Keyword: Glomerular Disease

ABSTRACT: Background: Pregnancy in women with kidney disease is associated with an increased risk of maternal and obstetric complications, including preeclampsia, preterm delivery, and deterioration of kidney function. The magnitude of risk increases with advancing chronic kidney disease (CKD) stage and is further influenced by hypertension and proteinuria. However, evidence describing the spectrum of kidney disease and predictors of adverse pregnancy outcomes in Central Asian populations remains limited. This study aimed to characterize the clinical and laboratory features of pregnant women with kidney disease and identify factors associated with adverse pregnancy outcomes.
Methods: We conducted a retrospective single-center cohort study including 80 hospitalizations of 79 pregnant women with kidney disease between 2022 and 2026. Demographic characteristics, kidney disease categories, comorbidities, laboratory parameters, and available pregnancy outcomes were analyzed. A combined adverse outcome was defined as at least one of the following: CKD progression, dialysis initiation, preeclampsia, eclampsia, HELLP syndrome, pregnancy termination for medical indications. Bias-reduced logistic regression was used to identify factors associated with adverse outcomes.
Results: Urinary tract infections accounted for 49.4% of kidney-related diagnoses and glomerular diseases for 35.4%. Hypertension was present in 28.8% and anemia in 61.8% of cases. Women with glomerular diseases had significantly higher 24-hour proteinuria than women with other kidney disorders (1.3 [0.6–3.3] vs 0.1 [0.0–0.5] g/day; p<0.001). A combined adverse outcome occurred in 10/80 (12.5%) hospitalizations. The incidence was markedly higher in women with CKD stage ≥3 than in those with CKD stage <3 or without CKD (83.3% vs 7.2%; p<0.001). In univariable analysis, CKD stage ≥3 (OR 43.00; 95% CI 5.07–364.80), hypertension (OR 24.68; 95% CI 3.93–154.88), higher admission creatinine (OR 2.70 per 1 SD; 95% CI 1.43–5.09), and higher 24-hour proteinuria (OR 2.20 per 1 SD; 95% CI 1.17–4.16) were associated with adverse outcomes. In the multivariable model, CKD stage ≥3 (OR 20.29; 95% CI 1.58–260.05) and hypertension (OR 18.62; 95% CI 2.61–132.74) remained independently associated with adverse outcomes.
Conclusion: Advanced CKD and hypertension were the strongest predictors of adverse pregnancy outcomes. Assessment of kidney function, blood pressure, and quantitative proteinuria may facilitate early risk stratification and identify women requiring intensive multidisciplinary nephrology and obstetric surveillance.
 

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.

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.