Nurse practitioners improve quality of care in chronic kidney disease: two-year results of a randomised study.

BACKGROUND: Chronic kidney disease (CKD) is associated with increased cardiovascular risk. Here we evaluate whether strict implementation of guidelines aimed at multiple targets with the aid of nurse practitioners (NP) improves management in patients with CKD. METHODS: MASTER PLAN is a randomised controlled clinical trial, performed in nine Dutch hospitals. Patients with CKD (estimated glomerular filtration rate (eGFR) 20-70 ml÷min) were randomised to receive NP support (intervention group (IG)) or physician care (control group (CG)). Patients were followed for a median of five years. Presented data are an interim analysis on risk factor control at two-year follow-up. RESULTS: We included 788 patients (532 M, 256 F), (393 CG, 395 IG), mean (±SD ) age 59 (±13) years, eGFR 38 (±15) ml÷min÷1.73m(2), blood pressure (BP) 138 (±21)÷80 (±11) mmHg. At two years 698 patients (352 IG, 346 CG) could be analysed. IG as compared with CG had lower systolic (133 vs 135 mmHg; p= 0.04) and diastolic BP (77 vs 80 mmHg; p=0.007), LDL cholesterol (2.30 vs 2.45 mmol(-l); p= 0.03), and increased use of ACE inhibitors, statins, aspirin and vitamin D. The intervention had no effect on smoking cessation, body weight, physical activity or sodium excretion. CONCLUSION: In both groups, risk factor management improved. However, changes in BP control, lipid management and medication use were more pronounced in IG than in CG. Lifestyle interventions were not effective. Coaching by NPs thus benefits everyday care of CKD patients. Whether these changes translate into improvement in clinical endpoints remains to be established.

Hospital specific factors affect quality of blood pressure treatment in chronic kidney disease.

BACKGROUND: Blood pressure (BP) is the most important modifiable risk factor for cardiovascular (CV) disease and progression of kidney dysfunction in patients with chronic kidney disease. Despite extensive antihypertensive treatment possibilities, adequate control is notoriously hard to achieve. Several determinants have been identified which affect BP control. In the current analysis we evaluated differences in achieved BP and achievement of the BP goal between hospitals and explored possible explanations. METHODS: At baseline, BP was measured in a supine position with an oscillometric device in 788 patients participating in the MASTER PLAN study. We also retrieved the last measured office BP from the patient records. Additional baseline characteristics were derived from the study database. Univariate and multivariate analyses were performed with general linear modelling using hospital as a random factor. RESULTS: In univariate analysis, hospital was a determinant of the level of systolic and diastolic BP at baseline. Adjustment for patient, kidney disease, treatment or hospital characteristics affected the relation. Yet, in a fully adjusted model, differences between centres persisted with a range of 15 mmHg for systolic BP and 11 mmHg for diastolic BP. CONCLUSION: Despite extensive adjustments, a clinically relevant, statistically significant difference between hospitals was found in standardised BP measurements at baseline of a randomised controlled study. We hypothesise that differences in the approach towards BP control exist at the physician level and that these explain the differences between hospitals.

Nephrotic syndrome induced by pamidronate.

Two patients developed nephrotic syndrome and progressive loss of renal function following treatment with i.v. pamidronate. Renal biopsy revealed collapsing focal segmental glomerulosclerosis (FSGS) in both the patients. In one patient, renal function recovered and the nephrotic syndrome disappeared after discontinuation of pamidronate. The second patient became dialysis dependent despite discontinuation of therapy. Nephrotic syndrome due to collapsing FSGS is a serious complication of treatment with bisphosphonates, especially of i.v. pamidronate. Bisphosphonates may also cause renal insufficiency as a result of tubular toxicity. In order to prevent severe nephrotoxicity clinicians should check urinary protein excretion and renal function regularly in patients who receive long-term treatment with i.v. bisphosphonates. In patients with pre-existing renal impairment (estimated GFR below 30 ml/min), bisphosphonates should be used with caution.

Toxicity of contrast media: an update.

Renal toxicity of iodinated radiocontrast media (contrastinduced nephropathy; CIN) is a major cause of acute renal failure in hospitalised patients. Magnetic resonance imaging (MRI) is applied as an alternative technique but the use of gadolinium (Gd) containing contrast media carries the risk of nephrogenic systemic fibrosis (NSF), a potentially lethal disorder that occurs especially in patients with renal failure. In this article we give an update of the literature on toxicity of radiocontrast media and on preventive measures. Risk of nephrotoxicity of iodinated contrast media can be reduced by identification of high-risk patients. In these patients pre- and post-hydration with isotonic saline should be applied. When there is insufficient time to prehydrate, a short infusion protocol with sodium bicarbonate is preferable. There is a lack of evidence to support the use of oral or intravenous N-acetylcysteine or iso-osmolar contrast media. In order to prevent NSF , linear gadolinium chelates should not be used in patients with an estimated glomerular filtration rate (eGFR) of less than 30 ml/min. In patients with eGFR between 10 and 30 ml/min the small chance of NSF with cyclic Gd-containing chelates must be balanced against the high risk of developing CIN, and the morbidity and mortality associated with the start of dialysis. In patients without residual renal function, the small chance of developing NSF after macrocyclic Gd-enhanced MRI imaging may tip the balance to the use of iodine containing contrast media.

[Guideline 'Precautionary measures for contrast media containing iodine']. / Richtlijn 'Voorzorgsmaatregelen bij jodiumhoudende contrastmiddelen'.

Annually, 0.5-1 million injections of contrast media containing iodine are administered in the Netherlands. Almost all contrast media nowadays are low-osmolar and nonionic. Nevertheless, the development ofcontrast-induced nephropathy is still a relevant clinical problem. Through an initiative by the Radiological Society of the Netherlands and with aid of the Dutch Institute for Healthcare Improvement (CBO), a guideline was conceived for the intravascular use of iodine-containing contrast media, based on recent scientific literature. The guideline defines the risk factors for contrast-induced nephropathy. One of the major risk factors is an impaired renal function. It is important to measure the glomerular filtration rate (GFR) in patients with a possible impaired kidney function, preferably by using the 'Modification of diet in renal disease' (MDRD)-study formula. The key measures for avoidance of contrast nephropathy are: limiting the amount of contrast agent used and to assure good hydration, by infusion of sodium chloride 0.9% 12-16 ml/kg body weight, both prior to and after contrast infusion. If time is limited, intravenous administration of sodium bicarbonate is an option. The guideline recommends discontinuation of metformin use from the day of contrast injection, if the GFR < 60 ml/min/1.73 m2, and to restart metformin 2 days following contrast infusion providing the GFR has not significantly deteriorated. Only in the case of previous moderate or severe adverse reactions to contrast media, prophylaxis with corticosteroids and antihistamines is recommended. Iodine allergy or an atopic condition is not a contraindication for the use of iodine-containing contrast media, and no prophylaxis is required. No specific measures are indicated in case of hyperthyroidism, acute pancreatitis, or phaeochromocytoma. Injection of contrast media is not contraindicated in case of pregnancy or lactation.