Physiological Hemodynamic Controls
Live Direct Manipulation
0%
92 mmHg
210 mg/dL
Nephron Microcirculation & Tubuloglomerular Feedback
Afferolar Resistance
1050dynes
Intraglomerular Pressure
58.0mmHg
Single-Nephron eGFR
138mL/min
Macula Densa NaCl
Low(Signal)
Renal Functional MRI Oxygenation (R2*)
BOLD Tissue Mapping
Medullary Hypoxia / Hyperfiltration State
High SGLT2 workload consumes oxygen, elevating medullary R2* relaxation rates.
Medullary R2*:
24.2 s⁻¹
Cortical Perfusion:
112%
RNA-seq & Proteomic Biomarker Panel
| Marker | Target/Pathology | Simulated Conc. | Expression |
|---|---|---|---|
| HAVCR1 / KIM-1 | Tubular Injury / Stretch | 380 pg/mL | Elevated |
| TGFB1 | Pro-Fibrotic Signaling | 28.4 pg/mL | Elevated |
| COL1A1 | Extracellular Matrix Synthesis | 18.2 ng/mL | Elevated |
| EDN1 | Vascular Endothelin-1 Stress | 8.5 pg/mL | Elevated |
Simulation State: SGLT2 inhibition at 0% allows hyperfiltration (P_gc: 58.0 mmHg, eGFR: 138 mL/min). Medullary R2* is elevated at 24.2 s⁻¹ due to metabolic solute overload.