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Abstract: SA-PO129

Through the Haze: Sailing the Turbid Waters of Uremic Ophthalmopathy

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Pacheco-Molina, Caleb Samuel, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Vega-Colon, Jesus Daniel, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Rivera, Maria Eugenia, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Rivera Rios, Jeaneishka Marie, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Ocasio Melendez, Ileana E., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Andujar-Rivera, Krystahl Z., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Rivera-Bermudez, Carlos G., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
  • Pérez Westerband, Lydwan, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico
Introduction

Ophthalmic disease can be a consequence of many metabolic conditions, rarely is caused by uremia. This is an uncommon etiology of ophthalmic disease and there are only a few cases reported.

Case Description

A 45-year-old man with arterial hypertension, horseshoe kidney and a previous episode of acute kidney injury (AKI) presented complaining of a three-month history of bilateral blurry vision, eye pain and fatigue. Denied changes in urinary habits, recent infections, travel, toxic habits, NSAIDs use, or family history of kidney disease. Evaluation was remarkable for elevated blood pressure, 168/85 mmHg, and bilateral lower extremity edema. Ophthalmologic evaluation was notable for bilateral optic nerve inflammation. Laboratory results were remarkable for anemia, azotemia with BUN of 182.9 mg/dL, creatinine level of 29.5 mg/dL, severe hyperkalemia, and metabolic acidosis with HCO3 level of 7.5 mEq/L. Urinalysis with findings of proteinuria, and hematuria with positive RBCs and WBCs without casts. Urine protein-creatinine ratio of 3.5 g/g. Workup for glomerular disease, vasculitides, HIV, HBV and HCV yielded negative results. Renal US showed small kidneys with increased cortical echogenicity compatible with intrinsic parenchymal disease, without hydronephrosis or nephrolithiasis. CT scan confirmed the presence of horseshoe kidney. Patient was started on hemodialysis with immediate improvement in visual symptoms. Follow up ocular evaluation was notable for improved optic nerve inflammation bilaterally. Head CT scan was negative for intracranial pathologies, as well as orbital CT scan. Patient was discharged home on hemodialysis and ophthalmologic symptoms continued improving.

Discussion

Uremic ophthalmopathy is a rare finding worth sharing. In the case of our patient that a clear etiology of renal injury was not found, it is more likely that the subject had progressive renal function decline for which he was not receiving appropriate care, and this finding might be secondary to chronic uremia. For this reason, it is fair to consider uremia as the cause of ophthalmopathy in patient in which other metabolic causes are not a clear culprit.