Journal of the American Society of Nephrology
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J Am Soc Nephrol 19: 13-, 2008
© 2008 American Society of Nephrology
doi: 10.1681/ASN.2007111196
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This Month's Highlights


   BASIC RESEARCH
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 BASIC RESEARCH
CLINICAL EPIDEMIOLOGY
 CLINICAL RESEARCH
 
Activating HIF Is Renoprotective

Figure 1
Hypoxia activates the transcription factor hypoxia inducible factor (HIF), and accumulating evidence suggests that HIF protects tissues against hypoxic injury. Hill et al. subjected mice to renal ischemia-reperfusion and found that the resulting injury was more severe in hif+/– mice than in wild-type controls. Moreover, increasing HIF levels by treating with inhibitors of HIF hydroxylases was renoprotective in wild-type mice. This study suggests that pharmacologic activation of HIF is a potential future therapeutic strategy for ischemic renal injury. See Hill et al., pages 39–46.

A New Look at NaCl Regulation

Figure 2
Little is known about the regulation and mechanisms of transcellular Cl– transport in the collecting duct. Pech et al. perfused mouse cortical collecting ducts in vitro and report that angiotensin II redistributes H+-ATPase to the apical plasma membrane of type A intercalated cells and stimulates H+ secretion. This, in turn, reduces the luminal HCO3– concentration, thereby providing a driving force for Cl– reabsorption via pendrin, the apical Cl–/HCO3– exchanger in type B intercalated cells. Angiotensin II–stimulated H+ secretion may also increase the electromotive force for epithelial sodium channel (ENaC)–mediated Na+ reabsorption. These results suggest that the H+-ATPase may regulate NaCl homeostasis in addition to acid/base balance. See Pech et al., pages 84–91.

AVP Promotes Cystogenesis

Figure 3
Vasopressin V2 receptor antagonists inhibit cystogenesis in animal models of polycystic kidney disease (PKD), but the mechanism of this inhibition has not been conclusively determined. Wang et al. generated rats with PKD and varying levels of arginine vasopressin (AVP) by breeding Pkhd1–/– with AVP–/– rats. Cystogenesis was almost completely inhibited in rats that had PKD and lacked AVP, but the addition of the V2 receptor agonist dDAVP promoted cyst formation in these animals. This study strengthens the rationale for the further study of V2 receptor antagonists to treat PKD. See Wang et al., pages 102–108.


   CLINICAL EPIDEMIOLOGY
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 BASIC RESEARCH
 CLINICAL EPIDEMIOLOGY
CLINICAL RESEARCH
 
CKD and 10-Yr Mortality after Acute MI

Figure 4
Renal insufficiency increases short-term mortality after acute myocardial infarction, but the persistence of its effect on long-term mortality is unknown. Smith et al. studied a cohort of nearly 120,000 elderly Medicare patients who were hospitalized with acute myocardial infarction and report that severe renal impairment on admission doubles the 10-yr risk for mortality, and even mild impairment increases risk by 10%. In addition, the influence of renal insufficiency on 10-yr mortality is rivaled only by age, surpassing traditional factors such as blood pressure and systolic function. This highlights the power of renal dysfunction as a risk factor for cardiovascular mortality. See Smith et al., pages 141–150.

Low Birth Weight Increases ESRD Risk

Figure 5
Case-control studies have suggested that intrauterine growth restriction may increase the risk for chronic kidney disease, but this hypothesis has not been previously tested in a cohort study. Vikse et al. combined the birth and renal registry data of Norway to evaluate the relationship between birth weight and ESRD risk in a cohort of >2 million people. They found that birth weight below the 10th percentile conferred a 70% increased risk for ESRD during a maximum follow-up period of 38 yr, even after adjusting for multiple birth-related confounders. This association was particularly strong during the first 14 yr of life. See Vikse et al., pages 151–157.


   CLINICAL RESEARCH
Top
 BASIC RESEARCH
 CLINICAL EPIDEMIOLOGY
 CLINICAL RESEARCH
 
Pioglitazone May Be Cardioprotective in CKD

Figure 6
The PROactive study compared the effects of pioglitazone with placebo on cardiovascular outcomes in a large cohort of patients with type 2 diabetes and a history of macrovascular disease. In a post hoc analysis, Schneider et al. evaluated the relationship between chronic kidney disease (CKD) and incident cardiovascular disease in this high-risk cohort, as well as the effects of pioglitazone treatment on recurrent cardiovascular disease. Compared with patients without renal disease, patients with CKD were nearly twice as likely to experience composite outcomes of death and cardiovascular events. Among those with CKD, pioglitazone treatment reduced the risk for all-cause mortality, myocardial infarction, or stroke by 34%. See Schneider et al., pages 182–187.





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