Prevention of contrast-induced acute kidney injury in patients with stable chronic renal disease undergoing elective percutaneous coronary and peripheral interventions: randomized comparison of two preventive strategies.

OBJECTIVE: We compared use of intravenous (IV) normal saline (NS) to sodium bicarbonate (NaHCO(3)) with or without oral N-acetylcysteine (NAC) for prevention of contrast-induced acute kidney injury (CI-AKI). BACKGROUND: CI-AKI is associated with significant adverse clinical events. Use of NAC has produced variable results. Recently, intravenous hydration with NaHCO(3) for CI-AKI prophylaxis has been adopted as standard treatment for patients with stable chronic renal disease undergoing catheterization procedures. METHODS: We prospectively enrolled 320 patients with baseline renal insufficiency scheduled to undergo catheterization. Patients were randomly assigned to receive either IV NS ± NAC (n = 161) or IV dextrose 5% in water containing 154 mEq/l of NaHCO(3) ± NAC (n = 159). IV NS was administered at 1 ml/kg body weight for 12 hr preprocedure and 12 more hr postprocedure. IV NaHCO(3) was administered at 3 ml/kg body weight for 1 hr preprocedure followed by 1 ml/kg body weight postprocedure. A 1,200 mg oral dose of NAC was given 2-12 hr preprocedure and 6-12 hr postprocedure in 50% of patients in each study arm. CI-AKI was defined as an increase of >0.5 mg/dl or >25% above baseline creatinine. RESULTS: Overall incidence of CI-AKI was 10.3%. There was no significant difference in incidence among the two groups (NS ± NAC 11.8% vs. NaHCO(3) ± NAC 8.8%, p = ns). Incidence of CI-AKI increased with increasing age (p = 0.001), contrast agent use >3 ml/kg body weight (p = 0.038) and diuretic use (p = 0.005). CONCLUSION: Incidence of CI-AKI was no different in the NaHCO(3) group compared to NS group, and NAC did not reduce CI-AKI in the two study arms.

Podocyte injury associated glomerulopathies induced by pamidronate.

BACKGROUND: Pamidronate has been demonstrated to decrease bone-related complications in multiple myeloma and delay progression of the disease. This has led to its use in supportive and maintenance therapy of myeloma in conjunction with steroids and chemotherapy. It has also been selectively used in patients with breast cancer and other neoplasms. METHODS: We report on five patients who developed glomerular disease induced by pamidronate. Pamidronate was the only drug common to all patients. Tests for hepatitis B and C and human immunodeficiency virus (HIV) were negative for all patients. The first two patients received a high dose of pamidronate for 8 weeks, whereas the other three patients were on monthly therapy for a prolonged period of time. Sources of data included chart review and pathologic analysis of kidney biopsy. RESULTS: Three patients were female and two were males and all were Caucasian, ranging in age from 58 to 71 years. Renal biopsy findings included minimal change disease in two, focal segmental glomerulosclerosis in two, and collapsing focal segmental glomerulosclerosis in one. Immunofluorescence was essentially negative in all cases. Electron microscopy showed variable podocyte injury and extensive foot process effacement. There was no evidence of multiple myeloma-related renal disease. After the biopsy, pamidronate was discontinued and renal function stabilized in all patients except the one with the collapsing variant of focal segmental glomerulosclerosis who required hemodialysis. Three patients had resolution of proteinuria, one patient continued to have proteinuria without deterioration in renal function. CONCLUSION: Pamidronate has been mainly associated with collapsing focal segmental glomerulosclerosis. This report expands that relationship and adds other glomerular diseases linked with podocyte injury. Additional studies are needed to define the cause of the variability of renal histology with this agent.