A unique evolution of the kidney phenotype in a patient with autosomal recessive Alport syndrome.

Alport syndrome is due to mutations in one of the genes encoding (α3,4,5) type IV collagen resulting in defective type IV collagen, a key component of the glomerular basement membrane (GBM). The GBM is initially thin and, with ongoing remodeling, develops a thickened basket-woven appearance. We report a unique case of a 9-year-old boy who underwent biopsy for hematuria and proteinuria, diagnosed as IgA nephropathy, with normal GBM appearance and thickness.

Nitric oxide does not mediate promotion of cellular potassium release by phenolphthalein in COS-7 cells.

1. It has been proposed that phenolphthalein exerts its laxative effect via an intracellular cascade that begins with the activation of nitric oxide synthase (NOS) and ends with an inhibition of NaCl and water reabsorption from the colon. Phenolphthalein also promotes the release of potassium from cells, but it is not known how this is related to its effect on sodium and water uptake.

Development of IgA nephritis following cat scratch disease in a 13-year-old boy.

We describe a 13-year-old boy who presented with hematuria and intermittent low-grade proteinuria at the time when he was diagnosed with cat scratch disease. Two months before presentation, he had a negative urinalysis during a routine physical evaluation. He continued to have microscopic hematuria for the next 6 months, when he developed gross hematuria and recurrence of low-grade proteinuria.

Regulation of 86Rb+ ion transport across polarized human colonocytes by bis-phenolic compounds.

1. Phenolphthalein, a well-known laxative, stimulates the secretion of Na+ and Cl- ions and accompanying water into the intestinal tract. Measurement of 86Rb+ efflux from several, but not all, cell types indicates that phenolphthalein also results in release of cellular K+ ions.