Renal AA-amyloidosis in intravenous drug users – a role for HIV-infection?
1 Department of Nephrology, Goethe University, Frankfurt/Main, Germany
2 Department of Nephrology, Agaplesion Markus Krankenhaus, Frankfurt/Main, Germany
3 Institute of Pathology, Nephropathology, Friedrich-Alexander-University, Erlangen, Germany
4 Department of Infectious Disease, Goethe University, Frankfurt/Main, Germany
5 Klinikum der Goethe-Universität, Zentrum der Inneren Medizin II, Infektionsambulanz, Haus 68, 1 OG, Theodor Stern Kai 7, 60590, Frankfurt/Main, Germany
BMC Nephrology 2012, 13:151 doi:10.1186/1471-2369-13-151Published: 21 November 2012
Chronic renal disease is a serious complication of long-term intravenous drug use (IVDU). Recent reports have postulated a changing pattern of underlying nephropathy over the last decades.
Retrospective investigation including all patients with prior or present IVDU that underwent renal biopsy because of chronic kidney disease between 01.04.2002 and 31.03.2012 in the city of Frankfurt/Main, Germany.
Twenty four patients with IVDU underwent renal biopsy because of progressive chronic kidney disease or proteinuria. Renal AA-amyloidosis was the predominant cause of renal failure in 50% of patients. Membranoproliferative glomerulonephritis (GN) was the second most common cause found in 21%. Patients with AA-amyloidosis were more likely to be HIV infected (67 vs.17%; p=0.036) and tended to have a higher rate of repeated systemic infections (92 vs. 50%; p=0.069). Patients with AA-amyloidosis presented with progressive renal disease and nephrotic-range proteinuria but most patients had no peripheral edema or systemic hypertension. Development of proteinuria preceded the decline of GFR for approximately 1–2 years.
AA-amyloidosis was the predominant cause of progressive renal disease in the last 10 years in patients with IVDU. The highest rate of AA-amyloidosis observed was seen in HIV infected patients with IVDU. We speculate that chronic HIV-infection as well as the associated immunosuppression might promote development of AA-amyloidosis by increasing frequency and duration of infections acquired by IVDU.