Bone Marrow Cells Can Fuse with Injured Renal Cells
Afteracute renal injury, bone marrow cells infiltrate the kidneyand convert into renal cells. Using two different methods ofdetection, Li et al. demonstrate that some bone marrow cellsundergo this conversion by fusing with injured renal cells afterischemia-reperfusion injury. The low frequency of fusion, approximately7 per 10,000 tubular cells, however, suggests that the majorityof bone marrow cells become renal cells by other mechanisms.If alternative mechanisms are identified, then future therapiesfor acute kidney injury could incorporate methods to promotebone marrow cell conversion into tubular epithelial cells. SeeLi et al., pages 3067–3077.
PPAR Protects against Fatty Acid Toxicity
Excessivedelivery of albumin-bound fatty acids to the proximal tubulemay contribute to the tubular toxicity associated with proteinuria.Peroxisome proliferator-activated receptor- (PPAR) is importantin fatty acid metabolism and is highly expressed in the proximaltubule. For this reason, Kamijo et al. used PPAR–/–mice to explore fatty acid–mediated tubular toxicity.Significant toxicity to proximal tubular cells is observed whenPPAR–/– mice—but not wild-type mice—areadministered an injection of fatty acids bound to albumin, suggestinga protective role for PPAR. Little injury occurs when PPAR–/–mice are administered an injection of albumin alone, implicatingthe fatty acids in the toxicity. See Kamijo et al., pages 3089–3100.
Renal Progenitors Enhance ARF Recovery
Interestin stem cell–based therapies for acute renal failure (ARF)is increasing. Lazzeri et al. characterized multipotent renalprogenitor cells that can be identified from early nephrogenesisto the adult kidney. When isolated and cultured ex vivo, thesecells demonstrate multidifferentiation potential. When injectedinto mice that have ARF, they incorporate into multiple nephronsegments, improve renal function, and reduce interstitial fibrosis.Unlike embryonic stem cells, which may form teratomas when transplantedbefore differentiation, they show that these renal progenitorcells are not tumorigenic; therefore, these progenitors mayhave a future role in the treatment of ARF. See Lazzeri et al.,pages 3128–3138.
The seriesof hemoglobin levels over time for an individual hemodialysispatient can be described by the absolute levels themselves,the trend over time, or a measure of variability. Yang et al.used linear regression–based techniques to describe hemoglobinlevels over time in nearly 35,000 dialysis patients and foundthat variability in hemoglobin concentration is independentlyassociated with increased mortality. A causal relationship cannotbe concluded on the basis of this retrospective cohort study,but hemoglobin variability may be an important metric to includein future studies comparing strategies for anemia management.See Yang et al., pages 3164–3170.
HPLC-Detected Albuminuria Predicts Mortality
Albuminuria,usually measured by immunonephelometry, is associated with all-causeand cardiovascular mortality. HPLC can detect urinary proteinthat is presumed to be albumin but is not identified by theimmunochemical methods. Magliano et al. measured baseline urinaryalbumin by immunonephelometry and HPLC in more than 10,000 community-basedparticipants in the Australian Diabetes, Obesity, and Lifestylestudy and followed them for more than 5 yr. Albuminuria detectedby HPLC and/or immunonephelometry increases the risk for mortalityapproximately two-fold, but HPLC identifies at-risk patientswhom immunonephelometry does not detect. See Magliano et al.,pages 3171–3176.
The clinicalimportance of sustained proteinuria or its remission has notbeen completely described for IgA nephropathy. Reich et al.followed 542 patients with primary IgA nephropathy for 6.5 yrand report a 10- to 25-fold increased rate of renal declinefor each incremental gram of proteinuria, averaged over time,above 1 g/d. Patients who achieve a "partial remission" (i.e.,proteinuria <1 g/d), whether spontaneous or by intervention,have similar rates of renal decline regardless of their peaklevel of proteinuria and fare better than those who do not achieveremission. See Reich et al., pages 3177–3183.
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Protects against Fatty Acid Toxicity
