Acute kidney injury due to anabolic steroid and vitamin supplement abuse: report of two cases and a literature review.

BACKGROUND: The use of anabolic steroids and vitamin supplements has reached alarming proportions in the last decades. Adverse effects have been documented and include virilization, feminization, adverse lipid profile, psychiatric disorders, cardiac and liver disease. Acute kidney injury (AKI) is not frequently described. The purpose of this study is to report two cases of AKI associated with anabolic steroid and vitamin supplement abuse. CASE REPORT: Two men, aged 21 and 30 years, presented to the Emergency Department with abdominal pain, nausea and vomiting. They reported the use of anabolic steroids and veterinary supplements with vitamins A, D and E. Laboratory tests showed AKI (serum urea 79 and 52 mg/dl, serum creatinine 3.9 and 1.9 mg/dl) and hypercalcemia (calcium 13.2 and 11 mEq/l). Kidney biopsies showed inflammatory interstitial nephritis and acute tubular necrosis. Treatment consisted of vigorous hydration with simultaneous use of furosemide and discontinuation of the vitamins and anabolic substances, and resulted in recovery of renal function. CONCLUSIONS: AKI is an important complication of anabolic steroid and vitamin supplement abuse. The exact pathophysiology of this type of AKI remains unclear. The main cause of renal dysfunction in these cases seems to be the vitamin D intoxication and drug-induced interstitial nephritis. It is mandatory to start early treatment for serious hypercalcemia, with vigorous venous hydration, diuretics and corticosteroids.

Behcet's disease and IgA nephropathy: report of this association in a patient from Brazil and literature review.

Behcet's disease (BD) is associated with renal involvement in about one-third of the cases and a variety of renal lesions have been reported. A 27-year-old man presented a history of recurrent oral and genital ulcers, associated with pseudofoliculitis and arthritis in his left knee. The first laboratory tests revealed: urea = 53mg/dL, creatinine = 1.8 mg/dL. The urinalysis showed leukocyturia. Initial treatment with ceftriaxone, thalidomide and prednisone was instituted. He became clinically stable, with normal renal function, but presenting hematuria and proteinuria. One year later the patient presented dark urine. The new laboratory tests showed urea=58 mg/dL, creatinine = 1.4 mg/dL, and mild proteinuria (500-1000 mg/24h). Two years later the proteinuria was 2230 mg/day. The renal biopsy showed one glomerulus with severe glomerular sclerosis, mild tubular atrophy, mild interstitial fibrosis and thickening of arterial walls. Treatment with captopril was started to decrease proteinuria. Two years later, the patient presented creatinine = 1.7 mg/dL and proteinuria = 2509 mg/day. A new renal biopsy evidenced proliferative crescentic glomerulonephritis, with diffuse granullary deposits of IgA, IgM and C3. It was instituted pulsotherapy with metilprednisolone, monthly endovenous cyclophosphamide and maintenance prednisone. The patient became clinically stable, with creatinine of 1.3 mg/dL and proteinuria of 500 mg/day. BD could be one of the various causes of secondary IgA nephritis. It is important to periodically perform renal function evaluation in patients with BD, through urinalysis and measurement of serum creatinine and its clearance, in order to detect any abnormality and provide an early adequate treatment.