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Clinical Case Study |
1 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Divisions of 2 General Internal Medicine and 3 Infectious Diseases, University Health Network, University of Toronto, Toronto, Ontario, Canada; 4 Division of Clinical Biochemistry, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; 5 Division of Clinical Biochemistry, The Hospital for Sick Children, Toronto, Ontario, Canada.
aAddress correspondence to this author at: The Hospital for Sick Children, 555 University Ave., Rm. 3653–Atrium, Toronto, Ontario, M5G 1X8 Canada. Fax (416) 813-6257; e-mail khosrow.adeli@sickkids.ca.
| The first 300 words of the full text of this article appear below. |
CASE
A 57-year-old man was referred for assessment and management of malaise and leg edema, which had increased 2 weeks after the onset of a productive cough, for which clarithromycin had been prescribed. His course was complicated by the development of a pruritic skin eruption. The patients medical history included type II diabetes mellitus of 5 years duration and stage III chronic kidney disease. He also had a chronic infection with hepatitis C virus (HCV)1 (genotype 1A) and had been lost to follow-up for the previous 19 years. Medications included antihypertensive drugs (calcium channel blocker, β-blocker, angiotensin-converting enzyme inhibitor, and furosemide), a lipid-lowering drug (ezetimibe), analgesics (hydromorphone HCl and acetaminophen), and ipratropium bromide aerosol. A physical examination revealed the following: blood pressure, 140/65 mmHg; pulse, 55 beats/min; temperature, 36.9 °C; oxygen saturation, 94% on room air; body mass index, 46 kg/m2. Abdominal distention was noted and felt to be compatible with the presence of ascites. The spleen was palpable. There was bilateral lower-extremity pitting edema and a hyperpigmented pretibial rash that was not palpable.
Initial laboratory investigations included typical findings for electrolytes, aspartate aminotransferase, alanine aminotransferase, total bilirubin, and the international normalized ratio. The patients laboratory test results are summarized in Table 1
. His fasting plasma glucose concentration was impaired, and his alkaline phosphatase was slightly raised. The patient was anemic and thrombocytopenic with hypoalbuminemia and an increased serum creatinine concentration. A urinalysis dipstick screen and a microscopy evaluation revealed hematuria, proteinuria, and the presence of red blood cell casts in the urine. A 24-h evaluation of urine protein excretion confirmed an abundance of protein in the urine. The glomerular filtration rate, as estimated with the Cockcroft–Gault equation, was very low. An ultrasound analysis revealed bilateral echogenic kidneys of typical size. In the setting of a chronic, untreated HCV
DISCUSSION
patient follow-up
patient diagnosis
adult nephrotic syndrome
hcv and cryoglobulinemia
differential diagnosis for adult glomerular disease
collection, analysis, and reporting of cryoglobulins and pitfalls
diagnosis and management of chronic hepatitis
POINTS TO REMEMBER
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