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Acute kidney injury (AKI) due to the precipitation and deposition of intratubular crystals is common and occurs in various clinical contexts, glycols and alcohols poisoning within know causes, predominantely secondary to accidentaly ingestion. Here, we would like to highlight a rarely suspected cause of calcium oxalate crystal nephropathy: polyethylene glycol as an excipient.
Case Presentation: A 72-year-old woman with hepatitis C-related liver cirrhosis and venous insufficiency treated with diosmin-hesperidin started a two weeks ago, presented to the emergency department brough by her family due to decreased alertness, oliguria, nausea, and vomiting. At inicial examination, she was found to be stuporous, with a blood pressure of 169/91, and anasarca. First blood tests showed metabolic acidosis of high anion gap, acude kidney injury with seric creatinine of 5.1 mg/dL (baseline 0.6 md/dL), blood urea nitrogen (BUN 117), albumin 2.5 g/dL, sodium (Na) 128 mmol/L and potassium (K) 7.38 mmoL/L. Urgent hemodialysis and intubation were required. Central nervous system injury was ruled out with a CT scan, and other etiologies were excluded, including immunological and infecious. Clinical improvement was observed after two sessions of hemodialysis, so percutaneous renal biopsy was performed which revealed nephropathy due to calcium oxalate crystals. (Figure 1). The patient did not have medical history of diarrhea and she and the family denied any glycol or alcohol ingestion, either accidentaly or voluntary. We performed a detailed investigation and we found that polyethylene glycol is used as excipient in diosmin-hesperidin, so we concluded that this fact in asocciation with the inability to metabolize such alcohol due to hepatitis C-related liver cirrhosis were the ethiology of the oxalate nephropathy. The drug was immediately suspended, substitutive kidney therapy whith hemodialysss was required for 5 months, since she later recovered kidney function with adequate diuresis and seric creatinine in 1.5 mg/dl without other abnormalities in her blood tests.
The presence of excipients in commonly used medications -such as diosmin-hesperidin- for venous insufficiency is not always innocuous. Polyethylene glycol ingestion (mostly associated with intoxication or poisoning) can cause hyperoxalemia and acute kidney injury due to intratubular deposition of oxalate crystals. Affected patients often have predisposing risk factors, such as depletion of effective intravascular volume or hepatic metabolism impairment (as in cirrhosis), especially with some degree of renal disease. When suspicion arises, potential aggressors should be discontinued, and supportive management provided until the damage resolves and no longer require it.
Calcium oxalate crystal nephropathy can be a severe cause of AKI. Renal biopsy allows for identification, and upon suspicion of the causal agent, it should be discontinued, and renal support measures, including hemodialysis, should be initiated.
Figure 1. Nephropathy due to calcium oxalate crystals. Histological data of acute kidney injury characterized by tubular dilation, desquamation, regenerative changes, and simplification of the epithelium (A, B), associated with mild tubular atrophy and interstitial fibrosis (G, Masson's trichrome staining). The crystals are polyhedral, transparent, brown, and colorful, some with a fan-like shape in the tubular lumen (C, E); they refract under polarized light (D, F).