In This Issue
Drug monitoring of mycophenolic acid (MPA) is not frequently applied in patients with autoimmune diseases. An interesting clinical study and accompanying editorial comment discuss this issue. The study showed that prevention of recurrence of disease was associated with higher trough levels (>3.0 mg/L), but that adverse events were clustered in patients with high MPA exposure.See editorial comment by de Winter and van Gelder, pages 3386–3388 and article by Neumann et al., pages 3514–3520
The ALLHAT study has in the past already stirred the emotions among the "hypertension specialists". A recent sub-analysis of the study was published in the Archives of Internal Medicine and in view of the ongoing controversy we asked our hypertension experts to comment on this paper. Our experts do not agree with some of the ALLHAT investigators and present arguments for their recommendation to prefer ACEI over thiazide diuretics at least in non-black patients.
See editorial comment by Hilgers and Mann, pages 3389–3391
An interesting editorial comment discussed the recent paper published in JASN on postprandial mineral metabolism and secondary hyperparathyroidism in early CKD. Whereas in the JASN paper the role of fibroblast growth factor (FGF) 23 was emphasized, the editorial made some interesting comments on some details of the methodology used. However, the main message remains that abnormal mineral metabolism is present in early CKD even when PTH is not significantly increased.
See editorial comment by Rodriguez and Felsenfeld, pages 3391–3393
A nice physiological study investigated the role of the Klotho hormone on epithelial calcium channels in the distal tubule and found a modulating effect, primarily restricted to epithelial channels TRPV5 and TRPV6.
See article by Lu et al., pages 3397–3402
Preconditional activation of hypoxia-inducible factors (HIF) with specific prolyl hydroxylase inhibitors attenuates not only proximal tubular injury, induced by warm ischaemia/reperfusion, but an elegant series of experiments now demonstrate that also tubular injury to the medullary thick ascending limbs was significantly attenuated by this treatment. These results provide further insight into the molecular mechanisms of acute ischaemia/reperfusion kidney damage.
See article by Rosenberger et al., pages 3472–3478
Several formulae have been proposed to guide infusion therapy for correction of hypernatraemia. This elegant clinical study demonstrates that these formulae do not accurately predict changes of serum sodium and concluded that infusion therapy should be based on the reasons for hypernatraemia and serial measurements of serum sodium.
See article by Lindner et al., pages 3501–3508
Congenital nephrotic syndrome (CNS) of the Finnish type is caused by recessive mutations in the NPHS1 gene encoding nephrin and more than 80 different mutations of NPHS1 causing CNF have been published. The current paper describes mutation analysis of NPHS1 by exon sequencing in a worldwide cohort of 32 children with CNS from 29 different families, an expansion of the spectrum of known NPHS1 mutations by >15%.
See article by Heeringa et al., pages 3527–3533
The effects of amlodipine (10 mg once daily) on cardiovascular events were investigated in a prospective RCT in hypertensive haemodialysis patients. Although the primary outcome (overall mortality) was not different between amlodipine and placebo, the secondary endpoint (a composite variable consisting of mortality from any cause or cardiovascular event) was significantly lower in the amlodipine group.
See article by Tepel et al., pages 3605–3612
A Japanese study examined the evolution of PTH levels and the maximum and total parathyroid (PT) volume in mildly hyperparathyroid patients treated either with oral or IV calcitriol over a 12-month study period. Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, while IV calcitriol successfully suppressed this progression.
See article by Taniguchi et al., pages 3662–3669 (This article was also discussed in a letter and reply–-see our website.)
A Canadian study retrospectively examined the association between therapy with ACE inhibitor/ARB and mortality in patients undergoing chronic peritoneal dialysis. It appeared that ACE inhibitor/ARB therapy dramatically reduced mortality in patients on peritoneal dialysis, independent of blood pressure and other clinical and demographic variables.
See article by Fang et al., pages 3704–3710
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