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Kidney Weight in Living and Postmortal Kidney Donation

2015; Wolters Kluwer; Volume: 100; Issue: 1 Linguagem: Inglês

10.1097/tp.0000000000000964

1534-6080

Sofie C. M. Tops, Jack F.M. Wetzels, Ine M. M. Dooper, Johan F. Langenhuijsen, Frank d’Ancona, J. Adam van der Vliet, Heleen M. Dekker, Aswin L. Hoffmann, Heinrich J. Kloke,

Renal and Vascular Pathologies

A reduction in nephron number results in compensatory glomerular hyperfiltration. This initiates a vicious circle of glomerular hypertrophy and sclerosis, continued nephron loss and worsening hyperfiltration, clinically characterized by proteinuria and progressive renal function loss.1,2 Glomerular hyperfiltration may be particularly important in kidney transplantation. Indeed, it has been suggested that posttransplant graft function and long-term outcome can be improved by matching nephron supply and recipient needs.1,2 In humans, nephron number cannot be measured noninvasively. It is suggested that donor kidney weight provides a suitable estimate of the number of nephrons.3-5 Several studies have reported on a positive association between donor kidney weight and glomerular filtration rate after transplantation.3-5 We regularly measured weights of living and postmortal donor kidneys between 1997 and 2001. Kidneys of living donors were weighed after donor nephrectomy, perfusion with cold preservation solution, and preparation by the surgeon. Postmortal donor kidney weight was determined after cold storage, immediately before implantation into the recipient. The average living donor kidney weight (n = 85) amounted to 167 g (Table 1). However, mean kidney weights of postmortal donors were clearly higher: +32 g (+19%) and +71 g (+43%) for donor kidneys after brain death (DKBD) (n = 95) and donor kidneys after cardiac death (DKCD) (n = 35), respectively. The higher weight of postmortal donor kidneys could not be explained by a higher donor body length, donor body weight, or donor body mass index (Table 1). There was a moderate correlation between donor kidney weight and donor body mass index in postmortal kidney donation (r = 0.465 [DKBD] and r = 0.391 [DKCD]).TABLE 1: Donor characteristicsCold ischemia time and type of preservation fluid are given in Table 1. There was only a weak correlation between cold ischemia time and kidney weight in DKBD and DKCD (r = 0.26). Unfortunately, the type of preservation solution differed between the 3 donor populations. However, the differences in kidney weight remained when limiting the analysis to donor kidneys perfused with the same (HTK) preservation solution (Table S2, SDC, https://links.lww.com/TP/B207). We also evaluated the possible role of perfusate pressure. Kidneys of brain death donors were perfused with higher perfusate pressures (300 mm Hg) than kidneys of cardiac death donors or kidneys of living donors (both 110 mmHg). These differences are not associated with the observed differences in kidney weight. We hypothesize that in postmortal kidney transplants prolonged ischemia will cause tubular necrosis and edema formation resulting in increased kidney weights. In this case, a relatively high kidney weight does not reflect a high number of functional nephrons but rather represents more severe kidney damage. Our findings indicate that measurement of kidney weight in postmortal kidney transplantation is unreliable, thus invalidating reliable conclusions. We observed no association between donor kidney weight and renal allograft function at 2 years after transplantation.