PROTEIN-MALNUTRITION AND DECREASED PROTEIN-TURNOVER IN CHRONIC RENAL-ALLOGRAFT FAILURE

Object: To define the longitudinal relationship of declining renal fun ction to protein consumption and turnover in the failing renal allogra ft model of chronic renal failure. Method: The study group is our firs t eight consecutive cadaveric renal graft recipients who after attaini ng a normal creatinine clearance, then developed chronic renal failure . We analysed their urea and creatinine clearances (Cur, Ccr), serum u rea (SU), urinary urea and creatinine (Ur, Ucr), serum albumin (SA), u rinary protein (Upr), body weight (EW), and steroid dose. Steady state Uur is also dietary protein intake (DPI) and protein catabolic rate ( PCR). Ucr measures body protein mass. Ucr/Uur measures the ratio of bo dy protein mass to urea excretion. Mean follow-up 4.7 years, range 1.5 -8.7 years. Results: Mean changes: (1) Body weight (BW) rose from 56 t o 65 and then fell to 61 kgms. (2) Cur fell 65 to 5 and Ccr from 92 to 12 ml/min/70 kg. (3) Uur fell from 369 to 107 and Ucr from 16.8 to 9. 5 mmols/day/70 kg. (4) Uur/Ucr indexed at 1:1 fell to 0.49. (5) SU ros e from 8.8 to 34.9 mmol/l; SA fell from 36.1 to 31.0 gms/l; Upr rose f rom 1.4 to 2.3 gms/day. (6) Prednisone rose from 26 to 66 and then fel l to 33 mgms/day. Correlations: (1) Cur and Uur (r = 0.99, p < 0.001). (2) Ccr and Uur (r = 0.99, p < 0.001). (3) Cur and Uur/Ucr (r = 0.88, p < 0.01) with a decelerating breakpoint at Cur 18 and Ccr 32 ml/min/ 70 kg (p < 0.01). (4) SU and Uur negatively (r = 0.90, p < 0.01. (5) C ur and SA albumin (r = 0.82, p < 0.05). (6) Cur and prednisone, Upr an d SA do not correlate. Conclusions: In this model of chronic renal fai lure: (1) Renal function controls protein intake. (2) Body protein mas s is relatively well preserved despite the decreased protein intake im plying a decrease in the protein turnover rate and a consequent increa se in body protein average age. (3) Protein malnutrition, protein agei ng, and decreased protein turnover are likely pathophysiological react ions to chronic renal failure and may be part of the pathogenesis of c hronic uremia.