Keyword: Disease Progression
3 results found.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A31, https://doi.org/10.63946/cajn/19522
ABSTRACT:
Background: The early onset of chronic kidney disease often lacks symptoms, leading to delayed diagnosis and treatment. Regular laboratory testing can detect the disease before it begins, which helps clinicians determine the appropriate treatment for patients. This review sought to assess how ongoing tracking of estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) contributes to understanding the progression of chronic kidney disease (CKD) and determining the risk levels for patients.
Methods: A thorough review of evidence from international clinical practice guidelines, systematic reviews, meta-analyses, and extensive observational cohort studies was conducted. Special attention was given to how eGFR and UACR changed over time and how these changes were linked to the development of advanced CKD, kidney failure, cardiovascular issues, and death. The most recent recommendations from the 2024 KDIGO CKD guideline were included.
Results: Evidence shows that regularly checking eGFR and UACR is essential for effectively monitoring chronic kidney disease. In a group of 91,319 people, a reduction of 30% or more in estimated glomerular filtration rate (eGFR) was linked to a significantly higher risk of developing advanced chronic kidney disease, with a hazard ratio of 7.53 (95% CI, 6.70–8.45).Similarly, an increase of 30% or more in urinary albumin-to-creatinine ratio (UACR) was associated with a hazard ratio of 1.78 (95% CI, 1.59–1.98). At the same time, when both UACR increased and eGFR decreased, the hazard ratio was 15.15 (95% CI, 12.43–18.46) compared to when these values remained stable. KDIGO suggests that patients with chronic kidney disease should have their glomerular filtration rate and albuminuria checked at least once every year.For those at greater risk, more regular check-ups are advised, especially if the results could impact treatment choices. Even though these recommendations were provided, a systematic review of 59 studies that included 3,036,41 patients showed significant shortcomings in standard monitoring practices: the estimated glomerular filtration rate (eGFR) was checked in 81.3% of patients, but testing for albuminuria was done in just 47.4%.
Conclusion: Regular laboratory testing, especially repeated checks of eGFR and UACR, is important for early identification of CKD progression and for assessing individual risk levels. The continued limited use of albuminuria testing highlights a significant gap in care that aligns with established guidelines. Integrating structured laboratory surveillance into routine clinical practice may facilitate timely therapeutic optimization and contribute to delaying kidney failure and reducing cardiorenal complications.
Methods: A thorough review of evidence from international clinical practice guidelines, systematic reviews, meta-analyses, and extensive observational cohort studies was conducted. Special attention was given to how eGFR and UACR changed over time and how these changes were linked to the development of advanced CKD, kidney failure, cardiovascular issues, and death. The most recent recommendations from the 2024 KDIGO CKD guideline were included.
Results: Evidence shows that regularly checking eGFR and UACR is essential for effectively monitoring chronic kidney disease. In a group of 91,319 people, a reduction of 30% or more in estimated glomerular filtration rate (eGFR) was linked to a significantly higher risk of developing advanced chronic kidney disease, with a hazard ratio of 7.53 (95% CI, 6.70–8.45).Similarly, an increase of 30% or more in urinary albumin-to-creatinine ratio (UACR) was associated with a hazard ratio of 1.78 (95% CI, 1.59–1.98). At the same time, when both UACR increased and eGFR decreased, the hazard ratio was 15.15 (95% CI, 12.43–18.46) compared to when these values remained stable. KDIGO suggests that patients with chronic kidney disease should have their glomerular filtration rate and albuminuria checked at least once every year.For those at greater risk, more regular check-ups are advised, especially if the results could impact treatment choices. Even though these recommendations were provided, a systematic review of 59 studies that included 3,036,41 patients showed significant shortcomings in standard monitoring practices: the estimated glomerular filtration rate (eGFR) was checked in 81.3% of patients, but testing for albuminuria was done in just 47.4%.
Conclusion: Regular laboratory testing, especially repeated checks of eGFR and UACR, is important for early identification of CKD progression and for assessing individual risk levels. The continued limited use of albuminuria testing highlights a significant gap in care that aligns with established guidelines. Integrating structured laboratory surveillance into routine clinical practice may facilitate timely therapeutic optimization and contribute to delaying kidney failure and reducing cardiorenal complications.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A39, https://doi.org/10.63946/cajn/19520
ABSTRACT:
Background: Chronic kidney disease (CKD) is characterized by progressive loss of kidney function associated with intraglomerular hypertension, hyperfiltration, podocyte injury, tubular damage, and tubulointerstitial fibrosis. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated nephroprotective effects beyond glycemic control. This study aimed to quantitatively assess the effect of SGLT2 inhibitors on CKD progression and to summarize the morphological mechanisms underlying their nephroprotective effects.
Methods: A systematic review and quantitative meta-analysis of randomized controlled trials (RCTs) evaluating SGLT2 inhibitors and renal outcomes was performed. The primary quantitative analysis included the CREDENCE, DAPA-CKD, and EMPA-KIDNEY trials. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Statistical heterogeneity was assessed using the I² statistic and Cochran’s Q test. Published evidence on morphological and structural renal changes associated with SGLT2 inhibition was additionally analyzed.
Results: SGLT2 inhibitors reduced the risk of the primary renal composite endpoint in CREDENCE (HR 0.70; 95% CI 0.59–0.82), DAPA-CKD (HR 0.61; 95% CI 0.51–0.72), and EMPA-KIDNEY (HR 0.72; 95% CI 0.64–0.82). The pooled analysis demonstrated a significant reduction in the risk of CKD progression (HR 0.68; 95% CI 0.62–0.75), corresponding to an approximately 32% relative risk reduction. Heterogeneity between studies was low (I²=17.5%). Morphological evidence demonstrated attenuation of glomerular hyperfiltration, preservation of podocytes and the glomerular filtration barrier, reduction of tubular injury, and attenuation of tubulointerstitial fibrosis.
Conclusion: SGLT2 inhibitors are associated with a significant reduction in the risk of CKD progression. Their nephroprotective effects appear to involve complementary hemodynamic, glomerular, tubular, and tubulointerstitial mechanisms. The consistency between clinical trial findings and morphological evidence supports a multifactorial basis for SGLT2 inhibitor-mediated nephroprotection.
Methods: A systematic review and quantitative meta-analysis of randomized controlled trials (RCTs) evaluating SGLT2 inhibitors and renal outcomes was performed. The primary quantitative analysis included the CREDENCE, DAPA-CKD, and EMPA-KIDNEY trials. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Statistical heterogeneity was assessed using the I² statistic and Cochran’s Q test. Published evidence on morphological and structural renal changes associated with SGLT2 inhibition was additionally analyzed.
Results: SGLT2 inhibitors reduced the risk of the primary renal composite endpoint in CREDENCE (HR 0.70; 95% CI 0.59–0.82), DAPA-CKD (HR 0.61; 95% CI 0.51–0.72), and EMPA-KIDNEY (HR 0.72; 95% CI 0.64–0.82). The pooled analysis demonstrated a significant reduction in the risk of CKD progression (HR 0.68; 95% CI 0.62–0.75), corresponding to an approximately 32% relative risk reduction. Heterogeneity between studies was low (I²=17.5%). Morphological evidence demonstrated attenuation of glomerular hyperfiltration, preservation of podocytes and the glomerular filtration barrier, reduction of tubular injury, and attenuation of tubulointerstitial fibrosis.
Conclusion: SGLT2 inhibitors are associated with a significant reduction in the risk of CKD progression. Their nephroprotective effects appear to involve complementary hemodynamic, glomerular, tubular, and tubulointerstitial mechanisms. The consistency between clinical trial findings and morphological evidence supports a multifactorial basis for SGLT2 inhibitor-mediated nephroprotection.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A1, https://doi.org/10.63946/cajn/19504
ABSTRACT:
Background: Diabetic chronic kidney disease (DKD) is a leading cause of kidney failure and cardiovascular morbidity worldwide. Although albuminuria and estimated glomerular filtration rate (eGFR) remain central markers of risk stratification, early progression is frequently driven by a broader cluster of metabolic, hemodynamic, inflammatory, and cardiometabolic factors. Identification of simple clinical predictors may support earlier intensification of nephroprotective therapy. This study aimed to evaluate clinical, biochemical, and renal predictors associated with early DKD progression.
Methods: This prospective observational study included 112 patients with type 2 diabetes mellitus and established chronic kidney disease. Baseline assessment included age, sex, diabetes duration, body mass index, systolic and diastolic blood pressure, glycated hemoglobin (HbA1c), fasting plasma glucose, lipid profile, serum creatinine, eGFR, urinary albumin-to-creatinine ratio (UACR), hemoglobin, uric acid, C-reactive protein, smoking status, hypertension, obesity, dyslipidemia, and cardiovascular disease history. Early CKD progression was defined as clinically significant eGFR decline during follow-up. Patients were divided into early progression and stable/slow progression groups. Between-group comparisons and multivariable logistic regression were performed.
Results: Early DKD progression was observed in 34 of 112 patients (30.4%), while 78 patients (69.6%) had stable or slowly progressive disease. Patients with early progression had longer diabetes duration (12.8±4.1 vs 8.9±3.6 years; p<0.05), higher systolic blood pressure (148±16 vs 134±14 mmHg; p<0.05), higher HbA1c (8.7±1.1 vs 7.6±0.9%; p<0.01), greater UACR (286 [164–420] vs 118 [62–210] mg/g; p<0.01), and lower baseline eGFR (52.4±13.8 vs 64.7±15.2 mL/min/1.73 m²; p<0.05). Progressors also had higher body mass index (31.2±4.6 vs 28.7±4.2 kg/m²; p=0.006), triglycerides (2.3±0.7 vs 1.8±0.6 mmol/L; p<0.01 ), uric acid (421±76 vs 368±69 µmol/L; p=0.05), and C-reactive protein (5.8 [3.4–8.6] vs 3.1 [1.8–5.2] mg/L; p=0.002), with lower hemoglobin (118±14 vs 126±13 g/L; p=0.004). In multivariable analysis, independent predictors of early progression were UACR above 300 mg/g (odds ratio [OR] 3.42, 95% confidence interval [CI] 1.48-7.91; p=0.004), HbA1c at least 8.0% (OR 2.76, 95% CI 1.27-6.01; p=0.011), uncontrolled hypertension (OR 2.58, 95% CI 1.17-5.68; p=0.018), and hyperuricemia (OR 2.21, 95% CI 1.02-4.79; p=0.044).
Conclusion: Early DKD progression affected nearly one-third of patients. Albuminuria, poor glycemic control, uncontrolled hypertension, hyperuricemia, reduced baseline eGFR, obesity, dyslipidemia, inflammation, and anemia were associated with accelerated renal decline. These clinically accessible variables may improve early risk stratification and guide individualized nephroprotective management.
Methods: This prospective observational study included 112 patients with type 2 diabetes mellitus and established chronic kidney disease. Baseline assessment included age, sex, diabetes duration, body mass index, systolic and diastolic blood pressure, glycated hemoglobin (HbA1c), fasting plasma glucose, lipid profile, serum creatinine, eGFR, urinary albumin-to-creatinine ratio (UACR), hemoglobin, uric acid, C-reactive protein, smoking status, hypertension, obesity, dyslipidemia, and cardiovascular disease history. Early CKD progression was defined as clinically significant eGFR decline during follow-up. Patients were divided into early progression and stable/slow progression groups. Between-group comparisons and multivariable logistic regression were performed.
Results: Early DKD progression was observed in 34 of 112 patients (30.4%), while 78 patients (69.6%) had stable or slowly progressive disease. Patients with early progression had longer diabetes duration (12.8±4.1 vs 8.9±3.6 years; p<0.05), higher systolic blood pressure (148±16 vs 134±14 mmHg; p<0.05), higher HbA1c (8.7±1.1 vs 7.6±0.9%; p<0.01), greater UACR (286 [164–420] vs 118 [62–210] mg/g; p<0.01), and lower baseline eGFR (52.4±13.8 vs 64.7±15.2 mL/min/1.73 m²; p<0.05). Progressors also had higher body mass index (31.2±4.6 vs 28.7±4.2 kg/m²; p=0.006), triglycerides (2.3±0.7 vs 1.8±0.6 mmol/L; p<0.01 ), uric acid (421±76 vs 368±69 µmol/L; p=0.05), and C-reactive protein (5.8 [3.4–8.6] vs 3.1 [1.8–5.2] mg/L; p=0.002), with lower hemoglobin (118±14 vs 126±13 g/L; p=0.004). In multivariable analysis, independent predictors of early progression were UACR above 300 mg/g (odds ratio [OR] 3.42, 95% confidence interval [CI] 1.48-7.91; p=0.004), HbA1c at least 8.0% (OR 2.76, 95% CI 1.27-6.01; p=0.011), uncontrolled hypertension (OR 2.58, 95% CI 1.17-5.68; p=0.018), and hyperuricemia (OR 2.21, 95% CI 1.02-4.79; p=0.044).
Conclusion: Early DKD progression affected nearly one-third of patients. Albuminuria, poor glycemic control, uncontrolled hypertension, hyperuricemia, reduced baseline eGFR, obesity, dyslipidemia, inflammation, and anemia were associated with accelerated renal decline. These clinically accessible variables may improve early risk stratification and guide individualized nephroprotective management.