Table 1 Potential etiology of lipofuscin deposits in the kidney

 Aging [6,7,8]

Strongest correlate of lipofuscin levels and deposition

 Hermansky-Pudlak syndrome [9,10,11]

Diffuse tubulopathy from deposition of cytoplasmic irregular waxy brown-yellow ceroid-lipofuscin-like pigment accumulations. This is thought to be pathogenic and leads to chronic kidney disease

 Diabetes Mellitus [3, 8, 12]

Patients have more lipofuscin deposits that are larger in size

 Hypertension [3, 12]

Lipofuscin deposits may increase in number

 Uremia [13]

High oxidative stress is presumed to be the cause

 Beta-Thalassemia Major [14]

This feature may be related to vitamin E deficiency secondary to fat malabsorption or hyper-consumption of Vitamin E

 Vitamin E deficiency [15]

Large amount of lipid peroxides that was produced in the kidney for the period of vitamin E deficiency reacted with amino acids or protein-amino acids to produce lipofuscin by glutathione depletion.

 Neurodegenerative disorders [5]

Studies have focused on increased lipofuscin deposits in neuronal cells only

 Amiodarone [2, 16, 17]

Cutaneous deposition occurs after 20 months of amiodarone use (dose: ≥160 mg/day) and is considered reversible

 Aluminum Exposure [18, 19]

Chronic exposure to aluminum sulfate (33 mg/day) in rats led to lipofuscin depositions. In hemodialysis patient, increased membrane lipid peroxidation of red blood cells has been described

 Analgesics [20, 21]

Seen with large doses of Acetophenetidin, Phenacetin and Acetaminophen

 Estrogen [22]

Only described in rats

 Rejection

Current case