Abstract

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and end-stage kidney disease (ESKD) in the United States and worldwide. Alterations in glomerular hemodynamics, inflammation, and fibrosis are primary mediators of kidney tissue damage, although the relative contribution of these mechanisms likely varies between individuals and over the course of the natural history of diabetic kidney disease. The presence of DKD is also strongly associated with cardiovascular morbidity/mortality and has a major influence on survival. Clinical presentation and prognosis of DKD are heterogeneous and vary between individuals, although the severity of albuminuria, particularly when combined with elevated blood pressure, remains an important marker of those at higher risk of progression. Management of DKD requires a holistic approach that combines cardiovascular risk reduction with elements to slow the progression of kidney disease, namely glycemic control, RAAS inhibition and blood pressure lowering. Effective delivery of these interventions in combination reduces the risks of DKD progression, as well as other microvascular complications, cardiovascular events, and mortality. Several international groups have issued clinical guidelines that largely agree on recommended targets, and in clinical practice these should be tailored for each individual patient. SGLT2 inhibitors are exciting new options now available to slow the progression of diabetic nephropathy.

Highlights

  • “Diabetic nephropathy” is a diagnosis that refers to specific pathologic structural and functional changes seen in the kidneys of patients with Diabetes Mellitus (DM) that result from the effects of DM on the kidney

  • A patient may even present with proteinuria and on kidney biopsy have diabetic nephropathy before T2DM is diagnosed. Another important difference in the natural history of patients with T1 versus T2DM is that the major macrovascular complication, namely cardiac disease and death due to cardiac disease, can occur at any point along the course of a patient with T2DM from the onset of DM and early diabetic nephropathy, whereas the elevated risk for cardiovascular disease is not apparent until advanced kidney disease has developed in patients with T1DM [14]

  • Suggested by vascular disease elsewhere, smoking history, hypertension, aortic disease, or asymmetric kidneys on renal ultrasound. This scenario is incorporated under the umbrella term of Diabetic kidney disease (DKD), and several of the risk factors for ischemic nephropathy are very common in people with diabetes

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Summary

Introduction

2. Diabetic Nephropathys vs Diabetic Kidney Disease “Diabetic nephropathy” is a diagnosis that refers to specific pathologic structural and functional changes seen in the kidneys of patients with DM (both type 1 and type 2 Diabetes Mellitus [T1/T2DM]) that result from the effects of DM on the kidney. Diabetic Nephropathys vs Diabetic Kidney Disease “Diabetic nephropathy” is a diagnosis that refers to specific pathologic structural and functional changes seen in the kidneys of patients with DM (both type 1 and type 2 Diabetes Mellitus [T1/T2DM]) that result from the effects of DM on the kidney It is characterized by persistent albuminuria and a progressive decline in renal function, and the term infers the presence of a typical pattern of glomerular disease. “Diabetic kidney disease” (DKD) is a clinical diagnosis based upon the presence of proteinuria, decrease estimated glomerular filtration rate (eGFR), or both in diabetes It does not indicate a specific pathological type. It is highly likely that diabetic nephropathy is the cause of diabetic kidney disease in type 1 diabetes of five or more years duration with albuminuria, but the frequency can range widely in type 2 diabetes

Epidemiology
Pathophysiology
Natural History of Diabetic Nephropathy
Screening
Confirmation of Persistent Abnormalities
Diagnosis of Diabetic Nephropathy
Features That May Indicate Alternative Forms of Kidney Disease
Differential Diagnoses to Consider in the Setting of Non-Albuminuric DKD
Treatment of Diabetic Nephropathy
Cardiovascular Risk Reduction
Glycemic Control
Achieved Findings in Intensive Intervention Care Group
RAS Inhibition
Emerging Therapies
Conclusions
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