The patient is a 28-year-old Hispanic female with a past medical history of\nhypertension, high serum cholesterol, and gastritis who presented to the emergency\nroom for the evaluation of abdominal pain of 2 days duration. Six months prior, she\nhad similar pain. An upper gastrointestinal (GI) endoscopy at that time showed\npeptic ulcer disease and no other mucosal lesions. The patient had a strong family\nhistory of renal disease and 2 of her siblings required a renal transplant, but she\ndid not know what kidney pathology they had. Her medications included Lisinopril\noral 10 mg tablet daily and Pantoprazole oral 40 mg daily. On presentation at the\nemergency room (ER), her height and weight were 157 cm and 61 kg, respectively, and\nher blood pressure was 206/121 mm Hg. On physical examination, the patient had\nepigastric tenderness. The rest of her physical examination was unremarkable.\nRadiology was ordered to exclude any anatomical abnormality. A computed tomography\nscan showed neither atrophy nor enlargement of the kidneys. She then followed up as\nan outpatient with a nephrologist shortly after her ER visit. Her laboratory work up\nduring that visit revealed the following: nephrotic range proteinuria (9.2 g protein\non 24-hour urine collection; reference range, 0-2.5 g/d), hypoalbuminemia (300\nµmol/L; reference range, 421-662 µmol/L), hypoproteinemia (50 g/L; reference range,\n60-80 g/L), elevated serum creatinine (148.5 µmol/L; reference range, 44-80 μmol/L),\nhigh chloride (110 mmol/L; reference range, 98-106 mmol/L), and low hemoglobin (100\ng/L; reference range, 120-160 g/L). The lipid profile showed an increased total\ncholesterol level (8.3 mmol/L; reference range, <5.2 mmol/L), elevated\ntriglycerides (3.7 mmol/L; reference range, <1.70 mmol/L), elevated low-density\nlipoprotein fraction (5.9 mmol/L; reference range, <2.6 mmol/L), and decreased\nhigh-density lipoprotein fraction (1.1 mmol/L; reference range, ≥1.55 mmol/L). After\ntreating her blood pressure, the patient underwent a US-guided renal biopsy.
A 66-year-old male was referred to our center by his primary care physician because of the increase of proteinuria. He was diagnosed with diabetes at the age of 50 years but remained untreated. At the age of 60 years, he started voglibose at the diabetes center of our hospital. At the age of 66 years, urinary abnormality of protein 3+ and occult blood 1+ was pointed out, combined with simple diabetic retinopathy and a serum creatinine level of 0.96 mg/dl. He was referred to our center for further investigation, and a renal biopsy was performed. One of 11 glomeruli showed global sclerosis, and the other glomeruli showed massive foam cell infiltration in the glomerular capillaries and mildly expanded mesangium (fig. ). These foam cells immunohistochemically stained positive for cluster differentiation 68 (CD68) (not shown). Transmission electron microscope images also revealed foam cell infiltration mainly located in the capillaries containing scattered lipid droplets and lamellar bodies in their cytoplasm (fig. ). The glomerular basement membrane (GBM) showed mild thickening, and nodular lesions were formed in some glomeruli. The interstitium and tubules showed mild fibrosis and atrophy (25% of the cortical region), and a moderate degree of arteriolar hyalinosis was also found. No interstitial foamy cells or foamy tubular degeneration was found. Immunofluorescence study revealed no significant glomerular deposits. The patient's lipid profile showed type III HLP (table ). Apolipoprotein phenotype analysis showed a homozygosity of apoE2. A further DNA sequence analysis was performed as described previously [] and showed a nucleotide substitution of cysteine for arginine at codon 158 (Arg158Cys) of the apoE gene and no other mutations. Eicosapentaenoic acid was added to his statin therapy, but he progressed to end-stage renal failure and was started on dialysis 8 years after the diagnosis.