QUALITY IMPROVEMENT: Supporting a hospital in difficulty: -experience of a '-buddying' agreement to implement a new medical pathway.

Increased NHS regulation has identified many healthcare organisations with operational and/or financial difficulties. Although the causes are often complex, most cases are effectively managed internally with limited input from external agencies. How best to support the few organisations needing additional support has not been established. 'Buddying', in which senior clinical and managerial teams from a well performing organisation work with colleagues from an organisation in difficulty has been proposed as a potential solution. Previous reports suggest that these partnerships are generally valued by the organisation in difficulty but there is a paucity of measured operational benefit. In this article we present our experience of a 'buddying agreement' and its impact on the introduction of a new 'whole system' medical pathway (ie rotas, staffing, process) at an organisation in difficulty. We describe the process, problems, effect on operational performance, staff survey feedback six months post-implementation and the lessons learned. Factors critical to success were good communication; clear responsibilities, common values and strong governance; incorporation into an effective local improvement programme; targeting of specific issues; ability to influence people and foster relationships; adequate 'manpower' and gradual transition to local 'ownership'.

Case report: making the CONN-ection: two cases of persistent hypertension and hypokalaemia following renal transplantation.

Conn's syndrome following renal transplantation is extremely rare. Here, we present two cases of persistent hypertension and hypokalemia, emerging after kidney transplantation, which proved resistant to medical treatment. In both patients, biochemical investigations elicited massively elevated plasma aldosterone levels and suppressed renin activity. Abdominal MRI demonstrated a 90- and 20-mm right adrenal tumour in cases 1 and 2, respectively. For both patients, curative treatment was achieved via laparoscopic right adrenalectomy.

The Pan-Thames EPS study: treatment and outcomes of encapsulating peritoneal sclerosis.

BACKGROUND: Encapsulating peritoneal sclerosis (EPS) is a disease process that can occur as a complication of peritoneal dialysis (PD). The aim of this study was to make a general assessment of the clinical features, diagnosis, management and outcome of PD-related EPS cases from London and South-East England. METHODS: Questionnaires were sent to 11 PD units in March 2007; cases were identified retrospectively. Outcome data on surviving patients were collected in March 2008. RESULTS: A total of 111 patients were identified; the mean time on PD was 82 months (range 8-247). Mortality increased with length of time on PD, being 42% at <3 years (n = 12), 32% at 3-4 years (n = 19), 61% at 5-6 years (n = 31), 54% at 7-8 years (n = 24), 75% at 9-10 years (n = 8) and 59% at >10 years (n = 17). Twelve patients had no previous peritonitis episodes, 28 had one previous episode, 30 had two previous episodes and 33 had three or more previous episodes. Of the patients with PD details available, 41/63 were high (>0.81) transporters and 44/71 had ultrafiltration <1 l/24 h, but 7/63 were low average transporters (0.5-<0.65) and 27/71 had ultrafiltration >1 l/24 h and a few had significant residual renal function. Sixty-five (59%) patients had their PD discontinued prior to diagnosis (51 HD; 14 transplanted). CT scans were performed on 91 patients and laparotomy on 47 patients. Drug treatment consisted of tamoxifen, immunosuppression or both. The median survival was 15 months in patients treated with tamoxifen (n = 17), 12 months in patients treated with immunosuppression (n = 24) and 21 months in patients who received both (n = 13), against 13 months (n = 46) in patients who received no specific treatment. Adhesionolysis was performed in 5 patients, and 39 patients were given parenteral nutrition. The overall mortality was 53% with a median survival of 14 months and a median time to death of 7 months. Conclusion. This is one of the largest cohorts of patients with EPS in the literature. Long-term survival occurred in over 50%, regardless of the various treatments strategies undertaken by the centres.

Calcimimetics and calcilytics--fooling the calcium receptor.

CONTEXT: Just a decade after the the calcium-sensing receptor (CaR) was identified, pharmacological manipulation of the CaR is about to enter routine practice. For hyperparathyroid states, calcimimetics, which increase activation of the CaR, have been licensed in Europe and the USA. Calcilytics, which decrease CaR function and increase secretion of parathyroid hormone (PTH), might allow the anabolic effects of PTH on bone to be harnessed for the prevention and treatment of osteoporosis. STARTING POINT: In a multicentre randomised double-blind placebo-controlled study, Munro Peacock and colleagues recently confirmed the efficacy of the oral calcimimetic cinacalcet for achieving long-term reductions in serum calcium and PTH concentrations in primary hyperparathyroidism (J Clin Endocrinol Metab 2005; 90: 135-41). The arrival of a non-surgical option for this common disorder is important. WHAT NEXT? Study in primary and uraemic secondary hyperparathyroidism will indicate whether the efficacy of calcimimetic agents extends into the longer term. The extracellular relation between the CaR and its ligands and the intracellular signalling cascades that modify PTH gene transcription and secretion need further study. Drugs acting on the CaR might treat other disorders of bone remodelling, including osteoporosis. CaR expression in tissues beyond those involved in mineral ion homoeostasis should remain an important focus of research.

New prospects for the management of renal bone disease.

The last decade has been a remarkably productive one in the field of bone biology. New insights into the maintenance of a normal bone microenvironment have led to significant advances in our understanding of many important skeletal disorders, including renal osteodystrophy. Novel targets for therapeutic manipulation have been exposed and encouraging progress made towards new treatments. In addition, just as clinical studies have alerted us to the potential hazards of vascular calcification, basic science has unearthed the intimate nature of the relationship between the previously separate disciplines of bone and vascular biology. The clinical nephrologist, however, may be forgiven a little cynicism at this point. If such progress has been made, why do the same proverbial difficulties confront us in day-to-day practice? Control of phosphate remains inadequate, despite a literature which constantly reaffirms its crucial importance, and parathyroid hyperplasia seems inevitable in many patients. Furthermore, even the satisfaction of successful control of serum parathyroid hormone concentration must now be tempered by disquiet regarding the skeletal and cardiovascular consequences of oversuppression. This review aims to provide an update of the latest developments in relevant skeletal research and to assess how recently acquired knowledge may improve clinical nephrological practice over the next five years.

Impaired release of interleukin-6 from human osteoblastic cells in the uraemic milieu.

BACKGROUND: Osteoblast-derived interleukin-6 (IL-6) affects bone metabolism and is linked with a number of pathological states characterized by increased bone resorption, including osteoporosis and renal osteodystrophy. To examine the possibility that uraemia directly influences the release of this cytokine in bone, we have investigated the effect of human uraemic serum on the release of IL-6 from human osteoblast-like cells. METHODS: Individual serum samples collected from healthy male volunteers or male haemodialysis patients prior to and during a dialysis treatment were assayed for IL-6, interleukin-1beta (IL-1beta) and soluble IL-6 receptor (sIL-6R) using specific enzyme-linked immunosorbent assays. MG-63 and SaOS-2 cells were cultured in media containing pooled sera from both groups and alongside matching charcoal-stripped sera. IL-6 concentrations were determined in harvested cell supernatants after 24 h. In further experiments, media containing individual sera obtained from five patients at regular intervals during their haemodialysis treatment were incubated with MG-63 cells to determine the effects of the dialysis process on IL-6 secretion. RESULTS: Haemodialysis patients had significantly higher (n = 10, P < 0.001) circulating concentrations of IL-6 (7.0 +/- 1.6 pg/ml) than normal subjects (0.4 +/- 0.1 pg/ml), but there were no significant differences in the concentrations of either IL-1beta or sIL-6R. These serum concentrations did not change significantly during 80 min of dialysis. IL-6 release by MG-63 cells incubated with charcoal-stripped serum from normal or from uraemic subjects was similar. Incubation with untreated sera from normal subjects increased IL-6 release by approximately 6-fold above the charcoal-stripped control, whereas sera from uraemic subjects increased IL-6 release by only approximately 2- to 3-fold (normal vs uraemic of 6878 +/- 595 and 2579 +/- 169 pg/ml, respectively, P < 0.001). Similar results were seen with SaOS-2 cells. Haemodialysis did not restore the capacity of uraemic serum to augment IL-6 release to the same degree as normal serum. CONCLUSIONS: These data show that the augmentation of IL-6 release from human osteoblastic cells after incubation with normal serum is greater than after uraemic serum. This may indicate the presence of an inhibitor of IL-6 release in uraemic serum that is involved in the deranged bone turnover of uraemic patients.