Nonglycemic targets in diabetes.

In conclusion, targets for patients with diabetes have actually become simpler with the release of new guidelines. The targets discussed in this article are summarized in Box 3. Finally, as clinicians and patients with diabetes struggle with the overwhelming burden of care, clinicians should consider the increasingly codified ethic of minimally disruptive medicine, which considers not just what patients and doctors can do but what patients' priorities, wishes, and needs are rather than the many specialist tests and treatment options available. Finding the balance may be easier with the new evidence-based and more straightforward guidelines.

Safety and efficacy of vemurafenib in end stage renal failure.

BACKGROUND: Serine-threonine inhibitors, such as vemurafenib, are being used increasingly in cancer treatment, and the toxicity and therapeutic benefit need to be balanced carefully both before and during treatment. CASE PRESENTATION: A patient with metastatic melanoma and end stage renal failure who was on peritoneal dialysis was treated with the serine-threonine kinase inhibitor, vemurafenib. After 5 months of treatment, a substantial response to vemurafenib was observed using imaging, but when he developed a prolonged QTc interval (common toxicity criteria (CTC) grade 3), treatment was interrupted. Vemurafenib was restarted at a reduced dose when the QTc interval returned to normal. The patient has had a significant response to vemurafenib and continued on treatment for 12 months after beginning the therapy. CONCLUSION: This is the first reported case of end stage renal failure in a patient who is taking vemurafenib. Although the patient developed QTc prolongation, it appears to be asymptomatic, and was managed with dose reduction. This case highlights the need for closer QTc monitoring at the start and during treatment.

Hypothesis: a simple algorithm to distinguish between hypoaldosteronism and renal aldosterone resistance in patients with persistent hyperkalemia.

AIM: Many patients with hyperkalemia have a readily identifiable cause, which leads to appropriate management. In others, particularly those with a reduced glomerular filtration rate, differentiating between (relative) hypoaldosteronism (HA) and renal aldosterone resistance (RAR) can be problematic. The aim of this study was to see if a plasma aldosterone to potassium algorithm could be defined which would help identify patients with hyperkalemia owing to suboptimal levels of aldosterone, thereby validating treatment with 9-alpha-fluhydrocortisone, instead of cation exchange resins, if more conservative treatment fails. METHODS: A literature search for, and analysis of, studies providing details of plasma aldosterone and plasma potassium in normals (made hyperkalemic)and patients with a plasma potassium >5.3 mmol/L, and a contemporaneous plasma aldosterone. RESULTS: One study was found in which normals were made significantly hyperkalemic (to 6.3 mmol/L). These subjects, while on a high sodium, low potassium (western) diet (n = 5), provided an arbitrary definition of a simple aldosterone to potassium algorithm for diagnosis (factored aldosterone (FAldo) = plasma aldosterone/(plasma K - 4.2)). The limit for FAldo is set at 280(pmol/L) or 10(ng/dL): results below the limit suggest HA; above the limit, RAR. This algorithm was then tested against, and, when plasma potassium was greater than 5.3, found to be consistent with, reported patients with confirmed HA (n = 33) and pseudohypoaldosteronism (n = 23). The ratios in reported patients with renal failure (n = 43) were consistent with either HA (n = 30) or RAR(n = 13). HYPOTHESIS: In hyperkalemic patients a plasma aldosterone to potassium algorithm may help distinguish HA from RAR, thereby guiding therapy.