<p>SGLT2 inhibitors have demonstrated robust cardiorenal benefits across diverse chronic kidney disease populations but remain underutilized in autosomal dominant polycystic kidney disease (ADPKD) due to lack of disease-specific data and theoretical safety concerns. We report a 58-year-old man with genetically confirmed <i>PKD2</i>-associated ADPKD who developed progressive proteinuria (0.8&#xa0;g/24&#xa0;h increasing to 2.0&#xa0;g/24&#xa0;h over three years) despite optimal ACE inhibition. Clinical findings suggested concomitant IgA nephropathy, but biopsy was contraindicated. Empagliflozin 10&#xa0;mg/day was initiated off-label. Proteinuria decreased progressively to 0.9&#xa0;g/24&#xa0;h at one month, 0.645&#xa0;g/24&#xa0;h at three months, 0.4&#xa0;g/24&#xa0;h at six months, and stabilized between 0.3 and 0.4&#xa0;g/24&#xa0;h through 18 months (82–85% reduction sustained to date). Renal function remained stable (eGFR 33–35 mL/min/1.73&#xa0;m²). No infections or adverse events occurred. This case supports safety and antiproteinuric efficacy of empagliflozin in ADPKD with superimposed glomerular disease and provides context for broader therapeutic potential of SGLT2i in this systemic cardiorenal-metabolic disorder.</p>

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Empagliflozin in ADPKD with suspected IgA nephropathy: antiproteinuric response without adverse events

  • Sindi Uruci,
  • Elena Tanzarella,
  • Pierpaolo Bianca,
  • Michele Paolisi,
  • Kristiana Kola,
  • Liliana Italia De Rosa,
  • Martina Catania,
  • Alessandro Barruscotti,
  • Rodolfo Fernando Rivera,
  • Chiara Livia Lanzani,
  • Giuseppe Vezzoli,
  • Maria Teresa Sciarrone Alibrandi

摘要

SGLT2 inhibitors have demonstrated robust cardiorenal benefits across diverse chronic kidney disease populations but remain underutilized in autosomal dominant polycystic kidney disease (ADPKD) due to lack of disease-specific data and theoretical safety concerns. We report a 58-year-old man with genetically confirmed PKD2-associated ADPKD who developed progressive proteinuria (0.8 g/24 h increasing to 2.0 g/24 h over three years) despite optimal ACE inhibition. Clinical findings suggested concomitant IgA nephropathy, but biopsy was contraindicated. Empagliflozin 10 mg/day was initiated off-label. Proteinuria decreased progressively to 0.9 g/24 h at one month, 0.645 g/24 h at three months, 0.4 g/24 h at six months, and stabilized between 0.3 and 0.4 g/24 h through 18 months (82–85% reduction sustained to date). Renal function remained stable (eGFR 33–35 mL/min/1.73 m²). No infections or adverse events occurred. This case supports safety and antiproteinuric efficacy of empagliflozin in ADPKD with superimposed glomerular disease and provides context for broader therapeutic potential of SGLT2i in this systemic cardiorenal-metabolic disorder.