Kidney Week

Abstract: PUB121

A Horseshoe Full of Stones: Proteus mirabilis Bilateral Urolithiasis and Postobstructive AKI in a Fused Kidney

Session Information

• Publication Only

Category: Genetic Diseases of the Kidneys

• 1202 Genetic Diseases of the Kidneys: Non-Cystic (Complex and Non-Cystic Monogenic)

Authors

• Inacio, Maithe Caroline, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, N.L., Mexico

Maithe Caroline Inacio, MD

• Cardenas, Hector Alejandro, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, N.L., Mexico

Hector Alejandro Cardenas, MD

• Haddad Rodriguez, Jorge Efren, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, N.L., Mexico

Jorge Efren Haddad Rodriguez

• Rizo Topete, Lilia Maria, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, N.L., Mexico

Lilia Maria Rizo Topete, MD

Introduction

Horseshoe kidney (HSK), the most common renal fusion anomaly (1:400), predisposes to urolithiasis and obstructive uropathy through urinary stasis. Proteus mirabilis, a urease-producing pathogen, alkalinizes urine and drives struvite stone formation, creating a cycle of infection and obstruction. We report post-obstructive acute kidney injury (AKI) in a young woman with HSK and bilateral Proteus-associated nephrolithiasis.

Case Description

A 23-year-old woman with known HSK and prior left renal lithotripsy presented with 5-day vomiting, fever (40°C), and syncope from severe dehydration. CT confirmed HSK with bilateral calculi and obstructive uropathy. Labs showed AKI (creatinine 2.9 mg/dL), leukocytosis (WBC 16,000/µL, 89% neutrophils), severe hypophosphatemia (0.6 mg/dL), high anion gap (18.8), and metabolic acidosis by day 2 (pH 7.26). Urinalysis showed pyuria, hematuria, positive nitrites, and urinary pH 8.5. Urine culture identified P. mirabilis >100,000 CFU/mL, resistant to fluoroquinolones and TMP-SMX. Urgent double-J stenting was performed with IV ceftriaxone and tamsulosin. PCNL was performed: complete stone clearance was achieved endoscopically in the left kidney, while residual right-sided lithiasis remained due to operative time constraints and is being managed with outpatient follow-up. Creatinine normalized to 0.7 mg/dL at follow-up.

Discussion

HSK anatomy promotes stasis and stone retention. P. mirabilis urease hydrolyzes urea to ammonia, raising urinary pH and precipitating struvite, compounding obstruction. Multidrug resistance (including to fluoroquinolones and aminoglycosides) underscores the need for culture-directed therapy in this population. HSK with P. mirabilis infection creates a high-risk triad of anatomical stasis, infectious lithogenesis, and obstruction. Early anatomical recognition, culture-guided antibiotics, and prompt decompression are critical to prevent irreversible AKI.