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PHYSICAL REVIEW LETTERS 10JULY1978 tion 14 of P(cr, t) reduce after a single RG step either to the form assumed in this work or to terms of second order in the intercell interaction. Of course, if the RG is performed to higher orders in the cumulant expansion, more terms must be used in

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Urinothorax should be considered when pleural effusion occurs in patients with urinary tract obstruction accompanied by retroperitoneal urinoma. This recommendation is based on our experience with 4 cases and a review of the literature. In 2 patients urinary obstruction was owing to retroperitoneal fibrosis secondary to malignancy, including one who had a neuroectodermal undifferentiated small round cell tumor and the other who had a metastatic epithelial neoplasm. In the 2 other patients urinary obstruction resulted from a failed ureteroneocystotomy following renal allograft transplantation. All 4 patients had a urinoma, which may be a predisposing factor to urinothorax.

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The cationic fluorescent probe, DiSC,(5) was used to measure the membrane potential in human platelets. Hyperpolarization was induced by the addition of Ca2+ to the medium and also by the addition of the Ca2+ ionophore, A23187. In the absence of extracellular Ca2+ ([Ca'+],) there was no response to A23187. The threshold concentration for [Ca2+]., was 20 fiM and for A23187 was 12 nM. The increase polarity induced by [Ca2+lO was not affected by various K' channel blockers. However, the effect of A23187 was inhibited by quinine and charybdotoxin, while apamin, tetraethylammonium, and the calmodulin inhibitors trifluoperarine and compound I324571 were ineffective. The resting membrane potential was -66 f 0.9 mV and was decreased by quinine. There are three conclusions from this study: (i) Ca2+-activated K+ channels exist in human platelets: (ii) they are the type that are apamin insensitive, charybdotoxin sensitive; and (iii) they may contribute to the resting membrane potential. [P.S.E.B.M. 1989[P.S.E.B.M. , VoI 1921 nimal cell plasma membranes possess K+ channels, which, when opened, induce cytoplasmic

Succinct aspects of clinical features, pathophysiology and prognosis of nephrotic syndrome in childhood, and indications for performing renal biopsy are enumerated in this review. Orthodox treatment of the nephrotic syndrome with more recent therapeutic approaches, and the role of diuretics, albumin infusions and immunizations in patients with the nephrotic syndrome are reviewed. The etiology of peritonitis, acute renal failure, and renal transplantation are re-examined to update nephrologists on the associated complications of this common childhood disease.

We present a 9-year-old boy, the product of a consanguineous marriage, with proteinuria, edema, and microscopic hematuria with mild renal impairment since age 2 yr. Renal biopsy showed the histopathologic electron microscopic changes seen in hereditary osteo-onchyodysplasia (HOOD) [Hoyer et al, 1972; Bennet et al, 1973; DelPozo and Lapp 1970; Vernier et al, 1974; Morita et al, 1973] or "nail-patella syndrome." Neither the patient nor his relatives had bone or nail abnormalities; however, 2 other sibs had died of complications of end-stage renal disease at age 6 and 9, leading us to suspect autosomal recessive inheritance of a severe nephropathy or glomerulodysplasia.