JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
RECURRENT GLOMERULONEPHRITIS
STATIN-INDUCED RHABDOMYOLYSIS WITHOUT THE STATIN?
S. Varakantam, MD; J. Samuel, MD Department of Medicine, Baton Rouge General Medical Center, Baton Rouge
J. Dubuc; A. Traina; H. Oddo Moise; A. Coulon, MD; A. Bourgeois, MD; J. Doan, MD; S. Guillory, MD; S. Sanne, MD Department of Internal Medicine, LSU Health Sciences Center - New Orleans are inflammatory myopathies with an incidence of 1-2 per 100,000 persons annually in the US and characterized by muscle inflammation and weakness in a proximal>distal distribution Statin-induced myopathy is a well described side effect of statin therapy occurring in 2-11% of all statin users. Both of these conditions can present similarly with rhabdomyolysis. Introduction: Polymyositis and Dermatomyositis Case: A 43-year-old man with history of multiple GSWs to the abdomen and face 3 months prior awoke with diffuse body aches, constipation and weakness for 8 days. He had no functional limitations at baseline. He denied strenuous activity, dehydration or trauma. The physical exam was remarkable for 3/5 strength in the bilateral upper and lower extremities, which was more pronounced in the lower extremities and in proximal muscle groups. Initial labs revealed an elevated CK to 32,740 u/L with normal creatinine and potassium. Aggressive intravenous fluid was begun for treatment of rhabdomyolysis, but after several dayswithout improvement, a rheumatologicworkupwas initiated. MRI of the lower extremity revealed diffuse myositis in all muscle compartments with surrounding edema. Further studies included negative ANA, but positive Anti-Jo1 and Mi-2 which are highly specific for dermatomyositis. A muscle biopsy was performed and demonstrated degenerative muscle fibers without inflammation. He was diagnosed with statin-induced rhabdomyolysis and his statin therapy was discontinued. His weakness improved following initiation of methotrexate and steroids, but he stopped taking this following his GSW 3 months prior without return of symptoms. During his hospitalization, he was started on high dosemethylprednisolone andmethotrexate with rapid improvement of symptoms and CK levels. Discussion: Statin-Induced Myopathy is a commonly made diagnosis when a patient presents with rhabdomyolysis in the setting of statin therapy. It is important to consider other etiologies of diffuse myopathy especially when discontinuation of the statin does not yield expected improvement.
Introduction: RecurrentGlomerulonephritisoccurs infrequently. We present a case of recurrent proliferative glomerulonephritis occurring in a patient after a lapse of 10 years. Case: A 74-year-old Caucasian man presented to the hospital withpetechial rash, swellingof the legs,decreasedurinaryoutput, and shortness of breath. He had a recent history of pneumonia 2 weeks prior and an uneventful aortic valve replacement for aortic stenosis 4 weeks prior to presentation. He had a remote history of acute glomerulonephritis with biopsy suggestive of type 1 membranous proliferative glomerulonephritis about 10 years prior that required temporary hemodialysis. Work up at that time demonstrated hypocomplementemia and low immunoglobulins. Cryolglobulins were marginally positive but were not characterized. He was treated with azathioprine and steroids which achieved complete remission after 9 months. Physical exam on this presentation showed petechial rash on pretibial area and buttocks, 2 + pitting edema of lower extremities, a prosthetic second heart sound with no murmurs. Labs revealed acute renal failure with a BUN/Cr of 60 and 2.01 respectively (baseline creatinine a month ago was normal). UA showed RBC casts, proteinuria and hematuria suggesting acute glomerulonephritis. Work up was negative for HIV, HCV, EBV, C–ANCA, P- ANCA. SPEP, UPEP, blood cultures were all negative. C3 was low normal, C4, total complements and immunoglobulins were low. Kidney biopsy revealed diffuse proliferative glomerulonephritis with IgG, IgM and C3 staining by immunofluorescence and differential included infectious vs cryoglobulinemic glomerulonephritis. Serum cryoglobulins were positive for type 2. Pulse steroids were started, but patient did not respond. Treatment with rituximab resulted in complete resolution of renal failure and proteinuria, and at 1 year after treatment he remained stable with normal creatinine and no proteinuria. Discussion: We believe that this patient had cryoglobulinemic glomerulonephritis on both occasions, and it recurred after his recent infection despite prior treatment with steroids and azathioprine. Treatment with rituximab for his recurrent episode proved to be more effective in achieving remission quickly and without the need to hemodialysis. Our patient appears to be immunologically predisposed and will be at risk for developing cryoglobulinemia in response to immune activation.
J La State Med Soc VOL 170 MARCH/APRIL 2018 65
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