Estimations of proximal tubule sodium reabsorption with the FELi method come closer to direct measurements than any other indirect method. There is little doubt that most lithium reabsorption takes place in the proximal tubules, very likely in proportion to the reabsorption of sodium and water. It is also likely that changes in proximal tubule sodium reabsorption due to changes in volume status are paralleled by changes in proximal tubule lithium reabsorption, at least in the superficial nephrons. Nonetheless, changes in FELi probably do not purely reflect changes in proximal reabsorption, since lithium is also handled beyond the proximal tubules. Acknowledged problems are lithium reabsorption in Henle's loop and in the late distal and collecting tubules. The latter occurs in the rat and the dog, but not or much less in men. Sodium restriction enhances this lithium transport considerably. It is as yet uncertain whether other conditions, such as increased vasopressin activity or lowering of renal perfusion pressure, also influence this transport. Amiloride appears to prevent this reabsorption of lithium. Therefore, this drug can be used in lithium clearance studies whenever unwanted "distal" lithium reabsorption is expected. Lithium reabsorption in Henle's loop forms a greater problem as it cannot be prevented by any drug without influencing proximal tubule reabsorption. It is estimated that about 7% of the filtered lithium (one-tenth of total lithium reabsorption) is normally taken up here, preferentially in deep nephrons. In view of studies with furosemide, this reabsorption probably varies with sodium intake, but the proportion of this variation to that of proximal tubule lithium reabsorption is obscure. This remains an uncertain factor in any circumstance where the lithium clearance method is used. In some conditions the change in FELi may be so large relative to the expected changes in proximal reabsorption, that use of FELi as marker of end-proximal solute delivery seems unjustified. Disproportionately large suppression is likely during mineralo-corticoid-induced volume expansion, and stimulation during prostaglandin synthesis inhibition and vasopressin. Based on observations in these conditions the potential range of lithium reabsorption in the loop of Henle would be 0 to 15% of filtered load. In this review attention was paid mainly to the validity of lithium clearance as a pure "proximal marker". Many of our interpretations suffer from incomplete certainty with respect to the renal effects of tested maneuvers, a problem which is acknowledged.(ABSTRACT TRUNCATED AT 400 WORDS)

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Encapsulating peritoneal sclerosis (EPS) is a rare but serious complication in patients on peritoneal dialysis (PD). We describe a cluster of 13 EPS cases occurring in 2 university hospitals in The Netherlands. Most of these cases were diagnosed after recent kidney transplantation, when the patients developed severe symptoms of bowel obstruction. This accumulation raised the question as to whether other than known risk factors, such as duration of PD treatment, could be involved in the development or course of EPS after transplantation. According to various publications, EPS has been diagnosed often after withdrawal from PD, suggesting that cessation in itself may be a risk factor. In addition, transplantation-related management should be considered to play a role, including the use of the profibrotic calcineurin inhibitors and the trend to reduce the load of corticosteroids in treatment regimes. To identify risk factors, further multicenter studies are required, paying special attention to alterations in immunosuppressive treatment regimens as well as PD prescriptions, including PD fluid characteristics. Transfer from PD to hemodialysis should be under serious consideration in patients eligible for kidney transplantation as soon as there are indications of ultrafiltration failure.

Background. Endothelial dysfunction contributes to accelerated atherosclerosis in chronic kidney disease (CKD). Bone marrow-derived endothelial progenitor cells (EPC) constitute an endogenous vascular repair system protecting against atherosclerosis. Smooth muscle progenitor cells (SPC) may stimulate atherosclerosis development. We hypothesized that an imbalance in EPC and SPC occurs in CKD, which may contribute to the increased cardiovascular disease (CVD) risk. Methods. EPC and SPC outgrowth from mononuclear cells (MNC), EPC migratory function and circulating CD34+ KDR + -EPC were measured in 49 patients with varying degrees of CKD on regular therapy and 33 healthy volunteers. Renal function, CKD cause, CVD history and endothelial dysfunction parameters were determined as factors of influence on progenitor cells. Results. Patients had reduced EPC outgrowth compared to controls [9 (2-22) vs 12 (1-38) cells/10 3 MNC, P = 0.026], independent of CKD cause and degree, whereas SPC outgrowth levels were higher in patients with more impaired kidney function (r = −0.397, P = 0.008). Patients had lower CD34 + KDR + -EPC compared to controls [9 (0-52) vs 19 (4-110) cells/10 5 granulocytes, P = 0.004]. CVD history and increased endothelial dysfunction markers were related to lower EPC levels. Progenitor cell outgrowth was shifted towards SPC with progression of endothelial damage. Reduction in EPC could not be attributed to decreases in progenitor cell-mobilizing factors SDF-1α and VEGF as levels increased with progressive kidney and endothelial dysfunction, while EPC remained low. Conclusions. Our data suggest that, already in mild CKD, EPC-mediated endogenous vascular regeneration is impaired, while SPC levels increase with declining kidney function.