BACKGROUND: Serum free carnitine is decreased and serum acylcarnitines are increased in maintenance hemodialysis (MHD) patients, and the causes for these abnormalities are not known. This study examined the role of renal failure in the occurrence of low serum carnitine and increased acylcarnitines in patients with advanced chronic kidney disease (CKD) by assessing the relationship between these compounds and renal function in normal individuals and patients with CKD. If these compounds decrease as glomerular filtration rate (GFR) decreases, this suggests that decreased intake or impaired synthesis in kidneys explain the low serum values. If serum compounds increase as GFR decreases, this suggests that impaired excretion may predispose to these values. METHODS: The study, conducted in Lyon, France (part A), and Los Angeles, California (part B), compared serum free carnitine and acylcarnitines to renal function in 20 normal patients, 65 CKD patients, and 29 MHD patients. GFR was measured using inulin (A) and iothalamate (B) clearances. Carnitine compounds were measured by tandem mass spectrometry (A) and electron spray mass spectrometry (B). RESULTS: There was no relationship between serum total carnitine or free carnitine and GFR in the normal subjects and CKD patients. In contrast, serum acylcarnitines were inversely correlated with GFR in these 2 groups. Serum free carnitine was significantly lower in MHD patients than in CKD patients and normal controls in study B, whereas acylcarnitines were significantly greater than controls in studies A and B and than in CKD patients in study A. CONCLUSIONS: Serum free carnitine is not reduced in CKD and decreases in MHD patients. Serum acylcarnitines increase in CKD and MHD patients primarily because of impaired excretory function in the failing kidney.
BACKGROUND: Serum free carnitine is decreased and serum acylcarnitines are increased in maintenance hemodialysis (MHD) patients, and the causes for these abnormalities are not known. This study examined the role of renal failure in the occurrence of low serum carnitine and increased acylcarnitines in patients with advanced chronic kidney disease (CKD) by assessing the relationship between these compounds and renal function in normal individuals and patients with CKD. If these compounds decrease as glomerular filtration rate (GFR) decreases, this suggests that decreased intake or impaired synthesis in kidneys explain the low serum values. If serum compounds increase as GFR decreases, this suggests that impaired excretion may predispose to these values. METHODS: The study, conducted in Lyon, France (part A), and Los Angeles, California (part B), compared serum free carnitine and acylcarnitines to renal function in 20 normal patients, 65 CKDpatients, and 29 MHD patients. GFR was measured using inulin (A) and iothalamate (B) clearances. Carnitine compounds were measured by tandem mass spectrometry (A) and electron spray mass spectrometry (B). RESULTS: There was no relationship between serum total carnitine or free carnitine and GFR in the normal subjects and CKDpatients. In contrast, serum acylcarnitines were inversely correlated with GFR in these 2 groups. Serum free carnitine was significantly lower in MHD patients than in CKDpatients and normal controls in study B, whereas acylcarnitines were significantly greater than controls in studies A and B and than in CKDpatients in study A. CONCLUSIONS: Serum free carnitine is not reduced in CKD and decreases in MHD patients. Serum acylcarnitines increase in CKD and MHD patients primarily because of impaired excretory function in the failing kidney.
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