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The average free choline level was determined to be 14 mumol/L in peritoneal dialysates and 22 mumol/L in the plasma of 30 patients on continuous ambulatory peritoneal dialysis (CAPD). Daily choline loss via dialysate averaged 129 mumol with 32 mumol choline lost per dwell. Daily choline loss via the dialysate was positively correlated with plasma choline concentrations. Choline levels in dialysate during CAPD exceed plasma levels of choline 9 mumol/L in healthy individuals.

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The average free choline level was determined to be 14 M in peritoneal dialysates and 22 M in plasma of thirty patients on continuous ambulatory peritoneal dialysis (CAPD). Daily choline loss via dialysate averaged 129 moles with 32 moles choline lost per dwell. Daily choline loss via the dialysate was positively correlated with plasma choline concentrations. Choline levels in dialysate during CAPD exceed plasma levels of choline (9 M) in healthy individuals.

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Renal cystic epithelia and peritoneal mesothelia from two humans with autosomal recessive polycystic kidney disease (ARPKD) were grown in culture. Cystic epithelial and mesothelial cells formed continuous monolayers in vitro. By electron microscopy, cystic renal cells exhibited a single apical cilium and numerous short, stubby microvilli, both in situ and in vitro. Mesothelial cells exhibited intra- and extracellular membrane-limited, lipid-filled vesicles and surface microvilli. Cystic kidney cells in vitro stained positive for lectins from Cancanavalia ensiformis (concanavalin A), Triticum vulgaris, Erythrina cristagalli, Ulex europeaus, and Arachis hypogaea. Immunocytochemical and lectin staining revealed the renal and peritoneal cells to be of collecting tubule and mesothelial origin, respectively. Both cell types showed large depositions of glycogen granules in the cytoplasm during propagation in certain culture media; in kidney cells, dibutyryl cyclic adenosine monophosphate (cAMP) abolished glycogen depositions. Glycogen deposition also was observed in liver tissue obtained by needle biopsy from one patient. No bacteria were cultured from nor endotoxin detected in the renal cyst fluid. Relative to serum, the cyst fluids contained low sodium, potassium, and chloride levels. Thus, cultured ARPKD cells demonstrate a number of characteristics that are different from cells derived from the autosomal dominant form of renal cystic disease (ADPKD).

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We describe five patients receiving long-term hemodialysis (mean duration of 6.4 years) in whom eight renal carcinomas were found. In four patients, the carcinoma was confirmed by tissue pathology, while the fifth patient had multiple (four) areas of neovascularity on selective renal arteriography. Two patients died of metastases. In four patients the diagnosis was initially made with selective renal arteriography and in the remaining one, with sonography and computerized tomography. In three of the four arteriography showed diffuse cystic degeneration; pathologic findings revealed renal carcinoma and the changes of "end-stage" disease. Two patients had brief pharmacologic immunosuppression during unsuccessful renal transplantation six years earlier. These cases demonstrate an apparently increased risk of renal carcinomas in end-stage renal disease, a risk that appears to be independent of pharmacologic immunosuppression.

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Behcet's syndrome is a multisystem disease complex, the major manifestions of which are oral and genital ulcers, arthritis, uveitis, and skin eruptions. Less frequently, CNS disturbances, colitis, thrombophlebitis, large-vessel vaculitis, and myocarditis occur. If renal involvement does occur, it is usually manifested by asymptomatic microhematuria and/or proteinuria. Recently, renal amyloidosis and focal necrotizing glomerulonephritis with immune complex deposition have been described. We describe a patient with Behcet's syndrome who experienced diffuse proliferative glomerulonephritis with epithelial cell crescent formation in 75% of glomeruli examined. Immune complexes were not identified. Renal function, impaired on admission, improved with no therapy.

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We have described a case of reversible acute renal failure caused by acute pyelonephritis. In this entity, the kidneys are swollen by an interstitial infiltrate and edema, and white cell tubular casts and microabscesses may be present. Fractional excretion of sodium is high, and nephrotic proteinuria may occur without glomerular abnormalities. Recovery of renal function may occur if antibiotics are promptly instituted. Renal size generally decreases after recovery.

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