Amir H. Qureshi1, Daniel J. Soberon1, Arif Asif2, Tushar Vachharajani3, Ali Nayer*
1 Division of Nephrology, University of Miami, Miami, FL, USA
2 Division of Nephrology, Albany Medical College, Albany, NY, USA
3 Division of Nephrology, W.G. (Bill) Hefner Veterans Affairs Medical Center, Salisbury, NC, USA
Methemoglobinemia refers to the presence of increased levels of methemoglobin (Fe3+) in the
blood. Methemoglobinemia can cause cyanosis, dyspnea, fatigue, seizure, arrhythmia, coma, and even death. Although
methemoglobinemia is shown to cause acute kidney injury in experimental settings, human case reports are exceedingly
rare. In addition, morphological features of methemoglobinemia-induced renal disease in humans remain undefined.
A 76-year-old man with a history of chronic obstructive pulmonary disease underwent bronchoscopy
following local anesthesia with a benzocaine spray. The patient developed benzocaine-induced methemoglobinemia and
acute renal failure. Urinalysis disclosed numerous dysmorphic erythrocytes, erythrocyte casts, and granular casts. Urine
protein excretion was approximately 1.1 g/day. Serologic tests were negative. Renal biopsy demonstrated minor
glomerular abnormalities, severe acute tubular necrosis, and numerous erythrocyte casts in the tubules. Despite supportive
care, renal function deteriorated necessitating hemodialysis. Four months later, the patient remained on hemodialysis. To
exclude a superimposed pathology, renal biopsy was repeated and showed numerous erythrocyte casts in the tubules and
severe tubular damage.
Methemoglobinemia can cause acute kidney injury in humans. Morphological features resemble those
observed in methemoglobin-induced acute kidney injury in experimental settings. This case calls for a heightened
awareness of potential adverse effects of methemoglobinemia on renal function.
* Address correspondence to this author at the Division of Nephrology and Hypertension, University of Miami, Clinical Research Building, Suite 825, 1120 NW 14th St., Miami, FL 33136, USA; Tel: 305.243.8491; Fax: 305.243.3506;