In this issue ...
Normalizing GFR for body surface area (BSA) is sometimes misleading; theoretically and physiologically it would be better to use extra-cellular fluid volume (ECFV) to index GFR. However, as elegantly argued by Geddes et al., for most situations it is much more practical to accept the physiological flaws and sacrifice the accuracy for the simplicity inherent in indexing GFR for BSA.(See editorial comment by Geddes et al., pages 4–6).
Circulating endothelial cells (CEC) in renal disease are both markers and mediators of vascular damage. It is hypothesized that phagocytosis of apoptotic and necrotic cells by the healthy endothelium may, on one hand, remove potentially dangerous debris from the circulation, but may, on the other, in itself trigger pro-inflammatory pathways.
(See editorial comment by Woywodt et al., pages 7–10).
The effect of oral calcium carbonate on aortic calcification in an apolipoprotein E-deficient mouse model of chronic kidney disease was to unexpectedly decrease vascular calcification; it is suggested that phosphorus plays a preponderant role in promoting vascular calcification.
(See article by Phan et al., pages 82–90).
Ketteler and Biggar have written a well-balanced editorial comment integrating the above study in an overview of this "hot topic" for the clinician and industry.
(See editorial comment by Ketteler and Biggar, pages 17–19).
A complete and informative editorial overview of access-related steal syndrome describes the clinical findings, diagnostic evaluation and treatment options.
(See editorial comment by Mickley, pages 19–24).
The status of glycaemic control in haemodialysis patients affects the serum levels of iPTH, and adequate control is required to prevent osteodystrophy.
(See article by Murakami et al., pages 315–320).
As a commentary to this paper, the treatment goals of serum levels of intact parathyroid hormone in diabetic patients on haemodialysis are further discussed.
(See editorial comment by Gnudi, pages 24–26).
The pathophysiologic and regenerative processes of acute kidney injury, whether induced by ischaemia-reperfusion (I/R) or after nephrotoxin exposure, are still being actively studied. Three original papers explore this subject by addressing three different issues: the blockage of the JAK/STAT signalling, the protective effect of intrarenal administration of recombinant human soluble thrombomodulin in I/R models and a description of the enhanced early tubular expression and urinary excretion of nephronectin in a nephrotoxic model of acute tubular necrosis.
(See articles by Yang et al., pages 91–100; Cheng et al., pages 101–109; Ozaki et al., pages 110–119).
Long-term peritoneal dialysis is hampered by the development of peritoneal fibrosis with functional deterioration of the membrane and loss of ultrafiltration. TGF-β is involved in these changes and its gene product βig-h3 has been suggested as a biological marker for active TGF-β.
An elegant study shows that in vitro, βig-h3 induced by TGF-β in cultured human peritoneal mesothelial cells improves adhesion and migration of these cells during wound healing. In vivo, using a chronic PD infusion model, βig-h3 plays a role in the functional deterioration of the membrane.
(See article by Park et al., pages 126–135).
Neseritide (NES), a recombinant brain natriuretic peptide, is a new agent used in the treatment of congestive heart failure (CHF). Recent meta-analysis suggests that this agent is associated with an increased risk of short-term mortality.
In a retrospective analysis including a cohort of 682 patients, NES was not independently associated with increased mortality in CHF patients; however, the development of acute renal failure in association with NES use may confer an increased risk of mortality.
(See article by Iglesias et al., pages 144–153).
Little information is available on the prognostic and therapeutic implications of the several pathological variants of focal segmental glomerulosclerosis (FSGS).
A retrospective analysis revealed that renal survival at five years was significantly better for patients with the tip variant compared to the not otherwise specified and perihilar forms of FSGS.
(See article by Deegens, et al., pages 186–192).
Different histopathological classifications of lupus nephritis exist, the latest one developed by the ISN/Renal Pathology Society.
The sobering conclusion of a study performed by five specialized nephropathologists in the Netherlands was that, although definitions were agreed upon beforehand, even these specialists had difficulties with scoring histopathological characteristics of lupus nephritis, particularly with the currently available classification systems.
(See article by Grootscholten et al., pages 223–230).
For many years, a relationship between high vascular access flow and increase in cardiac output (CO), the latter potentially causing cardiac failure, has been postulated.
A prospective study shows not only that the relationship between access flow and CO is quite complex, but demonstrates that an access flow of > 2 L/min has a high predictive power for high-output cardiac failure.
(See article by Basile et al., pages 282–287).
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