Monitoring radiofrequency renal lesions in real time using contrast-enhanced ultrasonography: a porcine model.

BACKGROUND AND PURPOSE: Ablation by cold (cryoablation) or radiofrequency energy (RFA), has been popularized for the treatment of small renal tumors. Regrettably, there currently is no reliable method of radiologically monitoring the propagation of RF lesions in real time. Ultrasonography enhanced by gas-filled microbubble contrast agents allows depiction of regions of tissue perfusion and has been described as a useful adjunct in diagnosing renal pseudotumors, improving prostate biopsy results, and confirming successful ablation of liver tumors. We hypothesized that contrast-enhanced ultrasonography (CEUS) would allow us to define, in real time, areas of cell death secondary to RFA and thus determine successful treatment. MATERIALS AND METHODS: Five female swine underwent initial laparoscopic exploration and creation of ipsilateral upper- and lower-pole renal RFA lesions. Lesion size was measured with standard gray-scale, Doppler, and microbubble CEUS. After 2 weeks, an identical procedure was performed on the contralateral kidney, including repeat sonographic measurements on the first kidney. All swine were then immediately sacrificed, and both kidneys (20 lesions) were harvested for pathologic analysis (hematoxylin-eosin and nicotinamide adenine dinucleotide stains). Radiographic lesion size was then compared with the gross and microscopic findings. RESULTS: The RFA lesions could not be imaged accurately in real time with standard gray-scale or Doppler sonography. However, microbubble CEUS was able to monitor parenchymal blood flow and, thus, the lesions (no blood flow) in real time. Hypoechoic lesions (no bubble enhancement) imaged during contrast sonography corresponded with regions of cell death as demonstrated on pathologic analysis. CONCLUSIONS: Microbubble CEUS is can monitor RFA lesions in real time. This novel imaging modality should allow more effective renal tumor ablation.

An unusual case of pulmonary-renal syndrome associated with defects in type IV collagen composition and anti-glomerular basement membrane autoantibodies.

Commercial serological assays for the presence of anti-glomerular basement membrane (GBM) antibodies are thought to be indicative of Goodpasture's syndrome. We report a case in which commercial tests inaccurately suggested that a patient with a pulmonary-renal syndrome had Goodpasture's disease. Additional laboratory testing using recombinant type IV collagen NC1 domain proteins showed that the autoantibodies in question were not directed against the Goodpasture antigen (the alpha3NC1 domain), but against the alpha2NC1 domain of type IV collagen. Our findings represent the first known case of human autoantibodies to the alpha2NC1 domain. Further investigation showed that this patient has decreased alpha3 and alpha5 chain expression in the GBM and defects in type IV collagen, resembling abnormalities in patients with Alport's syndrome.

Crescentic, proliferative IgA nephropathy: clinical and histological response to methylprednisolone and intravenous cyclophosphamide.

BACKGROUND: IgA nephropathy is an immune-complex glomerulopathy that can result in capillary or extra-capillary proliferation. Previous attempts to correlate specific histological findings including cellular crescents or endocapillary proliferation, with clinical outcomes, have produced conflicting results. METHODS: We conducted a prospective open-labelled trial of 12 patients with crescentic, proliferative IgA nephropathy and clinically progressive disease and treated them with pulse steroids and intravenous cyclophosphamide. Therapy included pulse solumedrol at 15 mg/kg/day for 3 days, followed by monthly intravenous cyclophosphamide at 0.5 g/m(2) body surface area for 6 months. Clinically significant proteinuria (>1.0 g/24 h) was present in all patients, while nephrotic-range proteinuria (>3.0 g/24 h) was observed in eight of 12 patients. All patients were hypertensive (BP >140/90 mmHg). RESULTS: After 6 months of treatment, the mean serum creatinine was reduced from a maximum of 2.65+/-0.39 to 1.51+/-0.10 mg/dl (P<0.03), while proteinuria was reduced from 4.04 to 1.35 g/24 h (P<0.01). The mean slope of 1/serum creatinine increased from -0.0398+/-0.02 to 0.0076+/-0.01 after 6 months of therapy, but this trend did not reach statistical significance (P<0.08). A repeat kidney biopsy was performed in all treated patients. Endocapillary proliferation, cellular crescents and karyorrhexis were eliminated in all 12 patients after 6 months of therapy, while interstitial fibrosis and tubule dropout remained unchanged. To determine the long-term efficacy of the treatment, treated patients were compared to 12 historical controls matched for severity of IgA on initial biopsy. After 36 months, the rate of end-stage renal disease in the treated group was lower (1/12) than in the historical controls (5/12). CONCLUSIONS: We conclude that steroids and intravenous cyclophosphamide reduce proliferative lesions, reduce proteinuria and stabilize renal function in patients with crescentic IgA nephropathy.