Neoplasia of the kidney--a rare event during pregnancy.

Sarcomas of the kidney during pregnancy are very rare and should be treated by an interdisciplinary team with respect to the actual trimester. Decisions regarding treatment have to be made with the patient and her family.

Cisplatin nephrotoxicity is critically mediated via the human organic cation transporter 2.

Cis-platin is an effective anti-neoplastic agent, but it is also highly nephrotoxic. Here, we clearly identify the human organic cation transporter 2 (hOCT2) as the critical transporter for cis-platin nephrotoxicity in isolated human proximal tubules and offer a potential mechanism for reducing nephrotoxicity in clinical practice. Interaction of cis-platin with hOCT2 in kidney or hOCT1 in liver was investigated with the fluorescent cation 4-[4-(dimethyl-amino)styril]-methylpyridinium in stably transfected HEK293 cells and for the first time in tissues physiologically expressing these transporters, human proximal tubules, and human hepatocyte couplets. Cis-platin (100 micromol/L) inhibited transport via hOCT2-HEK293 but not hOCT1-HEK293. In human proximal tubules cis-platin competed with basolateral organic cation transport, whereas it had no effect in tubules from a diabetic kidney or in hepatocytes. In hOCT2-HEK293 cells treated for 15 hours, incubation with cis-platin induced apoptosis, which was completely suppressed by contemporaneous incubation with the hOCT2 substrate cimetidine (100 micromol/L). These findings demonstrate that uptake of cis-platin is mediated by hOCT2 in renal proximal tubules, explaining its organ-specific toxicity. A combination of cis-platin with other substrates that compete for hOCT2 offers an effective option to decrease nephrotoxicity in the clinical setting.

Vasoactivity of diadenosine polyphosphates in human small renal resistance arteries.

BACKGROUND: We examined for the first time the vascular effects of purinergic agents that contribute to the regulation of peripheral vascular resistance in human small renal resistance arteries (hRRAs). METHODS AND RESULTS: Diadenosine polyphosphates (ApnAs, n = 3-6) and ATP, mounted in a microvessel myograph, caused vasoconstriction in hRRAs (rank order of potency: Ap5A > Ap6A = Ap4A > Ap3A = ATP). ADP, AMP and adenosine had less contractile potency than ApnA, suggesting that the observed effects were not induced by ApnA degradation products. The ApnA agent, Ap5A, but not Ap4A, induced vasoconstrictions that were inhibited by pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS; a P2X purinoceptor antagonist), but not by ADP3'5' (a P2Y purinoceptor antagonist). In pre-contracted hRRAs, all of the ApnA agents caused vasorelaxation, and the potencies did not differ from each other. The ApnA degradation products had less vasorelaxing potencies than ApnA, suggesting that the vasorelaxation was caused by the ApnA agents themselves. Ap4A-induced vasorelaxation was inhibited by ADP3'5' and PPADS. In contrast, Ap5A-induced vasorelaxation was not antagonized by ADP3'5', but was antagonized more strongly by PPADS than was Ap4A. CONCLUSIONS: We found that the tone of resistance arteries in human kidneys can be considerably influenced by these purinergic agonists, and most potently by ApnAs. Ap5A-induced vasoconstriction appeared to be mediated by P2X purinoceptors, whereas constriction due to Ap4A was caused by a different purinoceptor. Vasorelaxation due to Ap4A, but not Ap5A, appeared to be mediated by P2Y purinoceptors.

Accurate control of the superficial and deep dorsal veins during radical retropubic prostatectomy: the Münster clamp technique.

OBJECTIVE: To better control the superficial and deep dorsal veins during radical retropubic prostatectomy and, thus, to reduce blood loss. PATIENTS AND METHODS: A surgical technique is described which introduces a modified Babcock clamp to fully encompass all tissue above the prostatic capsule. In a prospective protocol, 30 consecutive patients (median age 64.5, range 57-76 years) were randomly assigned to either the standard technique or the Münster clamp method. Blood loss was estimated for the entire phase from teasing away the periprostatic fat until the apex had been mobilized. RESULTS: Median hemorrhage was 950 (range 300-2,100) ml for the standard technique and 800 (range 200-1,750) ml for the clamp procedure (Wilcoxon rank sum test, p = 0.17). CONCLUSIONS: The Münster clamp technique can reduce hemorrhage during radical retropubic prostatectomy. This method is easy to apply and is also suitable for cystoprostatectomy.