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临床试验/NCT07635797
NCT07635797尚未招募不适用

Effectiveness of Subgingival Instrumentation on Delaying End-stage Renal Disease Among Chronic Kidney Disease Patients: A Non-Randomized Clinical Study

Postgraduate Institute of Dental Sciences Rohtak1 个研究点 分布在 1 个国家目标入组 40 人开始时间: 2026年7月1日最近更新:
适应症
干预措施

试验速览

阶段
不适用
状态
尚未招募
入组人数
40
试验地点
1
主要终点
Soluble Urokinase Plasminogen Activator Receptor(suPAR)

研究概览

简要总结

Chronic kidney disease (CKD) and periodontitis share a bidirectional inflammatory relationship, with cytokines such as IL-6, TNF-α, and hsCRP driving progression in both conditions. Non-surgical periodontal therapy (NSPT) has shown reductions in systemic inflammatory markers with emerging evidence of improved renal function, yet robust randomized controlled trials targeting pre-dialysis stage IV-V diabetic CKD patients remain lacking. In the Indian context, where diabetes-related CKD is rapidly rising and access to dialysis is limited, there is a clear lacuna in literature regarding the effectiveness of NSPT in delaying progression to end-stage renal disease. Hence, the present non-randomized clinical study is undertaken to address this gap.

详细描述

Chronic kidney disease (CKD) is a major socio-economic and healthcare problem and represents a significant global public health challenge. The burden of disease is disproportionately higher in low- and middle-income countries. As per the Global Burden of Disease (GBD) 2023 estimates, approximately 788 million people were affected by CKD globally, with a global age-adjusted prevalence of 14.2% among adults aged 20 years and older. CKD has a significant global burden, affecting over 9% of the world population and was directly responsible for 1.2 million deaths worldwide in 2017 alone.

Chronic kidney disease is defined as the presence of kidney damage or an estimated glomerular filtration rate (eGFR) of less than 60 ml/min/1.73 m² persisting for three months or more, irrespective of the underlying cause. It represents a state of progressive loss of kidney function, ultimately resulting in the need for renal replacement therapy in the form of dialysis or kidney transplantation. Kidney damage refers to pathological abnormalities detected by imaging or renal biopsy, abnormalities in urinary sediment, or increased urinary albumin excretion rates.

The leading cause of CKD is diabetes mellitus, followed by hypertension and glomerular diseases. The prevalence of individuals with CKD due to type 1 diabetes has continued to increase globally, rising by 21.7% between 2007 and 2017 and reaching approximately 3.2 million individuals in 2017. These individuals are at increased risk of cardiovascular complications, and nearly 25-30% progress to kidney failure. Irrespective of the initial nephropathy, once a critical mass of nephrons is lost, kidney disease generally follows a progressive course toward advanced stages, resulting in increased morbidity and mortality.

The burden of CKD arises not only from the management of end-stage renal disease but also from complications related to CKD and its associated comorbidities. There are effective strategies to reduce the rate of CKD progression and improve patient outcomes; therefore, the need for therapies aimed at slowing disease progression is critical.

Periodontal bacteria, which cause chronic inflammation and the breakdown of tooth-supporting structures, are the cause of periodontal disease, a chronic infectious oral illness. One of the most prevalent oral illnesses worldwide is periodontitis, affecting almost 20-50% of the global population in varying degrees, and the percentage rises with advancing age. In India, 51% of people had periodontal disease overall. Periodontal disease is implicated as an independent risk factor for CKD. Periodontitis is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone, with periodontal pocket formation, gingival recession, or both.

研究设计

研究类型
Interventional
分配方式
Non Randomized
干预模型
Parallel
主要目的
Prevention
盲法
None

入排标准

年龄范围
40 Years 至 70 Years(Adult, Older Adult)
性别
All
接受健康志愿者

入选标准

  • Patients aged 40-70 years.
  • Type 2 diabetes mellitus with chronic kidney disease and currently on oral hypoglycaemic agents.
  • Diagnosed with Stage IV or V (eGFR between 15-20 mL/min/1.73m²).
  • Not undergoing dialysis.
  • Presence of ≥20 natural teeth.
  • Diagnosed with moderate (Stage II) (as per 2017 World Workshop classification) (Interdental CAL at site of greatest loss >2mm but <5 mm in ≥ 2 non-adjacent teeth).
  • Willingness to provide written informed consent.

排除标准

  • Patients already undergoing haemodialysis or renal transplantation.
  • Patients on insulin therapy or taking SGLT2 inhibitors and GLP-1 receptor agonists.
  • HbA1c level >8 %.
  • Any Periodontal therapy within past 6 months.
  • Immunocompromised patients.
  • Any history of tobacco use.
  • Pregnant or lactating women.

研究组 & 干预措施

Intervention Group

Experimental

Intervention Group participants will receive subgingival instrumentation using an ultrasonic scaler (NSK Variose 2 Ultrasonic Scaler) and hand instruments (Sickle scalers and Curettes, GDC) followed by oral hygiene instructions (OHI).

干预措施: Oral Hygiene Instructions (Other)

Comparator Group

Active Comparator

Control group participants will receive basic oral hygiene instructions

干预措施: Oral Hygiene Instructions (Other)

Intervention Group

Experimental

Intervention Group participants will receive subgingival instrumentation using an ultrasonic scaler (NSK Variose 2 Ultrasonic Scaler) and hand instruments (Sickle scalers and Curettes, GDC) followed by oral hygiene instructions (OHI).

干预措施: Subgingival Instrumentation (Procedure)

结局指标

主要结局

Soluble Urokinase Plasminogen Activator Receptor(suPAR)

时间窗: The estimation of soluble urokinase plasminogen activator receptor (suPAR) will be done at baseline and 12 months.

The estimation of soluble urokinase plasminogen activator receptor (suPAR) in plasma will be performed using a sandwich Enzyme-Linked Immunosorbent Assay (ELISA). The assay employs a sandwich ELISA technique, where suPAR in the plasma sample binds to specific antibodies immobilized on the microplate. Following incubation and washing steps, an enzyme-conjugated detection antibody and substrate solution will be added. The enzymatic reaction will produce a measurable colour change proportional to the concentration of suPAR. The absorbance will be recorded at 450 nm using an ELISA microplate reader, and the concentration was calculated using a standard curve.

Periodontal markers

时间窗: Measurement will be done at Baseline, 3, 6, 9 and 12 months.

Different periodontal markers including Pocket Probing Depth(PPD), Clinical Attachment Loss(CAL), Bleeding on Probing(BOP), Calculus Component of Oral Hygiene Index will be estimated. Measurement will be done at six sites (mesiobuccal, mid-buccal, distobuccal, mesiolingual/palatal, mid-lingual/palatal, and distolingual/palatal) on all maxillary and mandibular teeth. PPD will be measured from the gingival margin to the base of the pocket, while CAL will be measured from the CEJ to the base of the pocket/sulcus. All the measurements will be rounded to the nearest millimeter and will be recorded using a Williams probe. For BOP, WHO Probe will be used and bleeding areas will be documented at six sites per tooth.

次要结局

  • Glycated Haemoglobin (HbA1c) levels(Glycated haemoglobin (HbA1c) levels assessment will be done at baseline, 3, 6, 9 and 12 months.)

研究者

申办方类型
Other
责任方
Sponsor

研究点 (1)

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