Diabetic nephropathy

Mbbs, Fracp George Jerums; Mbbs, Fracp Elif I. Ekinci; Mbbs, Fracp Erosha Premaratne; Bs, Scott; Panagiotopoulos, Sianna; Bsc, Richard J. MacIsaac

doi:10.1002/9781118387658.ch62

Cited by 3 publications

(2 citation statements)

References 67 publications

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“…HbA1c, BP, albumin excretion rate, eGFR, microvascular complications and duration of diabetes Evidence from a range of studies in both type 1 diabetes mellitus and type 2 diabetes mellitus patients (as above) highlight the utility of the following clinical findings in the prediction of DKD progression: elevated baseline HbA1c, elevated BP (systolic or mean arterial, but not diastolic), elevated albumin excretion rate (AER), decreased pre-existing renal function (eGFR/mGFR), the presence and severity of concomitant microvascular complications (most especially retinopathy, but also peripheral/autonomic neuropathy, as has been corroborated by biopsy findings showing a link between retinopathy and renal structural changes 53 ), and duration of diabetes. Individual discussion of these risk markers and progressive DKD have been extensively reviewed previously 24,54 . Below, we review the evidence for other candidate clinical risk markers for progressive DKD.…”

Section: Evaluation Of Baseline Clinical Characteristics As Renal Rismentioning

confidence: 99%

Clinical predictive factors in diabetic kidney disease progression

Radcliffe

Seah

Clarke

et al. 2016

J of Diabetes Invest

Self Cite

156

109

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Diabetic kidney disease (DKD) represents a major component of the health burden associated with type 1 and type 2 diabetes. Recent advances have produced an explosion of ‘novel’ assay‐based risk markers for DKD, though clinical use remains restricted. Although many patients with progressive DKD follow a classical albuminuria‐based pathway, non‐albuminuric DKD progression is now well recognized. In general, the following clinical and biochemical characteristics have been associated with progressive DKD in both type 1 and type 2 diabetes: increased hemoglobin A1c, systolic blood pressure, albuminuria grade, early glomerular filtration rate decline, duration of diabetes, age (including pubertal onset) and serum uric acid; the presence of concomitant microvascular complications; and positive family history. The same is true in type 2 diabetes for male sex category, in patients following an albuminuric pathway to DKD, and also true for the presence of increased pulse wave velocity. The following baseline clinical characteristics have been proposed as risk factors for DKD progression, but with further research required to assess the nature of any relationship: dyslipidemia (including low‐density lipoprotein, total and high‐density lipoprotein cholesterol); elevated body mass index; smoking status; hyperfiltration; decreases in vitamin D, hemoglobin and uric acid excretion (all known consequences of advanced DKD); and patient test result visit‐to‐visit variability (hemoglobin A1c, blood pressure and high‐density lipoprotein cholesterol). The development of multifactorial ‘renal risk equations’ for type 2 diabetes has the potential to simplify the task of DKD prognostication; however, there are currently none for type 1 diabetes‐specific populations. Significant progress has been made in the prediction of DKD progression using readily available clinical data, though further work is required to elicit the role of several variables, and to consolidate data to facilitate clinical implementation.

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Section: Evaluation Of Baseline Clinical Characteristics As Renal Rismentioning

confidence: 99%

Clinical predictive factors in diabetic kidney disease progression

Radcliffe

Seah

Clarke

et al. 2016

J of Diabetes Invest

Self Cite

156

109

View full text Add to dashboard Cite

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“…The process begins with the formation of advanced glycation end products (AGEs) and the activation of their receptor (RAGE), initiating a cascade of signaling events, including the upregulation of protein kinase C, nuclear factor-kappa B, and transforming growth factor-β (TGF-β). This chain of events leads to the increased production of reactive oxygen species (ROS) and a chronic inflammatory response, pivotal in the development and progression of DKD [27].…”

Section: Understanding the Complex Pathophysiology Of Diabetic Kidney...mentioning

confidence: 99%

Transforming Diabetes Care: The Molecular Pathways through Which GLP1-RAs Impact the Kidneys in Diabetic Kidney Disease

Rroji,

Spasovski

2024

Biomedicines

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Diabetic kidney disease (DKD) is a substantial complication of type 2 diabetes (T2D), presenting challenges in chronic kidney disease (CKD) management. In addition to traditional and recent therapies, including angiotensin, converting enzyme (ACE) inhibitors, angiotensin receptor blockers, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and mineralocorticoid receptor antagonists, the evolution of antihyperglycemic treatments has introduced a promising agent, glucagon-like peptide-1 receptor agonist (GLP-1RA) for the management of DKD. GLP-1RAs enhance insulin release and reduce glucagon release, offering a novel approach to DKD management. This review analyzes the molecular pathways through which GLP1-RAs confer renal protection in T2D and DKD, which are complex and multifaceted. They include modulation of renal hemodynamics, antioxidative and anti-inflammatory actions, metabolic regulation, and direct cellular effects. These mechanisms highlight GLP1-RA’s potential as a therapeutic option for glycemic control and direct or indirect renal function protection in diabetic patients, emphasizing the potentiality of GLP-1RAs for dual therapy, with cardiovascular and renal protection as a holistic approach. Clinical evidence supports GLP-1RAs in reducing albuminuria and enhancing kidney outcomes, highlighting their value in a comprehensive DKD management strategy.

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Effects of glycaemic management on diabetic kidney disease

MacIsaac¹,

Jerums²,

Ekinci³

2017

WJD

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Hyperglycaemia contributes to the onset and progression of diabetic kidney disease (DKD). Observational studies have not consistently demonstrated a glucose threshold, in terms of HbA1c levels, for the onset of DKD. Tight glucose control has clearly been shown to reduce the incidence of micro- or macroalbuminuria. However, evidence is now also emerging to suggest that intensive glucose control can slow glomerular filtration rate loss and possibly progression to end stage kidney disease. Achieving tight glucose control needs to be balanced against the increasing appreciation that glucose targets for the prevention of diabetes related complications need be individualised for each patient. Recently, empagliflozin which is an oral glucose lowering agent of the sodium glucose cotransporter-2 inhibitor class has been shown to have renal protective effects. However, the magnitude of empagliflozin’s reno-protective properties are over and above that expected from its glucose lowering effects and most likely largely result from mechanisms involving alterations in intra-renal haemodynamics. Liraglutide and semaglutide, both injectable glucose lowering agents which are analogues of human glucagon like peptide-1 have also been shown to reduce progression to macroalbuminuria through mechanisms that remain to be fully elucidated. Here we review the evidence from observational and interventional studies that link good glucose control with improved renal outcomes. We also briefly review the potential reno-protective effects of newer glucose lowering agents.

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Diabetic nephropathy

Cited by 3 publications

References 67 publications

Clinical predictive factors in diabetic kidney disease progression

Clinical predictive factors in diabetic kidney disease progression

Transforming Diabetes Care: The Molecular Pathways through Which GLP1-RAs Impact the Kidneys in Diabetic Kidney Disease

Effects of glycaemic management on diabetic kidney disease

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