Lipoprotein pattern in end-stage renal disease (ESRD) and following successful renal transplantation

51 + 17 yrs (range 25-79 yrs) who have received nocturnal cyclic TPN for IO + 4 yrs (range 1.5-15 yrs). All subjects received 100 mg Vit C, 4 mg pyridoxine as part of their TPN regimen. Fifteen subjects had ileostomies (Group A) and 4 of these had a history of nephrolithiasis. Urine was collected for 24 hrs using a ‘pee-splitter’ to equally divide urine into an HCL and boric acid-washed containers for oxalate and citrate determinations. Approximately 4 hrs after completion of the urine collection and TPN infusion, true GFR was determined by Indium-111 DTPA plasma clearance. Serum and urine PO, were obtained at this time for tubular reabsorption of phosphate (TRP) determinations, 5/15, (33%) Group A, and 7/10, (70%) Group B had hyperoxaluria (> 140 mg/d) 5/l 0, (50%) Group A, and 2/l 5 (13%) Group B had hypocitraturia (1140 mg/d). All data are presented as mean + SD. lleostomy (A) No lleostomy (B) Avs B Total

GFR TRP (cc/mm/l -73 m2) (96) 67.2k32.5 68 Ok32.5 68.2+34 1 80.4+16 NS NS 649i34.5 72 9127.0

Oxalate @g/d) 40.2k30.2 63.2k53.3 NS 49.9+41 6

not account for the renal insufficiency TPN patients.

described in long-term

0.10 Lipoprotein pattern in end-stage disease (ESRD) and following successful transplantation

renal renal

S. Falger, K. Derfler, K. Swoboda, 0. Traindl, J. Kovarik, W. Drum1 and K. Widhalm’ Med. Clinic lit. Dept. of Nephrology; ‘Dept. of Pediatrics; Univ. of Vienna, Austria Hyperlipidemia is a common complication in patients maintained on dialysis treatment and may persist after successful renal transplantation (RT). This prospective study was designed to investigate changes in lipoprotein metabolism after RT in comparison to the chronic uremic state. For immunosuppression all RTRs (N = 67; 31 male; 36 female; age 50 _+ 12 yrs) received twice daily CsA orally. The dosage was adjusted to maintain CsA blood trough levels (RIA; monoclonal) of 90-130 ng/ml. In addition alternate-day corticosteroids were given in all RTRs.

Citrate (w/d) 324.4k239.0 4748+9363 NS 389.8+629.0

GFR was significantly correlated with TRP (r = 0.64, p = 0.0006). Urine oxalate and citrate had a significant negative relationship (r = -0.61, p = 0.002). However, there was no significant association between GFR or TRP, and urine oxalate, or citrate overall, in either groups A or B, or in those subjects who had abnormal urine oxalate and/or citrate excretion. In addition, there was no significant correlation between IV glycine intake and GFR, TRP or urinary oxalate. We conclude that urinary oxalate excretion may be increased not only in long-term TPN patients without ileostomies as expected, but also in patients with ileostomies. The mechanism for this finding is unexplained. We speculate that limited small bowel absorption in addition to overproduction of oxalate, even in the absence of excessive substrate, may account for the hyperoxaluria. However, hyperoxaluria does

After RT (E) Cholesterol” HDL-Chol’ LDL-Chol Chol/HDL Tnglycsrides APO-A-l APO-B” creat1n1ne

Before 209+60 38k14 141+54 6.1 +2.5 205kllO 127k25 96123 -

:52+64’ 50fl7’ 162+53 5.1 fl.8# 221 +129 149+27# 109+38# 1.4+0.5

‘mgidt &months; ‘p < 0.007; #p values obtained 3 months after RT.

!5, * 53’ 48k17’ 172+48# 5.8k2.5 212+112 146-)_25# 117+_26* 1.5f0.5 <

0.05

[versus

::9+53* 47Il7# 173?48’ 6 1 +3.0 233+152 149+31# 123128’ 1.6kl.O

::6&64’ 49k13’ 179k63’ 5.5k1.8 214+133 162*27# 130+35* 1.8kl.OS

before RT]; Sversus the

Prevalence of hyperlipoproteinemia increased from 32% at ESRD to 59% after RT. Predominantly an increase in LDLCHOL and APO-B has been observed. Thus, the increased risk for advanced atherosclerosis due to alterations in lipoprotein metabolism is present in both conditions, in ESRD and even more pronounced after RT.

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