Percutaneous US-guided renal biopsy: a retrospective study comparing the 16-gauge end-cut and 14-gauge side-notch needles.

PURPOSE: Assess glomerular yield and safety profile of two different types of needles for percutaneous ultrasound-guided kidney biopsy. MATERIALS AND METHODS: Over 24 months, 121 ultrasonographic ultrasound-guided renal biopsies were performed on native kidneys of 121 adults: 66 with 16-gauge, 29-mm end-cut (BioPince) needles and 55 with 14-gauge, 1.9-mm side-notch (Tru-Cut) needles. RESULTS: The mean number of complete glomeruli harvested per biopsy was 21.0 and 19.3, respectively, and the mean number of core samples required to obtain a satisfactory biopsy was 1.8 and 2.6, respectively. The ratio of glomeruli harvested to core samples needed with the end-cut needle was 58% greater than that with the side-notch needles (11.7 vs 7.4, respectively; difference of 4.3; 95% confidence interval: 2.0, 6.8). Procedures performed with end-cut needles were associated with fewer major complications (1.5% vs 7.3% with side-notch needles). CONCLUSIONS: Compared to the 14-g Tru-cut needle, the 16-g end-cut needle provided better glomerular yield per core sample, required fewer cores for satisfactory tissue specimen, and resulted in fewer major complications.

Primary hyperoxaluria: clinical course, diagnosis, and treatment after kidney failure.

Primary hyperoxaluria type 1 (PH1) is a rare autosomal recessive metabolic disorder resulting in the overproduction of plasma oxalate. Although the enzymatic defect is in hepatocyte peroxisomes, uncontrolled levels of oxalate result in calcium oxalate deposition in multiple organs. Because the primary route of elimination of oxalate is renal excretion, high levels are found in urine, which results in supersaturation and crystal nucleation. Patients typically present with recurrent nephrolithiasis and nephrocalcinosis. If not diagnosed early, end-stage renal disease (ESRD) and systemic calcium oxalate deposition can occur. Once ESRD develops, intensive dialysis therapy is unable to keep pace with the high oxalate production, and the preferred therapeutic intervention is combined kidney-liver transplantation. Here, we report a young man with a history of recurrent nephrolithiasis who presented to us with ESRD and subsequently developed manifestations of systemic oxalosis. The diagnosis of PH1 must be considered in the differential diagnosis of patients presenting with ESRD with a history of recurrent nephrolithiasis. The diagnosis of PH1 is more challenging in patients with ESRD, for whom urinary oxalate levels are often normal or only modestly increased because of decreased glomerular filtration, and recurrent nephrolithiasis is no longer the dominant clinical feature.

The EphB2 tumor suppressor induces autophagic cell death via concomitant activation of the ERK1/2 and PI3K pathways.

EphB2 is a tyrosine kinase receptor that has been shown to be a tumor suppressor gene in various cancers. However the mechanisms of this function are unknown. We report that EphB2 induces a form of cell death that does not involve the formation of apoptotic bodies or nuclear fragmentation and is instead accompanied by extensive vacuolization. Transmission electron microscopy demonstrates cytoplasmic vacuoles in EphB2-overexpressing cells that resembled autophagosomes. Using an EYFP-LC3 fusion protein and immunoblotting, we detected LC3 aggregation and conversion from form I to form II, both hallmarks of autophagy, in EphB2-transfected cells. Silencing of the autophagy regulating genes ATG5 or ATG7 using shRNAs, strongly prevented EphB2-induced cell death, further confirming its autophagic nature. EphB2 expression results in mitochondrial depolarization and translocation of cytochrome c from the mitochondria to the cytosol. Mapping of signaling pathways revealed novel information about the mechanisms of action of EphB2. We demonstrated that the MAPK pathway is important in the pro-death action of EphB2, through ERK1/2 phosphorylation and inhibition of this pathway using PD98059 counters EphB2-driven cell death. In addition, we found that inhibition of class III PI3K pathway, using the autophagy inhibitor 3MA, but not class I PI3K inhibition using LY294002, also effectively blocks EphB2- induced cell death. Finally, EphB2 expression inactivates Akt, which is a known inhibitor of autophagy. In conclusion, the EphB2 receptor induces an autophagic cell death that is mediated through the ERK1/2 and PI3K/Akt pathways.

Granulocytic sarcoma presenting as tumors of the cervix.

BACKGROUND: Granulocytic sarcoma of the cervix, leading to the diagnosis of acute myelogenous leukemia (AML), is a rare event. CASE: A 33-year-old woman presented with vaginal bleeding, pain, and a large pelvic mass involving the cervix, extending bilaterally to the pelvic side walls. A biopsy of the cervix revealed granulocytic sarcoma, and a subsequent bone marrow biopsy confirmed the diagnosis of AML. RESULTS: The majority of patients with cervical granulocytic sarcoma present with vaginal bleeding, sometimes with abdominal pain and other systemic symptoms. The overall 2-year survival rates for all patients with granulocytic sarcoma in the literature is 6%, and none of the patients lived 5 years. CONCLUSION: Granulocytic sarcoma of the cervix is rare. Awareness of this entity will allow earlier diagnosis and appropriate treatment.