Care for chronic renal patients - Role of multidisciplinary education.

The aim of this study is to summarize the beneficial effects of the holistic approach to patients living with chronic renal failure, including multidisciplinary education and psychosocial care. By education, we enable our patients to reach self-management, appropriate compliance, and coping, which may decrease progression of renal failure, avoid urgent need for starting dialysis and may facilitate better modality selection, access planning, renal transplantation activity, and rehabilitation. Psychosocial care reduces anxiety and fear, modifies perception of illness' burden, and increases quality of life. Yet, both patients and nephrologists feel that transmission of information is often insufficient. Different methods can effectively be utilized as educational interventions, meetings with staff, and also with expert patients, group education sessions, written or online materials, or multimedia presentations. Patient care of such a high complexity can be provided only by multidisciplinary teams. A special Hungarian example of holistic care is presented, and the favorable results of the education and lifestyle camps for patients accompanied by their relatives are discussed. Accordingly, complex care of patients living with chronic renal failure on the long run is cost saving.

An Overview of Preformed Metal Crowns. Part 1: Conventional Technique.

This article details the clinical techniques for conventional preformed metal crown placement. It aims to increase the readers' awareness of the clinical advantages of preformed metal crowns and the indications for their use. The second part will discuss the Hall Technique. CPD/Clinical Relevance: This two-part article aims to guide the reader through the conventional and alternative techniques available for placement of a preformed metal crown whilst providing an update of the evidence for each.

Reversal of adynamic bone disease by lowering of dialysate calcium.

Adynamic bone disease (ABD) is increasingly recognized, especially in dialysis patients treated with oral calcium carbonate, vitamin D supplements, or supraphysiological dialysate calcium. We undertook this study to assess the effect of lowering dialysate calcium on episodes of hypercalcemia, serum parathyroid hormone (PTH) levels as well as bone turnover. Fifty-one patients treated with peritoneal dialysis and biopsy-proven ABD were randomized to treatment with control calcium, 1.62 mM, or low calcium, 1.0 mM, dialysate calcium over a 16-month period. In the low dialysate calcium group, 14 patients completed the study. This group experienced a decrease in serum total and ionized calcium levels, and an 89% reduction in episodes of hypercalcemia, resulting in a 300% increase in serum PTH values, from 6.0+/-1.6 to 24.9+/-3.6 pM (P<0.0001). Bone formation rates, all initially suppressed, at 18.1+/-5.6 microm2/mm2/day rose to 159+/-59.4 microm2/mm2/day (P<0.05), into the normal range (>108 microm2/mm2/day). In the control group, nine patients completed the study. Their PTH levels did not increase significantly, from 7.3+/-1.6 to 9.4+/-1.5 pM and bone formation rates did not change significantly either, from 13.3+/-7.1 to 40.9+/-11.9 microm2/mm2/day. Lowering of peritoneal dialysate calcium reduced serum calcium levels and hypercalcemic episodes, which resulted in increased PTH levels and normalization of bone turnover in patients with ABD.

[Hypophosphatemic oncogenic osteomalacia]. / Hypophosphataemiával járó onkogén osteomalacia.

The first case of oncogen osteomalacia in Hungary is reported, to draw the attention of the medical profession to it and to present the new data about its pathomechanism. Pathological hip fracture caused by hypophosphataemic osteomalacia due to isolated renal phosphate wasting was found in a previously healthy 19 years old sportsman. In spite of daily 1.5 micrograms calcitriol treatment and phosphate supplementation, hypophosphataemia persisted for 13 years and he needed regular indometacin medication for his bone pain. During that time an 1.5 cm gingival tumour was found and radically removed. The serum phosphate level returned to normal in a few hours after the operation (preoperative 0.51, after 2, 4 and 8 hours 0.61, 0.68 and 0.79 mmol/l respectively), and remained normal without calcitriol. The histological examination showed epulis with fibroblast and vascular cell proliferation, which has never been previously reported in connection with oncogenic osteomalacia. The pain resolved after 3 months and the bone density became normal in one year. Oncogenic osteomalacia must be considered in every case presenting with atypical hypophosphataemic osteomalacia. Careful dental examination is needed also in the course of search for the underlying tumour. Every tumour-like growth, even the common epulis, has to be operated radically and serum phosphate monitored in the postoperative period in all such cases.

Patterns of potassium wasting in response to stepwise combinations of diuretics in nephrotic syndrome.

OBJECTIVE: To study the urinary potassium wasting patterns when the decreasing effectiveness of diuretics during repeated administrations are counterbalanced by stepwise increases of doses and combinations of them. PATIENTS: Eleven patients with renal edema. Seven patients suffered from advanced nephrotic syndrome and 4 patients were "forme fruste". METHODS: Urinary excretions and serum levels of potassium, sodium, creatinine, osmoles were determined; specific renal functions, glomerular filtration rate (GFR) fractional excretion of potassium (FE(K)), transtubular potassium gradient (TTKG) and free water reabsorption (TcH2O) were calculated. Nine different intervention-induced changes were followed daily: furosemide (FSD) alone, FSD with chlorthalidone (CTN), "low dose" and "high dose" potassium sparing drugs (PSD), FSD with CTN and "low dose" or "high dose" PSD, and "no drug" as well as "postdiuretic" periods with or without PSD. RESULTS: TTKG significantly decreased in response to FSD. It elevated during FSD with CTN, but remained lower than the baseline. The normal correlation between urinary potassium excretion (UKV) and TTKG became distorted under FSD. UKV and FE(K) were slightly increased by FSD and more markedly when given FSD together with CTN, probably because "distal volume flow" was elevated. In the "postdiuretic" periods TTKG increased, but this was reversed by PSD. In response to PSD, TTKG and UKV decreased, but both were elevated when combining with FSD + CTN. CONCLUSIONS: FSD caused relatively small potassium loss, because the enhanced "distal volume flow" was counterbalanced by a decrease of TTKG. FSD may have had a potassium secretion inhibitory influence as well. Potassium loss and TTKG were enhanced during coadministration of CTN, and decreased by PSD. "Postdiuretic rebound" increase of TTKG was reversed by PSD.

High-dose phosphate treatment leads to hypokalemia in hypophosphatemic osteomalacia.

The mechanism of the decrease in plasma potassium induced by phosphate treatment was investigated in a 24-year-old hypertensive patient with hypophosphatemic osteomalacia, who was the youngest of four patients, belonging to a 23 number kindred of five generations. Parameters of potassium, sodium, calcium, and phosphate metabolism as well as specific renal functions have been studied in the basal state and during administration of graded doses of phosphate (500-6000 mg). Progressive hypokalemia developed during phosphate treatment. An inverse correlation was found between plasma potassium and doses of phosphate (plasma potassium = -0.2 g phosphate + 3.9 r = -0.49; p < 0.05; N = 21). A renal route of potassium loss was suspected, but could not be confirmed as potassium excretion did not increase although sodium excretion was augmented [basal sodium output: 56.7 mmol/24 h; phosphate treatment: 153 mmol/24 h (p < 0.05)]. Transtubular potassium gradient (TTKG) also decreased and an inverse correlation was found between TTKG and doses of phosphate (r = -0.37; p < 0.02; N = 38). Decrease of TTKG was possibly the result of suppressed K+ secretion. It was concluded that potassium loss occurred by a non-renal (intestinal) route in phosphate-induced hypokalemia. Although major hazards of treatment of hypophosphatemic osteomalacia with phosphate and calcitriol are secondary hyperparathyroidism and vitamin D intoxication, potassium loss also should be kept in mind.

[Adult-onset sex-linked familial hypophosphatemic osteomalacia]. / Felnöttkori, nemhez kötötten öröklödö, családi hypophosphataemiás osteomalacia.

Three patients (a grandmother, her daughter and her grandson) belonging to a 23-number-kindred of five generations suffered from adult-onset, X-linked, familiar hypophosphataemic osteomalacia. According to the familiar anecdotes the great-grandmother also had the same disease. The clinical diagnosis was documented by X-ray pictures, scintigraphic and bone histological results, the laboratory diagnosis was proven by blood and urine analyses examined after phosphate loading. The youngest, 24-year-old patient was treated with daily 3 g phosphate and high doses of calcitriol for 2 years. As a new feature of our therapy, per os treatment with 1.25 micrograms calcitriol was supplemented by daily 2-4 micrograms iv. bolus calcitriol for one week every month. The osteomalacia, causing serious symptoms and complaints, healed. Our treatment seemed to be safe, as renal functions, serum total and ionized calcium and PTH levels (including midnight values) remained in normal range. On the basis of our results this disease can be treated by administration of high doses of phosphate, provided that development of hyperparathyroidism is prevented by the coadministration of high doses of calcitriol.