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En bloc pediatric kidneys have been used in adult renal transplantation for over 30 years. Despite the duration of this experience, issues such as increased technical difficulties and associated complications, hyperfiltration injury, and ultimately a limited allograft half-life have limited the use of these organs at many centers. To date, however, the collected experience suggests that these organs may in fact be an excellent source of allografts for adult transplantation. The present paper was a retrospective review of the experience using en bloc kidneys for adult transplantation from two institutions. These results support the use of these kidneys. Actual patient and graft survival at 2 years was 97% and 94% respectively.

Background: Early diagnosis and treatment of acute rejection is important to prevent continued renal injury. Acute rejection most commonly presents with asymptomatic rise in serum creatinine. Proteinuria associated with acute rejection is well established; however, there is limited documentation of the presentation of acute rejection as nephrotic syndrome in the literature., Methods and Results: We report a renal transplant patient who presented with early onset nephrotic syndrome without change in serum creatinine, whose allograft biopsy confirmed acute glomerulitis and vascular rejection. Treatment of the acute rejection was accompanied by resolution of the nephrotic syndrome. A second episode of acute rejection was also manifested as nephrotic range proteinuria., Conclusion: The nephrotic syndrome in early post-transplantation period should prompt a work-up for acute rejection even in the absence of the common findings of this complication.

Reports that examined the issue of whether transplantation of inadequate nephron mass may be a risk factor for long-term allograft failure yielded conflicting results. One of the more accurate methods of estimating glomerular mass is kidney weight. Most of the clinical studies used body surface area (BSA) or kidney length as estimates of kidney weight. To test the hypothesis that indirect measures of kidney weight are accurate estimates of kidney weight, we compared the kidney weight of 41 consecutive cadaveric kidneys to donor BSA, dimensions measured with calipers at the time of transplantation, and dimensions supplied by the Organ Procurement Agency (OPA). Linear regression analysis was used with kidney weight as the dependent variable and BSA, kidney length, or kidney volume as the independent variable. Kidney length measured with calipers was also compared to kidney length supplied by the OPA. Kidney weight had the best correlation with kidney volume and kidney length determined by caliper measurements (r = 0.640 and 0.646, respectively). The regression analysis showed that the correlation of kidney weight with BSA was 0.487. The correlation of OPA-provided kidney length with kidney weights was poor (r = 0.410). The linear regression of caliper-measured kidney length versus OPA length yielded a slope of 0.360, instead of an ideal slope of 1. The assumption has been made that kidney weight or a surrogate of kidney weight has an excellent correlation with nephron mass. Some of the variability in studies that attempted to examine the effect of transplanted nephron mass on allograft outcome may be due to inaccurate estimates used for kidney weight. Our data suggest that surrogate measurements of kidney weight may not be accurate. We recommend that measured kidney weight should be used in studies examining the effect of donor renal mass on allograft outcomes.

Prostaglandins of the E series have been shown to have immunosuppressive properties. To study the effects of the prostaglandin E1 analogue misoprostol on renal function and graft rejection after transplantation, we conducted a randomized, double-blind, placebo-controlled trial in 77 renal-allograft recipients. The subjects received misoprostol (200 micrograms four times daily by mouth; n = 38) or placebo (n = 39) for the first 12 weeks after transplantation, in addition to standard immunosuppression with cyclosporine and prednisone. They were then observed for an additional four weeks after the drug or placebo was discontinued. Treatment with misoprostol was associated with a significant improvement in renal function as judged by the mean (+/- SEM) serum creatinine concentration (128 +/- 7 vs. 158 +/- 11 mumol per liter after 12 weeks; P = 0.03) and creatinine clearance (84 +/- 6 vs. 69 +/- 5 ml per minute per 1.73 m2 of body-surface area; P = 0.05). There was a significant reduction in the incidence of acute rejection in the group treated with misoprostol as compared with the placebo group (10 of 38 vs. 20 of 39; P = 0.02), and there was less need for rehospitalization after transplantation (4 +/- 1 days with misoprostol vs. 10 +/- 2 days for placebo; P = 0.03). Although blood levels of cyclosporine did not differ significantly between the groups, they tended to be higher in the misoprostol group, as did the incidence of acute nephrotoxicity due to cyclosporine (13 of 38 vs. 8 of 39). Infectious complications tended to be fewer in the misoprostol-treated group (14 of 38 vs. 21 of 39). We conclude that misoprostol improves renal function and safely reduces the incidence of acute rejection in renal-transplant recipients treated concurrently with cyclosporine and prednisone.

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).