Nat. Rev. Nephrol. doi: /nrneph

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©2013 Astute Medical, Inc. PN 0138 Rev B 2013/03/19

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Nat. Rev. Nephrol. doi: /nrneph

Figure 5 A layered approach to the follow-up of patients with acute kidney disease (AKD) Figure 5 | A layered approach to the follow-up of patients with.

Figure 4 Interplay between acute kidney injury (AKI),

Figure 6 Effects of adiponectin on podocyte function

Figure 3 Energy metabolism regulation, cardiovascular and bone disease in CKD Figure 3 | Energy metabolism regulation, cardiovascular and bone disease.

Figure 6 Approach to drug management in patients with acute kidney disease (AKD) Figure 6 | Approach to drug management in patients with acute kidney disease.

Figure 4 Expression of coagulation protease receptors in renal cells

Figure 4 Interactions between adipose, the microbiome and kidney

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Mechanisms of kidney injury in the setting of obesity

Figure 2 Proinflammatory mechanisms in CKD

Figure 1 Circadian changes in energy metabolism and immune responses in CKD Figure 1 | Circadian changes in energy metabolism and immune responses in CKD.

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Role of the kidney in glucose homeostasis

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 6 The bioavailability of phosphate differs according to the protein source Figure 6 | The bioavailability of phosphate differs according to the.

Figure 7 The efficacy of phosphate-binder therapy

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Figure 2 Expression of complement activation products in renal samples

Figure 5 Risk factor control in the intensive treatment group

Figure 2 The network of chronic diseases and their mutual influences

Figure 2 Three distinct mechanisms of activation of

Figure 1 The burden of chronic kidney disease (CKD)

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Societal costs for the care of patients with chronic kidney disease in the UK Figure 3 | Societal costs for the care of patients with chronic.

Figure 5 Comparison of outcomes with belimumab or rituximab therapy

Figure 1 Overview of canonical TGF-β/Smad signalling in tissue fibrosis Figure 1 | Overview of canonical TGF-β/Smad signalling in tissue fibrosis. Once.

Figure 1 Acute kidney injury and chronic kidney disease

Figure 2 The continuum of acute kidney injury (AKI),

Figure 4 Model of changes in the serum levels

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney.

Figure 4 Potential therapeutic strategies to inhibit TGF-β1/Smad-induced tissue fibrosis Figure 4 | Potential therapeutic strategies to inhibit TGF-β1/Smad-induced.

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Altered innate immune functions after sepsis

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Specificity of the various epidermal growth factor (EGF)

Figure 3 Cascade of events leading from AKI to ALI

Volume 85, Issue 4, Pages (April 2014)

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

cardiovascular and renal systems

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Potential mechanisms of PAR activation by thrombin and aPC

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Hypothetical trajectories of acute kidney disease (AKD)

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 The nephron-centric model of renal transplant fibrosis based on the injury-related molecular events observed in biopsy samples in the first year.

Nat. Rev. Nephrol. doi: /nrneph

Figure 6 Hypothetical effect of starting therapy for autosomal

Figure 3 Biologics that attenuate effector responses in the kidney

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 The relationship between health fitness and pathogen load

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Principal pathogenic mechanisms of

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Patient, facility, health-care system and industry factors

Figure 3 Preventive strategies for CSA-AKI

Figure 4 The relationship between the time-dependent changes in the expression of immunoglobulin, mast cell, acute kidney injury (AKI), and fibrillar collagen.

The promise of biomarkers for personalized renal cancer care

Figure 1 Worldwide distribution of disease burden attributable to environmental risks in 2012 Figure 1 | Worldwide distribution of disease burden attributable.

Pediatric acute kidney injury: The use of the RIFLE criteria

Peter A. McCullough et al. JACC 2016;68:

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Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.186 Figure 4 Potential strategies for the assessment of renal tolerance in patients with sepsis Figure 4 | Potential strategies for the assessment of renal tolerance in patients with sepsis. a | Determination of tolerance (that is, reaction norms) could potentially be achieved at the bedside using existing kidney-specific markers of renal fitness and clinical surrogates of pathogen load. b | An alternative, potentially more feasible approach might be to determine the impact of immunopathology on renal fitness using clinical surrogates of inflammatory burden. CRP, C-reactive protein; IGFBP-7, insulin-like growth factor-binding protein; LPS, lipopolysaccharide; NGAL, neutrophil gelatinase-associated lipocalin; TIMP-2, urinary metalloproteinase inhibitor 2. Gómez, H. et al. (2017) Metabolic reprogramming and tolerance during sepsis-induced AKI Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.186