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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Adjunct hypertonic saline (HTS) can improve loop-diuretic response in heart failure. However, evidence outside heart failure is limited. We describe a diuretic-resistant congestive nephropathy without heart failure that improved with low-volume HTS.
A 61-year-old female with thymic carcinoma and myasthenia gravis was hospitalized for infection and developed respiratory failure complicated by carbon dioxide narcosis and shock. She required emergency endotracheal intubation, large-volume fluid resuscitation, and vasopressors. She subsequently developed stage 3 acute kidney injury (AKI) attributed to congestive nephropathy without heart failure. Physical examination showed marked generalized edema. Abdominal ultrasound indicated severe systemic venous congestion. Computed tomography demonstrated enlarged kidneys and distended inferior vena cava (Figure). Peak laboratory values were as follows: serum urea nitrogen 70.9 mg/dL, creatinine 4.22 mg/dL, sodium 152 mmol/L, potassium 3.2 mmol/L, chloride 108 mmol/L, uric acid 10.9 mg/dL (pre-AKI 2.0 mg/dL), and phosphate 1.25 mmol/L (pre-AKI 0.64 mmol/L). A continuous furosemide infusion, even with additional diuretics, did not achieve adequate urine output. Elevations in uric acid and phosphate implied reduced glomerular filtration rate (GFR) with enhanced proximal tubular sodium reabsorption, thereby reducing delivery of sodium chloride to the distal tubule. Norepinephrine was titrated to increase mean arterial pressure (~65→~80 mmHg) to support GFR, but diuresis remained minimal. Low-volume HTS (2.4% sodium chloride 120 mL every 8 hours) was added as adjunctive therapy. Following the introduction of low-volume HTS, urine output increased immediately, leading to the regression of clinical congestion and the normalization of creatinine levels to baseline within two weeks.
Congestive nephropathy—an AKI phenotype driven by venous congestion—can engender loop-diuretic resistance through reduced GFR (via elevated Bowman’s space pressure) and increased proximal tubular sodium reabsorption, which reduce delivery of sodium chloride to the distal tubule. The abrupt elevations in uric acid and phosphate in this case were compatible with the proposed mechanisms. HTS likely attenuated maladaptive tubuloglomerular feedback at the macula densa, thereby increasing delivery of sodium chloride to the distal tubule.
In congestive nephropathy without heart failure, adjunct low-volume HTS may restore diuretic responsiveness and promote decongestion with renal recovery. Prospective work is warranted to establish indications, dosing strategies, and safety profile.
