Francisco Llach

Dietary Management of Patients in Chronic Renal Failure

A new oral amino acid preparation was given to two groups of patients: group 1, five patients on hemodialysis; and group 2, five patients with chronic renal failure (CRF). In group 1 significant pre- and postdiet changes were: BUN 93-37 mg% (p smaller than 0.01); creatinine 13.0-9.7 mg% (p smaller than 0.001); phosphorus 6.6-4.2 mg% (p smaller than 0.05); uric acid 8.7-6.0 mg% (p smaller than 0.01); CO2 16.3-21.3 mEq/I (p smaller than 0.01); hematocrit 18.0-20.8% (p smaller than 0.05). In group 2: BUN 93-66 mg% (p smaller than 0.05); phosphorus 5.6-3.8 mg% (p smaller than 0.05); hematocrit 27.3-30.7% (p smaller than 0.05). Nitrogen balance was positive in all patients. It is concluded that this oral amino acid mixture is well-tolerated and can be utilized in CRF to attain protein anabolism.

Parathyroidectomy in Dialysis Patients: Indications, Surgical Approach, Complications and Clinical Management After Surgery

Over the last two decades significant advances have been made in the diagnosis and therapy of renal bone disease. Thus, it has become clear that both secondary hyperparathyroidism (HPTH) and aluminum-induced bone disease can co-exist in a large number of dialysis patients (1). Patients with overt HPTH are characterized by musculoskeletal symptoms, high PTH levels, X-ray manifestations showing subperiosteal bone erosions and bone histology findings of osteitis fibrosa (2). Over the last decades the number of patients developing overt secondary HPTH has steadily decreased, most likely due to better control of hyperphosphatemia and, most importantly, the widespread use of vitamin D analogs. On the negative side, the decrease in HPTH may be the result of the concomitant use of aluminum (Al) containing phosphate binders. Recent data show that in most Western countries A1 binders are still commonly used. The direct inhibition of PTH secretion by calcitriol ( 3 ) particularly with the availability of its intravenous form (4, 5) , has substantially reduced the need for parathyroidectomy (PTX). Nevertheless, in spite of recent therapeutic advances, some patients with severe overt secondary HPTH may receive surgical PTX. Subtotal PTX for renal HPTH was performed 35 years ago in two patients with chronic renal failure (6) . Since then, three surgical procedures have been developed for the management of overt secondary HPTH with subtotal PTX or total PTX with autotransplantation of parathyroid gland tissue having become the two established surgical approaches. However, recent data from Kaye, d’Amour and Henderson have questioned such procedures and have favored the use of total PTX (7). This controversial issue will be discussed later. The present review will focus on the indications and surgical approach to FTX, with some anatomical considerations and the clinical course after

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.

Treatment of Secondary Hyperparathyroidism by Intravenous Calcitriol

Secondary hyperparathyroidism resulting in osteitis fibrosa is the most common bone abnormality observed in dialysis patients. Most recent data strongly suggest that a deficit of calcitriol is an important factor in the high parathyroid hormone (PTH) levels of these patients (1, 2). Thus, it is not surprising that the administration of calcitriol orally (3, 4) has resulted in the amelioration or even dramatic improvement of secondary hyperparathyroidism. What makes the use of intravenous calcitriol an attractive modality of therapy is the recent observation that calcitriol per se, in the absence of hypercalcemia inhibit both synthesis and secretion of PTH (5, 6). In the present chapter we will briefly review the physiological action of calcitriol in dialysis patients in regard to divalent ion metabolism, then we will discuss new data on calcitriol and PTH interaction and finally, the available clinical data on the intravenous use of calcitriol will be reviewed.

Treatment of Secondary Hyperparathyroidism in Maintenance Hemodialysis Patients by Intravenous Calcitriol

Secondary hyperparathyroidism resulting in osteitis fibrosa is the most common bone abnormality observed in dialysis patients. Most recent data strongly suggest that a deficit of calcitriol is an important factor inducing the high parathyroid hormone (PTH) levels observed in these patients (1-2). Thus, it is not surprising that in initials studies the administration of calcitriol orally (3-4) has resulted in the amelioration or even dramatic improvement of secondary hyperparathyroidism. What makes the use of calcitriol an attractive modality of therapy is the recent observation that calcitriol per se, in the absence of hypercalcemia, inhibits both synthesis and secretion of PTH (5-6). In the present discussion, we will briefly review the physiological action of calcitriol in dialysis patients in regard to divalent ion metabolism. Then we will discuss recent data on the interaction of calcitriol and PTH; and finally, the available clinical data on the intravenous use of calcitriol will be reviewed.