The relationship between serum concentration of cardiac troponin I in chronic renal failure patients and cardiovascular events.

OBJECTIVE: The purpose of this study was to evaluate the relationship between serum cardiac troponin I in asymptomatic chronic renal failure patients and cardiovascular events. BACKGROUND: Short-term follow-up studies on this subject produced conflicting results. MATERIAL AND METHOD: A total of 63 asymptomatic patients with chronic renal failure (CRF) with regular hemodialysis were followed for 18 months for cardiac mortality, myocardial infarction events and interventional procedures such as percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG). Serum cTnI and other blood chemistries were measured at the time of the study. RESULTS: Forty seven chronic dialysis patients (75%) had an elevated level of cTnI concentration more than the 0.08 ng/ml cutoff but only fourteen patients (22%) had and elevated cTnI concentration of more than the AMI cutoff (0.4ng/ml). When using the 0.08 ng/ml cutoff, the NT-proBNP concentrations of the elevated groups were significantly higher than the normal groups. The authors also found that the elevated groups above the AMI cutoff had significantly higher cardiovascular events. CONCLUSION: Elevated cTnI concentrations are commonly found in chronic renal failure patients. The AMI cutoff level of cTnI (0.4 ng/ml) seem to have a benefit for predicting the cardiovascular events in asymptomatic chronic renal failure patients while the 0.08 ng/ml cutoff doesn't have usefulness for this purpose. Further studies are needed to clarify this hypothesis.

The renin--angiotensin system gene polymorphisms and clinicopathological correlations in IgA nephropathy.

Genetic variability in the renin-angiotensin system (RAS) may modify renal responses to injury and disease progression. We examined whether RAS alleles affect severity of IgA nephropathy. These genetic variants include angiotensin I converting enzyme deletion polymorphism in intron 16 (ACE I/D), a point mutation in the angiotensinogen (AGT) gene resulting in a methionine to threonine substitution at residue 235 (M235T) and an angiotensin receptor type I (ATR) A to C transition at bp 1166 (A 1166 C). A total of 53 patients with biopsy-proven IgA nephropathy and 80 normal control subjects were recruited for study. These patients were classified into two groups according to serum creatinine at renal biopsy. Group 1 patients (n = 40) had normal renal function, serum creatinine < or = 1.5 mg/dl and group 2 patients (n = 13) had renal insufficiency with serum creatinine > 1.5 mg/dl. The blood pressure and urinary protein of group 2 patients were higher than group 1 (p < 0.01). The mean scores of histological parameters including mesangial proliferation, glomerular sclerosis (global and segmental), the interstitial fibrosis and crescent formation in group 2 patients were significantly higher than in group 1 patients (p < 0.05). The most frequent genotype in IgA patients was ID (47%) genotype, followed by II (45%) and DD (8%) genotype of ACE gene. The mean serum ACE activity in the DD group was significantly higher than in the II group (p < 0.05) but was not significantly different from that of the ID group. No statistically significant differences were found with respect to allele frequencies between IgA group 1, group 2, or between controls and all IgA patients. Furthermore, no significant difference in AGT alleles, ATR alleles frequencies was detected between groups of IgA patients, although a trend for a higher frequency of DD genotype and AGT-TT genotype were noted in IgA group 2. The combined analysis of the ACE-DD and AGT-TT genotypes did not show any genetic influence on the risk of the disease susceptibility. To resolve the true role of ACE genotype and any dependent effect on progression, larger collaborative studies are required.

Lipoprotein(a) in nephrotic syndrome.

Serum lipoprotein(a) levels were measured in 27 patients with idiopathic nephrotic syndrome (NS), 14 patients with systemic lupus erythematosus (SLE) and 30 healthy controls. Lp(a) levels were significantly elevated in both idiopathic NS (53.4 + 36.2) and SLE (49.3+ 41.9) compared with controls (9.5+ 5.7) (p < 0.001). Fifty nine percent of idiopathic NS and 50 percent of SLE had Lp(a) more than 30 mg/dl. In 19 patients with idiopathic NS, serum Lp(a) levels fell markedly in 12 patients who responded to prednisolone therapy while, 7 patients with partial and no response had serum Lp(a), cholesterol, triglycerides and albumin levels not different from pretreatment period vs 6 months therapy. Lp(a) levels correlated significantly with proteinuria, serum cholesterol and triglycerides (r = 0.8, 0.6, 0.6) in idiopathic nephrotic syndrome and correlated inversely with serum albumin (r = -0.9). The SLE patients had the same pattern of correlation among these parameters and Lp(a) levels except for triglycerides. The high levels of Lp(a) in the NS could be one of the risk factors for atherosclerosis and thrombotic events associated with this disorder. In conclusion, the present study confirmed that patients with idiopathic NS and SLE had markedly increased serum level of Lp(a), in conjunction with other lipid abnormalities. The serum Lp(a) levels decreased substantially in all NS patients who experienced remission. In addition, the study also demonstrated a relationship between serum Lp(a) levels and serum albumin, cholesterol and triglycerides. An elevated Lp(a) level may be useful in guiding the physician towards more aggressive care to detect coronary artery disease early in patients at risk.

Lipoproteins and lipid peroxidation abnormalities in patients with chronic renal disease.

Increasing experimental and clinical evidence suggests that lipoproteins and lipid peroxidation can be important modulators in progressive kidney disease. A group of 54 patients with varying degrees of kidney impairment was studied to find the abnormalities in lipoproteins and lipid peroxidation. Lipoproteins and lipid peroxidation products, malondialdehyde (MDA) were measured in the plasma of 54 chronic renal disease patients CGN 33, nephrosclerosis 11, 7CTIN, 1PCKD, unknown 2 and compared with values obtained from 32 healthy controls. The patients were divided into 5 groups according to serum creatinine levels: Group 1 (serum creatinine of 2 mg/dl), group 2 (S. creatinine > 2-4 mg/dl), group 3 (S. creatinine > 4-8 mg/ dl), group 4 (S. creatinine > 8-12 mg/dl), group 5 (S. creatinine > 12 mg/dl). Plasma cholesterol was higher significantly than controls in patients with group 1, 2 and 3 (p < 0.01, < 0.001, < 0.05) respectively while plasma LDL-chol was statistically significantly different from controls only in group 2 patients (p < 0.001). Plasma VLDL-chol, beta-VLDL-chol, triglycerides, ratio of chol/HDL and LDL/ HDL showed high levels in all groups compared with controls but more evident in patients of group 2. Plasma HDL-chol decreased during the progression of renal failure. All groups had significantly elevated plasma malonyldialdehyde (MDA) vs controls (p < 0.001), especially highest value was found in group 2. Triglycerides, beta-VLDL chol, VLDL-chol LDL/HDL, chol/HDL correlated very closely with plasma MDA levels and also with serum creatinine. Patients with chronic renal disease showed lipoprotein abnormalities and accelerated lipid peroxidation. The evidence was more marked in patients with normal to mild renal insufficiency which suggested the role of oxidative stress early in the course of nephron injury.

Analysis of serum urinary proteins in normal and renal diseases by cellulose acetate electrophoresis.

A method using dried polyacrylamide gel to concentrate urine samples has been described, tested and used for the purpose of urine protein analysis. Concentrated urine samples from 10 normals and 100 patients with IgM nephropathy and systemic lupus erythematosus (SLE) were analysed by cellulose acetate electrophoresis (CAE). The results demonstrated that the patterns of proteins in the electrophoresis could be used to discriminate the two diseases. The best discriminating power was found in the logarithm of gamma globulin to albumin ratio. In IgM nephropathy the ratio of gamma globulin to albumin is much smaller than the ratio in SLE, indicating that relatively larger gamma globulins were excreted in SLE. In addition, the ratio can be used to discriminate subgroups of patients with IgM nephropathy. Urine from patients with IgM nephropathy with focal and segmental changes showed a significantly higher ratio. The study indicated the usefulness of the technique in discriminating the two common glomerular diseases.