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The tumors in 249 patients presenting initially with stages Ta and T1 bladder cancer were analyzed for tumor progression and recurrence. Only transurethral resection and/or fulguration was used before the first recurrence. Patients who received intravesical chemotherapy after the first tumor recurrence were excluded from an analysis of progression. Progression according to stages Ta and T1, and grades I, II and III was 4, 30, 2, 11 and 45 per cent, respectively. All differences were statistically significant. Progression also correlated with nontumor dysplasia and size. High tumor grade, lamina propria invasion, atypia elsewhere in the bladder, positive urinary cytology, tumor multiplicity and large tumors were associated with shorter intervals free of disease.

CONGENITAL, unilateral multicystic disease of the kidney is characterized by the replacement of one entire kidney by irregularly lobulated cystic masses of sizes varying from 1 to 30 mm which are held together by loose connective tissue (Figure). The cortical architecture, pyramids, and calyces are completely absent, and on the cut section no normal parenchyma except a very occasional scattering of solid tissue is seen. The ureter is characteristically absent or atretic, and the blood supply is variable, in some instances, being altogether absent. The cyst wall, on microscopic examination, is usually lined by a thin layer of flat cuboidal cells, and the occasional scattering of solid tissue often may contain a few immature glomeruli or tubules.The recognition of this deformity as an entity separate from other renal cystic disorders has come about slowly since its first description by Schwartz1 in 1936. Bunge and Harness2 described one

TWO English ophthalmologists, Laurence and Moon in 1886, directed attention to the fact that retinitis pigmentosa sometimes appears in combination with other defects, such as mental retardation, hypogenitalism, and obesity. In 1922, Biedl reported the additional observation of familial occurrence and polydactyly in association with the above findings. Thus, this complex became known as the Laurence-Moon-Biedl syndrome.1 By definition, it is characterized by familial occurrence, 48%; mental retardation, 80%; obesity, 83%; genital dystrophy, 60%; retinitis pigmentosa, 68%; and polydactyly or syndactyly, 75%.2-4 Numerous other anomalies such as skull defects, renal disease, and heart disease are often included but are not considered essential to the diagnosis.5-7 The syndrome is seen in all races and occurs in children with healthy parents, although consanguinity of parents has been reported.8,9Two theories of the genetic aspect of this syndrome have been proposed. One theory is that a single gene produces