Insights in Nutrition and Metabolism

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Short Communication - Insights in Nutrition and Metabolism (2023) Volume 7, Issue 4

A discussion of diabetic nephropathy diagnosis and therapy.

Samsu Lerner*

Department of Internal Medicine, University of Illinois at Chicago, Advocate Christ Medical Center, Chicago, IL, USA

*Corresponding Author:
Samsu Lerner
Department of Internal Medicine
University of Illinois at Chicago, Advocate Christ Medical Center
Chicago, IL, USA
E-mail:lerner.sam@hotmail.com

Received:24-Jun-2023,Manuscript No. AAINM-23-107292; Editor assigned: 27-Jun-2023, PreQC No. AAINM-23-107292(PQ); Reviewed:11-Jul-2023, QC No. AAINM-23-107292; Revised:17-Jul-2023, Manuscript No. AAINM-23-107292(R); Published:24-Jul-2023, DOI: 10.35841/aainm-7.4.153

Citation: Lerner S. A discussion of diabetic nephropathy diagnosis and therapy. Insights Nutr Metab. 2023;7(4):153

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Introduction

Diabetic nephropathy is a type of chronic kidney disease (CKD) that develops as a result of diabetes mellitus. It is one of the most prevalent and serious complications of diabetes, contributing significantly to morbidity and mortality rates worldwide. The condition arises due to long-standing uncontrolled diabetes and remains asymptomatic during its early stages. However, once symptoms manifest, the kidney damage is often irreversible, leading to end-stage renal disease (ESRD) and necessitating dialysis or kidney transplantation.

Pathophysiology

The pathogenesis of diabetic nephropathy is multifactorial and involves various molecular and cellular processes. Hyperglycemia, a hallmark of diabetes, plays a central role in initiating and perpetuating kidney damage. Elevated glucose levels activate multiple pathways, leading to the production of advanced glycation end products (AGEs), oxidative stress, and inflammation. These processes contribute to the dysfunction of endothelial cells and the renal filtration barrier, allowing proteins to leak into the urine (proteinuria) and trigger renal fibrosis. Furthermore, the renin-angiotensin-aldosterone system (RAAS) and the transforming growth factor-beta (TGF-β) pathway are also implicated in the development of diabetic nephropathy. These pathways exacerbate renal injury by promoting vasoconstriction, inflammation, and fibrosis, eventually leading to glomerulosclerosis and tubulointerstitial fibrosis[1].

Risk factors

While the primary risk factor for diabetic nephropathy is diabetes mellitus, several factors can influence its development and progression. Notable risk factors include:

  • Duration of diabetes: The longer a person has diabetes, the higher their risk of developing nephropathy
  • Poor glycemic control: Uncontrolled blood glucose levels increase the likelihood of kidney damage.
  • Hypertension: High blood pressure is a significant risk factor for diabetic nephropathy and can accelerate its progression.
  • Genetic predisposition: Some individuals may have a genetic susceptibility to diabetic nephropathy.
  • Smoking: Smoking can worsen kidney function and contribute to the development of nephropathy[2].

Clinical presentation

In its early stages, diabetic nephropathy may not cause any noticeable symptoms. As the disease progresses, the following clinical manifestations may become evident:

  • Proteinuria: Excessive protein in the urine, detected through routine urinalysis.
  • Hematuria: Presence of blood in the urine, indicating damage to the kidney's filtration system.
  • Hypertension: High blood pressure is common in diabetic nephropathy due to increased RAAS activity.
  • Edema: Swelling, particularly in the ankles and feet, due to fluid retention.
  • Fatigue and weakness: Kidney dysfunction can lead to anemia and fatigue.
  • Reduced urine output: In advanced stages, the kidneys may fail to produce an adequate amount of urine[3].

Diagnosis

Early detection and diagnosis of diabetic nephropathy are crucial to initiate timely interventions. Diagnostic methods and assessments include:

  • Urinalysis: Screening for proteinuria and hematuria.
  • Blood tests: Measurement of serum creatinine and blood urea nitrogen (BUN) to assess kidney function.
  • Albumin-to-Creatinine Ratio (ACR): ACR measurement to quantify proteinuria and assess disease progression.
  • Glomerular Filtration Rate (GFR): Estimation of GFR to assess kidney function.
  • Kidney biopsy: In some cases, a biopsy may be necessary to confirm the diagnosis and determine the extent of kidney damage.

Management

The management of diabetic nephropathy aims to slow disease progression, alleviate symptoms, and reduce complications. Key components of management include:

  • Glycemic control: Strict control of blood glucose levels through lifestyle modifications and antidiabetic medications.
  • Blood pressure control: Aggressive management of hypertension using antihypertensive medications.
  • RAAS Inhibitors: Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are beneficial in reducing proteinuria and slowing progression.
  • Lipid control: Management of dyslipidemia to reduce cardiovascular risk.
  • Dietary modifications: A low-sodium, low-protein diet may be recommended to reduce kidney burden.
  • Smoking cessation: Encouraging patients to quit smoking to improve kidney health[4].

Preventive measures

Prevention plays a pivotal role in combating diabetic nephropathy. Strategies to reduce the risk of developing nephropathy include:

  • Early diabetes detection: Identifying and treating diabetes as early as possible can reduce the risk of complications.
  • Regular monitoring: Regular screening for proteinuria and kidney function in diabetic individuals.
  • Blood pressure control: Maintaining optimal blood pressure levels can delay or prevent nephropathy.
  • Glycemic control: Tight glycemic control can significantly reduce the risk of diabetic nephropathy[5].

Conclusion

Diabetic nephropathy is a severe and prevalent complication of diabetes mellitus that poses a significant global health burden. Understanding the underlying pathophysiology and recognizing early clinical signs are essential for its successful management. By adopting preventive measures and optimizing glycemic and blood pressure control, healthcare providers can reduce the incidence and impact of diabetic nephropathy, improving the quality of life for countless individuals affected by this silent menace.

References

  1. Sheira G, Noreldin N, Tamer A, et al.Urinary biomarker N-acetyl-β-D-glucosaminidase can predict severity of renal damage in diabetic nephropathy.J Diabetes Metab Disord. 2015;14:1-5.

    2. Indexed at, Google Scholar, Cross Ref

  2. Kitada M, Ogura Y, Koya D.Rodent models of diabetic nephropathy: their utility and limitations.Int J Nephrol Renov Dis. 2016:279-90.

    3. Indexed at, Google Scholar, Cross Ref

  3. Fioretto P, Steffes MW, Brown DM, et al.An overview of renal pathology in insulin-dependent diabetes mellitus in relationship to altered glomerular hemodynamics.Am J Kidney Dis. 1992;20(6):549-58.

    4. Indexed at, Google Scholar,Cross Ref

  4. Kohan DE, Pollock DM.Endothelin antagonists for diabetic and non?diabetic chronic kidney disease.Br J Clin Pharmacol. 2013;76(4):573-9.

    5. Indexed at, Google Scholar, Cross Ref

  5. Chen X, Wang DD, Wei T, et al.Effects of astragalosides from Radix Astragali on high glucose?induced proliferation and extracellular matrix accumulation in glomerular mesangial cells.Exp Ther Med. 2016;11(6):2561-6.

    6. Indexed at, Google Scholar, Cross Ref

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