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Metabolic-associated chronic kidney disease (mCKD) represents a novel construct that recognizes CKD developing within a background of metabolic dysfunctions- diabetes, hypertension, obesity, dyslipidaemia, and metabolic dysfunction-associated steatotic liver disease (MASLD). The concept integrates metabolic and renal injury as a unified entity. This study aimed to apply and validate proposed diagnostic criteria for mCKD.
As a multi-centre cross-sectional study, thirty-two consecutive adults with evidence of CKD and at least two metabolic abnormalities were prospectively evaluated between January and May 2025. The diagnosis of mCKD required fulfilment of four diagnostic pillars: evidence of CKD, presence of ≥2 metabolic abnormalities, exclusion of primary renal disease, and at least one supportive feature (Table 1). All participants underwent comprehensive metabolic and renal evaluation including anthropometry, blood pressure, HbA1c, lipid profile, liver ultrasound, serum uric acid, bicarbonate, and urine albumin-creatinine ratio (UACR). Renal ultrasonography was used to rule out congenital or obstructive pathology. Data were analysed descriptively.
Table 1. Proposed Diagnostic Criteria for mCKD
Criterion
Details
Clinical Relevance
Evidence of CKD
• eGFR < 60 ml/min/1.73 m² for ≥3 months and/or • Albuminuria > 30 mg/gm creatinine
Confirms chronic kidney damage independent of cause
Presence of ≥2 metabolic abnormalities
• Type 2 diabetes mellitus (T2DM) • Hypertension (>140/90 mmHg or on antihypertensives) • Obesity (BMI >30 kg/m² or >25 kg/m² in Asians) or Overweight (BMI >23 kg/m²) • Dyslipidaemia (TG >150 mg/dL, HDL <40 mg/dL) • MASLD (ultrasound evidence)
Defines metabolic milieu contributing to kidney dysfunction
Exclusion of primary glomerular disease
Absence of: anasarca, nephrotic-range proteinuria (>3 g/day), haematuria, rapid eGFR decline, autoimmune/vasculitic serology, or biopsy-proven glomerulopathy
Ensures kidney injury not primarily glomerular
Exclusion of primary tubulointerstitial disease
Absence of: congenital anomalies, shrunken/single kidneys, polycystic kidneys, or obstruction on imaging
Excludes structural or obstructive renal disease
Supportive features (≥1)
Hyperuricemia, metabolic acidosis, cardiovascular disease, stroke, or obstructive sleep apnoea
Strengthens diagnosis and indicates systemic metabolic involvement
The baseline demographic and metabolic profile of mCKD patients have been depicted in Table 2. The mean age was 54 ± 10.8 years; 19 (59%) were male. All patients satisfied the mCKD diagnostic triad. Hypertension (84%) and T2DM (78%) were most common, followed by dyslipidaemia (72%), obesity/overweight (63%), and MASLD (41%). Mean BMI was 28.6 ± 3.9 kg/m² and waist circumference 96 ± 8 cm. Renal indices confirmed moderate CKD with significant metabolic overlap. Mean serum creatinine was 1.8 ± 0.6 mg/dL, mean eGFR 52 ± 12 ml/min/1.73 m², and albuminuria >30 mg/gm in 22 (69%) patients. Supportive features included hyperuricemia (47%), metabolic acidosis (34%), and cardiovascular disease (28%). Renal and metabolic laboratory characteristics have been depicted in Table 3.
Table 2. Baseline Demographic and Metabolic Profile of mCKD Patients (n = 32)
Parameter
Mean ± SD / n (%)
Interpretation
Age (years)
54 ± 10.8
Middle-aged cohort typical for metabolic CKD
Male: Female
19:13
Male predominance
BMI (kg/m²)
28.6 ± 3.9
Overweight/obese range
Waist Circumference (cm)
96 ± 8
High central adiposity
Hypertension
27 (84%)
Most prevalent abnormality
Type 2 Diabetes Mellitus
25 (78%)
Major metabolic contributor
Dyslipidaemia
23 (72%)
Coexistent lipid disorder
Obesity/Overweight
20 (63%)
Common in Asians
MASLD
13 (41%)
Liver-metabolic linkage
Cardiovascular Disease
9 (28%)
Reflects systemic vascular risk
Obstructive Sleep Apnoea
4 (13%)
Associated metabolic comorbidity
Table 3. Renal and Metabolic Laboratory Characteristics in mCKD (n = 32)
Clinical Implication
Serum Creatinine (mg/dL)
1.8 ± 0.6
Mild to moderate renal dysfunction
eGFR (ml/min/1.73 m²)
52 ± 12
Stage 3 CKD predominant
Albuminuria (>30 mg/gm)
22 (69%)
Marker of renal endothelial injury
HbA1c (%)
7.9 ± 1.2
Suboptimal glycaemic control
Serum Triglycerides (mg/dL)
182 ± 48
Elevated in majority
HDL (mg/dL)
39 ± 8
Consistently low, reflecting dyslipidaemia
Serum Uric Acid (mg/dL)
7.8 ± 1.3
Reflects metabolic overload
Serum Bicarbonate (mEq/L)
21 ± 3
Tendency to metabolic acidosis
Hyperuricemia
15 (47%)
Common supportive marker
Metabolic Acidosis
11 (34%)
Confirms metabolic derangement
This pilot validation confirms the feasibility, reproducibility, and clinical relevance of the proposed diagnostic framework for mCKD. The clustering of multiple metabolic derangements with chronic kidney impairment reinforces the concept of mCKD as a distinct metabolic-renal phenotype. Early identification through these criteria allows clinicians to target metabolic pathways for kidney protection. Larger multicentric studies are needed for external validation, prognostic correlation, and therapeutic stratification.
