Lipid abnormalities in uremia, dialysis, and transplantation

Chan, M.K.; Varghese, Z.; Moorhead, John F.

doi:10.1038/ki.1981.62

Cited by 237 publications

(99 citation statements)

References 91 publications

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“…Hypercholesterolemia occurs within 6 months in most patients (82%), whereas the peak incidence of hypertriglyceridemia is at 12 months after transplantation [11]. In the present study, an inverse correlation was observed between TG and TC levels and transplant duration as shown in Table 3 and Fig 1. This observation is also in accordance with other studies [9,12,13].The pathogenesis of hyerlipidaemia in renal Values are Mean ± SD; n -Number of patients; BMI -Body mass index; M -Males; F -Females; BP in mmHg Values are mean ±SD (range in parenthesis); n -Number of patients; TC -Total cholesterol ** ; TG -Total triglycerides; LDL-C -Low density lipoprotein cholesterol; HDL-C -High density lipoprotein cholesterol; ** p < 0.001 versus control and LDL-C was observed in 60% and 33.3% respectively in the transplanted patients. The mean TC levels, TG levels and HDL-C levels were significantly higher in the transplant group (p< 0.001) when compared to controls (Table 3).…”

Section: Methodssupporting

confidence: 94%

“…The investigations performed included blood urea, creatinine, glucose, albumin, ECG and chest X-ray. After 14 hours of overnight fast, blood samples were collected for serum total have lipid derangement before transplantation [9]. After a successful renal transplant, though the renal function returns to normal, the lipid profile is reported to remain abnormal.…”

Section: Methodsmentioning

confidence: 99%

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Lipid Profile In Transplant Patients: A Clinical Study

Baliga

Sharma

Prakash

et al. 2003

Medical Journal Armed Forces India

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Abstract15 renal transplant recipients were studied for their lipid profile. The patients were on regular post transplant follow up and had non clinical or laboratory evidence of graft dysfunction, intercurrent infection or post transplant diabetes mellitus for at least 3 months prior to the study. The mean duration of transplant was 15 ± 9.5 months (range 3-32 months). Majority (86%) were on triple immunosuppression therapy and received a mean prednisolone dose of 10.5 mg. An equal number of healthy subjects were randomly selected and studied for their lipid profile and served as control for the study group. There was no significant change in the HDL-cholesterol level as compared with controls. However, these patients showed a significantly higher LDL-cholesterol and total cholesterol levels. Further, a significant inverse correlation was observed between triglycerides and total cholesterol levels and transplant duration.

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Section: Methodssupporting

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Lipid Profile In Transplant Patients: A Clinical Study

Baliga

Sharma

Prakash

et al. 2003

Medical Journal Armed Forces India

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“…Abnormalities of lipid and lipoprotein metabolism are particularly marked in patients with nephrotic syn drome (31)(32)(33). Especially, hypercholesterolemia plays an important role in the progression of initial toxic glomerular injury by PAN to FSGS (34).…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Shirakura

Sano

Karasawa

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-An experimental focal segmental glomerular sclerosis (FSGS) was induced by the com bined administration of puromycin aminonucleoside (PAN) and protamine sulfate (PS). Blood collec tions were made on days 0, 37, 70 and 94. Urine collections were made on days 0, 24, 80 and 94. Vehicle-treated rats showed severe proteinuria and an increase in serum total cholesterol (sTC). Benidi pine (1 or 3 mg/kg, p.o.)-treated rats exhibited less proteinuria and lower sTC than the vehicle-treated rats. On days 70 and 94, both blood urea nitrogen (BUN) and serum creatinine (sCR) values in the vehicle-treated rats were significantly higher than those in normal rats (without treatment with PAN and PS). On the other hand, the treatment with benidipine (1 or 3 mg/kg, p.o.) attenuated the in creases in BUN and sCR. On day 94, vehicle-treated rats showed a significant decrease in creatinine clearance as compared with normal rats, but benidipine (1 or 3 mg/kg, p.o.)-treated rats did not. The histology was examined on day 94. Vehicle-treated rats demonstrated a significantly greater percentage of glomeruli with segmental areas of glomerulosclerosis/hyalinosis, mesangial cell proliferation, and mesangial foam cell. Benidipine (3 mg/kg, p.o.) ameliorated the development of renal regeneration as estimated by histological examination. These results suggest that the Ca-channel blocker benidipine is a favorable drug for preventing the progression of glomerular sclerosis.

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“…Hypertdglyceridemia isthe most common lipid abnormality in patients with renal failure (1). The major cause of death in about 30-65% of CRF patients is atherosclerotic cadiovascular disease with various predisposing factors like diabetes mellitus, essential hypertension and proteinuria (2). Abnormalities of liptds and lipoproteins occur early in clinical course of patients, but they are not always reflected by hyperlipidemia.…”

Section: Introductionmentioning

confidence: 99%

Lipid abnormalities in chronic renal failure

Bhagwat

Joshi

Salgia

et al. 1997

Indian J Clin Biochem

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:Lipid abnormalities remain to be a major cause of early mortality in patients with chronic renal failure (CRF). In present study, 114 (one hundred fourteen) CRF patients without any additional cause of dyslipidemia were divided into groups on the basis of etiologies of CRF. Blood samples from each group were analyzed for total cholesterol, triglyceride and HDL cholesterol along with blood urea nitrogen and serum creatinine. 25 healthy individuals without any obvious disease were taken as control. Patients from all the groups showed a marked hypertriglyceridemia of 232 (SD + 77) mg/dl (P < 0.001) as compared to control. Levels of HDL cholesterol were found to be significantly low 20 ( ~ 11) mg/dl (p < 0.001) in all the groups. LDL cholesterol showed an increase 104 ( _+ 30) mg/dl as compared to control group which is not statistically significant. Present study reveals that, CRF patients show an uniform dyslipidemia irrespective of etiologies leading to CRF. This dyslipidemia is also independent of serum creatinine levels. Although, these lipid abnormalities may not solely cause mortality in CRF patients, they may act as modulators in accelerating atherogenesis which in turn cause early mortality in CRF patients.

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Lipid abnormalities in uremia, dialysis, and transplantation

Cited by 237 publications

References 91 publications

Lipid Profile In Transplant Patients: A Clinical Study

Lipid Profile In Transplant Patients: A Clinical Study

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Lipid abnormalities in chronic renal failure

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