in osteomalacia as characterized by osteoid accumulation and decreased mineralization. Previous in vivo and in vitro studies have indicated that either aluminum directly inhibits mineralization or is toxic to the osteoblast. In the present study, PTH was continuously infused in rats with aluminum-induced osteomalacia to evaluate whether aluminum administration decreased mineralization without a concomitant decrease in osteoblasts. Four groups of rats were studied: chronic renal failure (CRF); CRF + aluminum (AL); CRF + PTH; and CRF + PTH + AL. Rats were sacrificed 5 and 12 days after aluminum or diluent administration; in the PTH groups, bovine PTH (1-34) was administered at 2 units/h via a subcutaneously implanted Alzet pump. Aluminum administration decreased osteoblast surface, increased osteoid accumulation, and produced a cessation of bone formation. The infusion of PTH alone increased osteoblast surface and bone formation. The simultaneous administration of aluminum and PTH resulted in an osteoblast surface intermediate between aluminum and PTH alone; however, despite a PTH-induced restoration of osteoblast surface, bone formation did not increase. These findings indicate (1) aluminum is toxic to osteoblasts and also directly inhibits mineralization even when osteoblasts are not decreased; (2) PTH is capable of increasing osteoblasts even in the presence of aluminum; and (3) despite a PTH-induced increase in osteoblast surface, mineralization of osteoid was not improved.

Aluminum↗
PubMed1990

Effect of parathyroidectomy on aluminum toxicity and azotemic bone disease in the rat.

In maintenance dialysis patients, low-turnover osteomalacia and aplastic bone disease are generally attributed to aluminum toxicity. Both groups of patients have a relative deficiency of PTH. The reason for the development of osteomalacia versus aplastic bone disease is unclear. The present study was performed to evaluate whether parathyroidectomy (PTX) modifies the effect of aluminum administration on bone histology in renal failure. Seven groups of pair-fed rats were studied: normals (N); renal failure (RF); RF + PTX; PTX; RF + aluminum (AL); RF + PTX + AL; and PTX + AL. Aluminum was administered intraperitoneally 5 days/week for 6 weeks. All groups were sacrificed at 6 weeks. Renal failure increased the serum calcium in both the parathyroid intact (RF versus N, 11 +/- 0.1 versus 10 +/- 0.3 mg/dl, X +/- SEM, P less than 0.05) and calcium-supplemented PTX groups (PTX + RF versus PTX, 9.7 +/- 0.2 versus 9.2 +/- 0.2 mg/dl, P less than 0.05). After PTX, aluminum administration increased the serum calcium (PTX + AL versus PTX, 9.8 +/- 0.3 versus 9.2 +/- 0.2, P less than 0.05, and PTX + RF + AL versus PTX + RF, 10.8 +/- 0.1 versus 9.7 +/- 0.2 mg/dl, P less than 0.05). In rats with renal failure receiving aluminum, PTX decreased osteoid volume and surface but not osteoid thickness. Rats receiving aluminum did not mineralize bone. Additionally, in PTX rats receiving aluminum, renal failure per se increased osteoblast surface, osteoid surface, osteoid volume, and osteoclast number.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1990

Insulin in the acute renal adaptation to dietary phosphate restriction in the rat.

Dietary phosphate restriction produces a rapid increase in tubular reabsorption of phosphate. To evaluate whether insulin is important in the acute renal adaptation following a low phosphate meal, four groups of conscious rats were studied by renal clearance methods, following a single meal by gavage. Group A received a normal (0.8%) phosphate meal, followed by saline infusion; Group B, a low (0.03%) phosphate meal, followed by saline infusion; Group C, a low phosphate meal, followed by infusion of somatostatin to suppress endogenous insulin secretion; and Group D, a low phosphate meal, followed by infusion of somatostatin plus insulin. Baseline plasma phosphate, insulin, glomerular filtration rate, and fractional excretion of phosphate were similar in all four groups. Following a low phosphate meal in Groups B, C, and D, there was a decrease in plasma phosphate, as compared with Group A. Whereas fractional excretion of phosphate decreased when plasma phosphate fell in Group B, administration of somatostatin (Group C) prevented the drop in fractional excretion of phosphate, despite a lower plasma phosphate. The addition of exogenous insulin (Group D) restored the antiphosphaturic effect of the low phosphate meal. These results suggest that insulin contributes to the acute decrease in phosphate excretion following a low phosphate meal.

Adaptation, Physiological↗
PubMed1990

[Osteomalacia and renal tubular acidosis associated with analgesic abuse. A clinical case].

Osteomalacia is a multifactorial bone disorder. Main causes are vitamin D deficiency and phosphorus depletion. Among patients with renal insufficiency the incidence of osteomalacia is variable and probable related to impairment of the synthesis of 1,25 dihydroxy-vitamin D3 (calcitriol). We report a patients with severe osteomalacia, hyperkalemic tubular acidosis, low serum calcitriol levels and insufficiency associated to a prolonged overuse of analgesic drugs. Differential diagnosis and pathophysiology are discussed.

Acidosis, Renal Tubular↗
PubMed1990

Parathyroidectomy in chronic renal failure: indications, surgical approach and the use of calcitriol.

The appropriate use of phosphate binders, calcium supplements and especially calcitriol therapy has significantly decreased the incidence of overt secondary hyperparathyroidism in dialysis patients. Nevertheless some patients may still need parathyroidectomy, especially in the event of severe clinical signs and symptoms such as persistent hypercalcemia, pruritus, calcifilaxis, or extensive extra-skeletal calcification. Since aluminum-induced bone disease may resemble hyperparathyroidism in dialysis patients, whenever parathyroidectomy is contemplated the diagnosis of secondary hyperparathyroidism must be firmly established. Thus, a bone biopsy is mandatory prior to parathyroidectomy. It is our experience that once the patient goes to surgery the most important factor in the surgical approach is the presence of a skilled surgeon who has extensive experience in parathyroid gland surgery. The data comparing subtotal parathyroidectomy with total parathyroidectomy and autotransplantation are similar. The most important shortcoming is the lack of long-term follow-up. Recently, new data by several investigators has been advanced reintroducing total parathyroidectomy. Long-term observations in patients who despite total parathyroidectomy still have normal PTH levels are of special interest. In addition, long-term follow-up of these patients has shown that normal plasma calcium and phosphorus levels may be maintained without the use of Vitamin D; this occurred in the presence of active mineralization. However, our major objection to this procedure is the risk of aluminum-induced bone disease. At the present time we feel that the relative high incidence of recurrent hyperparathyroidism following subtotal parathyroidectomy is a reasonable trade off for the risk of aluminum bone disease which may develop in absence of PTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗
PubMed1990

Two-needle calculation of recirculation compared with the standard three-needle method.

A two-needle method for calculating recirculation was compared with the standard three-needle method, substituting the standard phlebotomy of a remote vessel during dialysis with blood obtained from the dialyzer inlet needle 15 minutes after the termination of dialysis. Twenty patients were studied prospectively. There was no significant difference between corrected blood flow calculated with the standard and two-needle methods. The BUN obtained from the inlet line needle 15 minutes after conclusion of the treatment did not differ significantly from the BUN concentration in the specimen from a contralateral arm drawn five minutes before termination of dialysis. Recirculation calculated by the two-needle method correlated well with the results obtained with the standard three-needle method. The two-needle method provides a convenient alternative to the standard three-needle method of determining recirculation.

Aged↗