Keyword: Nephroprotection
2 results found.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A12, https://doi.org/10.63946/cajn/19521
ABSTRACT:
Background: Alport syndrome is an inherited disorder of the glomerular basement membrane caused by pathogenic variants in COL4A3, COL4A4, or COL4A5. The disease is characterized by persistent microscopic hematuria, progressive proteinuria and chronic kidney disease, with possible hearing and ocular involvement. Early recognition is important for timely nephroprotective management and family screening.
Methods: This narrative review synthesizes the available information on the molecular basis, inheritance patterns, clinical manifestations, diagnostic approaches, monitoring, and treatment of Alport syndrome. Particular attention was given to genetic testing, renal manifestations, extrarenal features, and nephroprotective strategies.
Results: Alport syndrome demonstrates X-linked, autosomal recessive, and autosomal dominant inheritance patterns. X-linked disease is associated predominantly with COL4A5 variants, whereas COL4A3 and COL4A4 variants are responsible for autosomal forms. Persistent hematuria is an important early renal manifestation and may progress to proteinuria, glomerulosclerosis, chronic kidney disease, and end-stage renal disease. Hearing impairment and ocular abnormalities may provide additional diagnostic clues. Molecular genetic testing is an important approach to diagnosis and classification. Screening of relatives is valuable for identifying affected or at-risk family members. Nephroprotective therapy, particularly renin–angiotensin–aldosterone system blockade with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, is emphasized in patients with persistent proteinuria. Long-term management also requires renal function monitoring and audiological and ophthalmological assessment.
Conclusion: Alport syndrome requires early recognition of persistent hematuria and appropriate genetic evaluation. Timely nephroprotective treatment, family screening, and multidisciplinary follow-up may help slow progression of kidney disease and improve comprehensive patient care.
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.