Reduction of Dialysate Calcium Level Reduces Progression of Coronary Artery Calcification and Improves Low Bone Turnover in Patients on Hemodialysis.

Exposure to high Ca concentrations may influence the development of low-turnover bone disease and coronary artery calcification (CAC) in patients on hemodialysis (HD). In this randomized, controlled study, we investigated the effects of lowering dialysate Ca level on progression of CAC and histologic bone abnormalities in patients on HD. Patients on HD with intact parathyroid hormone levels ≤300 pg/ml receiving dialysate containing 1.75 or 1.50 mmol/L Ca (n=425) were randomized to the 1.25-mmol/L Ca (1.25 Ca; n=212) or the 1.75-mmol/L Ca (1.75 Ca; n=213) dialysate arm. Primary outcome was a change in CAC score measured by multislice computerized tomography; main secondary outcome was a change in bone histomorphometric parameters determined by analysis of bone biopsy specimens. CAC scores increased from 452±869 (mean±SD) in the 1.25 Ca group and 500±909 in the 1.75 Ca group (P=0.68) at baseline to 616±1086 and 803±1412, respectively, at 24 months (P=0.25). Progression rate was significantly lower in the 1.25 Ca group than in the 1.75 Ca group (P=0.03). The prevalence of histologically diagnosed low bone turnover decreased from 85.0% to 41.8% in the 1.25 Ca group (P=0.001) and did not change in the 1.75 Ca group. At 24 months, bone formation rate, trabecular thickness, and bone volume were higher in the 1.25 Ca group than in the 1.75 Ca group. Thus, lowering dialysate Ca levels slowed the progression of CAC and improved bone turnover in patients on HD with baseline intact parathyroid hormone levels ≤300 pg/ml.

Prognostic value of glomerular C4d staining in patients with IgA nephritis.

INTRODUCTION: Mesangial IgA deposition is the initiative factor in the pathogenesis of IgA nephropathy (IgAN). Glomerular IgA depositon leads to activation local complement system. C4d positivity shows that complement activation occurs via alternative pathway. C4d positivity at the time of renal biopsy can be associated with poor prognosis in IgA nephropathy. We aimed to evaluate C4d deposition and renal outcome in patients with IgA nephritis. METHODS: Between January 2005 and December 2009, 40 patients with IgA nephritis were enrolled. Renal biopsy specimens of 33 patients have been evaluated. C4d immunohistochemical staining was performed 3-µm deparaffinized and rehydrated sections of formaldehyde-fixed renal tissues, using rabbit polyclonal anti-human C4d as the antibody. Baseline demographical, clinical and laboratory data were recorded retrospectively. RESULTS: Mean age of the patients was 35.9 ± 12.9 years and female/male ratio was 19/21. Mean duration of follow-up was 32.8 (12-60) months. Baseline glomerular filtration ratio (GFR) and proteinuria were 55.8 ml/min and 2.44 gr/day respectively at the time of renal biopsy. Eleven patients were C4d positive. Presence of hypertension (p=0.133), proteinuria (p=0.007), serum creatinine levels (p=0.056) and glomerulosclerosis (p=0.004), mesengial hypersellularity (p=0.0001) and interstitial fibrosis (p=0.006) at the time of renal biopsy were higher in C4d positive group rather than negative group. Evolution to renal failure were 63.6% in C4d positive group and 13.6% in negative group (p=0.006). Renal survival at 3 years was 39% in C4d-positive patients versus 66.7% in the C4d-negative patients (log rank- p=0.0072).

Quantitative evaluation of interstitial fibrosis with Sirius Red in IgA nephritis.

OBJECTIVE: Tubulointerstitial fibrosis is one of the strongest independent predictive factors in determining the prognosis in IgA nephritis. Recently, software-based quantitative measurement of interstitial fibrosis with Sirius Red staining has entered the practice. The objective of this study was to investigate the prognostic value of measurement of interstitial nephritis with this method in IgA nephritis. METHOD: Forty-three patients diagnosed with IgA nephritis with renal biopsy between the years 2005 and 2009 were included in this retrospective observational study. The diagnostic biopsies of 37 patients were examined. Basal data included age, gender, creatinine level, glomerular filtration rate (GFR), presence of proteinuria, hypertension, glomerulosclerosis, mesangial proliferation, and interstitial fibrosis and fibrosis index calculated by the measurement of computed images of Sirius Red positive areas. Final visit included evaluation of development of end-stage renal disease (ESRD), and GFR (whether = 60 mL/min or <60 mL/min). RESULTS: Numbers of patients with hypertension (75% vs. 34.5%; p = 0.050), ESRD development (62.5% vs. 20.7%, p = 0.035), GFR <60 mL/min (87.5% vs. 31%; p = 0.007) were greater; and basal GFR (34.25 ± 25.29 vs. 64.14 ± 35.34; p = 0.048) was lower in high-intensity interstitial fibrosis group (>1000 µm2) compared to low-intensity interstitial fibrosis group (≤1000 µm(2)). CONCLUSION: Quantitative analysis of computed imaging of areas of Sirius Red positive tubulointerstitial fibrosis might serve as an effective novel method to determine the prognosis in IgA nephritis.

Prognostic value of NGAL staining in patients with IgA nephropathy.

BACKGROUND: Renal tubulointerstitial injury plays an important role in disease progression of IgAN. Neutrophil gelatinase-associated lipocalin (NGAL) is a stress protein released by tubular cells. NGAL is a promising biomarker of acute kidney injury. There is a growing literature suggesting that NGAL is also a marker of chronic kidney disease and severity. Our aim was to evaluate the prognostic value of NGAL staining in patients with IgAN. METHODS: This retrospective study included all consecutive patients who underwent a renal biopsy at our center between January 2005 and December 2009. Forty-five patients with IgA nephritis were enrolled, and renal biopsy specimens of 29 patients were evaluated. We evaluated baseline age, sex, hypertension, serum creatinine, glomerular filtration rate (GFR), urine protein, NGAL staining, glomerulosclerosis, interstitial fibrosis, and extracapillary proliferation. The primary endpoint of this study was doubling of baseline serum creatinine and/or the onset of ESRD in the course of the study. At the end of the follow-up, patients whose estimated GFR (eGFR) was ≤15 mL/min/1.73 m(2) and/or baseline serum creatinine doubled, were defined as the progressor group. RESULTS: Nineteen patients (65.5%) were NGAL positive and 10 patients (34.5%) were NGAL negative. Female gender and hypertension were associated with NGAL-positive staining. Urinary protein excretion and serum creatinine levels were more elevated in the NGAL-positive group, but the difference was not significant. We found NGAL-positive staining in major proportion in the progressor group (88.9%) than the non-progressor group (55%) (p = 0.076). CONCLUSION: NGAL staining can be a new histological marker in IgAN progression.

Glomerular c4d staining can be an indicator of disease activity in lupus nephritis.

BACKGROUND: Abnormalities in complement activation and clearance of immune complexes by erythrocytes are the central pathogenic mechanisms in systemic lupus erythematosus (SLE). Serum C4d level, which is a degradation product of complement factor C4, was found to be a sensitive indicator of SLE activity. Our aim was to determine whether glomerular C4d staining could be a useful marker of disease activity in patients with lupus nephritis. METHODS: This retrospective study included all consecutive patients who underwent a renal biopsy at our center between January 2005 and December 2009. A total of 29 patients with IgA nephritis were enrolled, and renal biopsy specimens of 24 patients have been evaluated. We evaluated baseline age, sex, hypertension, serum creatinine level, glomerular filtration rate (GFR), urine protein, and glomerular C4d staining. The primary endpoint of this study was the onset of end-stage renal disease (ESRD) in the course of study. RESULTS: Fourteen (58%) patients were C4d+ and 10 (42%) patients C4d-. Urinary protein excretion was more elevated in C4d+ group (p = 0.0001). The renal biopsy showed that activity index score >12 was a higher proportion in C4d+ patients. The patients were followed up for 3.5 years. Four patients in the C4d+ group evolved to ESRD in the follow-up, but none of the patients in the C4d- group (p = 0.064). DISCUSSION: We found a relationship between glomerular C4d staining and activity of lupus nephritis. C4d staining may be a useful marker to predict the prognosis of lupus nephritis.

The value of serum immunoglobulin free light chain assessment in patients with monoclonal gammopathies and acute renal failure.

OBJECTIVE: Immunoglobulin free light chain (FLC) abnormalities are common in patients with monoclonal gammopathies and the kidneys are the most affected organs. Immunoassays that provide quantitative measurement of FLC in serum indicate monoclonal FLC production based on the presence of an abnormal FLC kappa:lambda (κ:λ) ratio. The aim of this study was to assess the utility of serum FLC measurement as a diagnostic tool for detecting plasma cell dyscrasias in comparison to standard assays, and to ascertain its sensitivity and specificity in patients with acute renal failure (ARF). MATERIAL AND METHODS: Sera from 82 patients with ARF were assessed using serum protein electrophoresis (SPE), serum immunofixation electrophoresis (SIFE), and FLC measurement. The sensitivity and specificity of the FLC ratio in identifying which ARF patients had multiple myeloma (MM) was compared to those of SPE and SIFE. RESULTS: Among the 82 patients with ARF, 7 were diagnosed as MM using SPE, SIFE, and bone marrow biopsy techniques. In total, 8 patients did not have a FLC κ:λ ratio that was within the published reference range (0:26-1:65); the FLC κ:λ ratio based on FLC measurement had a specificity of 96% and sensitivity of 71%, and positive and negative predictive values of 62.9% and 97.3%, respectively, for the diagnosis of MM. CONCLUSION: The sensitivity and specificity of the FLC κ:λ ratio for diagnosing MM in patients that presented with ARF were lower than those of SPE and SIFE. To further delineate the utility of the FLC κ:λ ratio additional prospective, well-designed large-scale studies are needed. CONFLICT OF INTEREST: None declared.

The role of nebivolol in the prevention of contrast-induced nephropathy in patients with renal dysfunction.

OBJECTIVE: This prospective study was designed to evaluate the potential protective effect of nebivolol compared with metoprolol on the development of contrast-induced nephropathy (CIN) following coronary angiography in patients with renal dysfunction. METHODS: Ninety patients with stable coronary angina pectoris with renal insufficiency (creatinine value ≥1.2 mg/dl) were included for this prospective study. Patients were divided into two groups. Patients in group 1 (n=55) received oral administration of nebivolol 5 mg/daily for coronary artery disease and/or hypertension. Group 2 consisted of 35 patients who received metoprolol 50 mg/daily for the same indications. All patients were hydrated with 0.9% NaCl at a rate of 1 mL/kg/hr for 12 hours before and 24 hours after the procedure. Patients were also given N-acetylcysteine (NAC) 600 mg twice a day, beginning 24 hours before and continuing 48 hours after the procedure. All patients underwent routine coronary angiography. Serum creatinine was assessed just before, immediately after and 48 hours after the procedure. CIN was defined as an increase in serum creatinine concentration of ≥25% within 48 hours after the procedure compared to the patient's baseline value. Tests for significance between groups were conducted using the independent sample t-test for continuous variables and Chi-square test for categorical variables. RESULTS: Baseline serum creatinine levels were statistically comparable in two groups. Following angiography, serum creatinine levels increased in both groups. Post-angiographic creatinine levels were not statistically different in the nebivolol and the metoprolol groups. Contrast induced nephropathy developed in 13 patients (24%) of the nebivolol group and in 12 patients (33%) of the metoprolol group. The incidence of CIN was statistically significantly lower in the nebivolol group comparing with the metoprolol group (p=0.03). CONCLUSION: The use of oral nebivolol for one week at a dose of 5 mg per day may decrease the incidence of contrast-induced nephropathy in patients who underwent coronary angiography with renal dysfunction. The small numbers of this study do not allow to draw final conclusion on the use of nebivolol in the prevention of CIN. Therefore, larger studies may be necessary to address the definite role of nebivolol in this setting.

TLR polymorphisms in FMF: association of TLR-2 (Arg753Gln) and TLR-4 (Asp299Gly, Thre399Ile) polymorphisms and myeloid cell TLR-2 and TLR-4 expression with the development of secondary amyloidosis in FMF.

Amyloidosis is the major complication of familial Mediterranean fever (FMF). Toll-like receptors (TLR) are involved in the activation of an innate immune system TLR-2 and TLR-4 recognize lipoteichoic acid and lipopolysaccharides (LPS), respectively. While TLR-2 Arg753Gln polymorphism upregulates, TLR-4 Asp299Gly and Thre399Ile polymorphisms downregulate inflammation. We investigated the effect of these polymorphisms on the development of amyloidosis in FMF patients. We also investigated myeloid cell TLR-2 and TLR-4 expressions in these patients. We studied 26 FMF patients and 13 FMF patients with amyloidosis. TLR-2 Arg753Gln and TLR-4 Asp299Gly and Thr399Ile polymorphisms were analyzed with the polymerase chain reaction-restriction fragment length polymorphism method. Myeloid cell baseline TLR-2 and TLR-4 and LPS-induced TLR-4 expressions were evaluated. The TLR-2 and TLR-4 polymorphism rate was compared with the results of 100 healthy subjects in our previous study. In addition, 13 healthy controls were enrolled for leukocyte TLR-2 and TLR-4 expressions. Serum amyloid A (SAA) levels were measured in these 13 control cases and in FMF patients during attack-free periods. The frequency of TLR-2 Arg753Gln, TLR-4 Asp299Gly, and Thr399Ile polymorphisms in healthy controls in our previous study were 1%, 3%, and 2%, respectively. The frequency of these polymorphisms were not different in FMF patients (with or without amyloidosis) compared to the control group. Likewise, myeloid cell TLR-2 and TLR-4 expressions were not different among the controls and FMF patients. However, LPS-induced TLR-4 expression in granulocytes was more prominent in FMF patients. There was no correlation between TLR-2 and TLR-4 expressions and SAA levels. Neither myeloid cell TLR-2 and TLR-4 expressions nor TLR-2 Arg753Gln, TLR-4 Asp299Gly, and Thr399Ile polymorphisms seem to affect the development of secondary amyloidosis in FMF patients in our study population.

The renal effect of replacement fluids in controlled severe hemorrhagic shock: an experimental study.

BACKGROUND: This experimental study examined the effects of resuscitation with Ringer's lactate (RL), 6% hydroxyethyl starch (130/0.4-HES), and the combination of RL and HES on renal function in hemorrhagic shock (HS). METHODS: Twenty-four male New Zealand white rabbits weighing 2198-3435 g were divided at random into four groups. HS was constituted by maintaining the mean arterial blood pressure at 30 mmHg and blood lactate at >4 mM/L. Subsequently, Group 1 (control) was not resuscitated, while the study rabbits' resuscitation was initiated with RL (Group 2), HES (Group 3), or the combination of RL and HES (Group 4). RESULTS: In all groups, the serum creatinine and blood urea nitrogen (BUN) levels were observed to be within normal limits, while the lactate dehydrogenase and alpha-1 microglobulin levels statistically significantly increased when time points were compared with beginning values (p<0.05). Furthermore, cystatin-C levels were observed to be increased after the HS (p<0.05), but returned to the normal level after resuscitation in all the study groups. Interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha levels were increased in all the rabbits after HS (p<0.05), and there were no significant differences among the study groups after resuscitation (p>0.05). There were no differences in the histological imaging between the groups (p>0.05). CONCLUSION: The 6% HES (130/0.4) did not have any harmful effects on the kidney when it was used alone or in combination with crystalloid for resuscitation of HS in rabbits.

Renal Behçet's disease: an update.

OBJECTIVE: The aims of this study are (1) to report 33 patients with Behçet's disease (BD) having various renal manifestations, and (2) to update current data using our patients and published papers about BD and renal manifestations. METHODS: The PubMed database was searched using the terms BD or Behçet's syndrome. We found reports of 94 patients (including ours) with BD and specific renal diseases (amyloidosis, 39; glomerulonephritis [GN], 37; renal vascular disease, 19; interstitial nephritis, 1). RESULTS: The presentation of renal disease was edema/nephrotic syndrome in 12 patients (36%). Renal disease was incidentally diagnosed by routine urine analysis and measurement of serum creatinine level in 20 patients (61%). Renal failure was present in 23 patients (70%) and 5 of them have had cyclosporine treatment. The frequency of renal disease among BD patients has been reported to vary from less than 1 to 29%. CONCLUSIONS: The clinical spectrum of renal BD shows a wide variation. Amyloidosis (AA type), GN, and macroscopic/microscopic vascular disease are the main causes of renal BD. Patients with vascular involvement have a high risk of amyloidosis and amyloidosis is the most common cause of renal failure in BD. Several types of glomerular lesions are seen in BD. Current treatment options for renal BD are not evidence based. Radiological vascular intervention combined with immunosuppressive drugs can be useful in selected cases. Routine urine analysis and measurement of serum creatinine level are needed for early diagnosis of renal BD.

Preventive effect of nebivolol on contrast-induced nephropathy in rats.

BACKGROUND: Altered renal vasodilatation and oxidative stress are important mechanisms of contrast-induced nephropathy (CIN). The aim of the present study was to assess the effect of nebivolol, a beta blocker, on prevention of CIN. We hypothesized that nebivolol may prevent CIN due to its renal vasodilatation and antioxidant effects. METHODS: Thirty-two Wistar-albino rats were divided into four groups (n = 8 each): control (C), contrast media (CM), nebivolol (N), and nebivolol + contrast media (NCM). CIN was induced by administration of intravenous high-osmolar contrast media diatrizoate (6 ml/kg) after 72 h of dehydration. Nebivolol (2 mg/kg) was given internally once daily for 5 days. Kidney function parameters, nitric oxide metabolites and oxidative stress markers were measured. Kidneys were excised for pathological evaluation. RESULTS: The decrease of creatinine clearance was 0.180 +/- 0.11 mg/dl in CM, and 0.030 +/- 0.10 mg/dl in NCM (P = 0.01). Microproteinuria was ameliorated using nebivolol (P = 0.001). Serum protein carbonyl content, malonyldialdehyde and kidney thiobarbituric acid-reacting substances levels were higher in CM than in C (P = 0.003, P < 0.001 and P = 0.034, respectively) and serum thiol was lower in CM than in C (P = 0.001). However, oxidative stress markers were similar in NCM and C. Diatrizoate decreased kidney nitrite levels, but nebivolol increased them (P = 0.027). Nebivolol attenuated the tubular necrosis, proteinaceous casts and medullary congestion, although significant protective effects, were observed in tubular necrosis (P = 0.001) and proteinaceous cast (P < 0.001). CONCLUSION: This study demonstrated the protective role of nebivolol against CIN.

Impact of diabetic and pre-diabetic state on development of contrast-induced nephropathy in patients with chronic kidney disease.

BACKGROUND: The aim of the present study was to assess the influence of diabetic and pre-diabetic state on the development of contrast-induced nephropathy (CIN) in chronic kidney disease patients undergoing coronary angiography. METHODS: A total of 421 patients with Cockcroft clearance between 15 and 60 ml/min were divided into three groups [diabetes mellitus (DM), n = 137; pre-diabetes (pre-DM), n = 140; and normal fasting glucose (NFG), n = 144]. CIN was defined as an increase of > or =25% in creatinine over baseline within 48 h of angiography, DM as glucose > or =126 mg/dl, pre-DM as glucose between 100 and 125 mg/dl and NFG as glucose <100 mg/dl. RESULTS: CIN occurred in 20% of the DM [relative risk (RR) 3.6, P = 0.001], 11.4% of the pre-DM (RR 2.1, P = 0.314) and 5.5% of the NFG group. The decrease of glomerular filtration rate (GFR) was higher in DM and pre-DM (P = 0.001 and P = 0.002, respectively). GFR < or =30 ml/min (RR 19.22), multivessel involvement (RR 7.59), hyperuricaemia (RR 3.95), use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blocker (RR 2.70) and DM (RR 2.34) were predictors of CIN. Length of hospital stay was 2.45 +/- 1.45 day in DM, 2.27 +/- 0.68 day in pre-DM and 1.97 +/- 0.45 day in NFG (P < 0.001, DM vs NFG and P = 0.032, pre-DM vs NFG). The rate of major adverse cardiac events was 8.7% in DM, 5% in pre-DM and 2.1% in NFG (P = 0.042, DM vs NFG). Haemodialysis was required in 3.6% of DM and 0.7% in pre-DM (P = 0.036, DM vs NFG), and the total number of haemodialysis sessions during 3 months was higher in DM and pre-DM (P < 0.001). Serum glucose > or =124 mg/dl was the best cut-off point for prediction of CIN. CONCLUSION: Our data support that patients with DM are at a higher risk of developing CIN, but patients with pre-DM are not at as high a risk for developing CIN as diabetes patients.

Risk factors and therapy strategies for contrast-induced nephropathy.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality, as well as increased costs for medical care, particularly in patients with diabetes mellitus and chronic renal failure. A key step to safer CIN is to identify patients at risk and applying proven preventive interventions. Extracellular volume expansion, minimizing the dose of contrast media, using low-osmolar non-ionic contrast media, stopping the intake of nephrotoxic drugs, and avoiding short intervals between procedures have all been shown to be effective in reducing CIN. The aim of the present review is to summarize the knowledge about the risk factors and prophylactic treatments of CIN.

Angiotensin-converting enzyme inhibitors as a risk factor for contrast-induced nephropathy.

BACKGROUND/AIMS: The aim of the present study was to assess the influence of chronic angiotensin-converting enzyme (ACE) inhibitor administration on the development of contrast-induced nephropathy (CIN) in patients undergoing coronary angiography. METHODS: A total of 230 patients with renal insufficiency and age > or =65 years were divided into two groups according to prior use of ACE inhibitors (ACE inhibitor group, n = 109; control group, n = 121). CIN was defined as an increase of > or =25% in creatinine over the baseline value within 48 h of angiography. RESULTS: CIN occurred in 17 patients (15.6%) in the ACE inhibitor group and 7 patients (5.8%) in the control group (p = 0.015). Serum creatinine level increased from 1.34 +/- 0.20 to 1.53 +/- 0.27 mg/dl in the ACE inhibitor group and from 1.33 +/- 0.18 to 1.45 +/- 0.19 mg/dl in the control group (p < 0.001). Chronic ACE inhibitor administration was a risk indicator of CIN [odds ratio 3.37; 95% confidence interval 1.14-9.94; p = 0.028]. Multi-vessel coronary involvement (p = 0.001), hypoalbuminemia (p = 0.005), diabetes mellitus (p = 0.006), GFR < or =40 ml/min (p = 0.010), and congestive heart failure (p = 0.024) were other risk indicators of CIN. CONCLUSION: Chronic ACE inhibitor administration is a risk for developing CIN in elderly patients with renal insufficiency.

Risk factors for contrast-induced nephropathy.

An increasing number of diagnostic imaging and interventional procedures require the use of radiographic contrast agents which has led to a parallel increase in the incidence of contrast-induced nephropathy (CIN). CIN is a serious clinical problem associated with increased morbidity and mortality, particularly in patients with chronic renal failure (see the Case Report). A key step to minimize CIN is to identify patients at risk of CIN. The aim of the present review was to summarize the knowledge about the risk factors of CIN, including the review of ultimate clinical research and developments.

Metabolic syndrome as a risk factor for contrast-induced nephropathy in non-diabetic elderly patients with renal impairment.

BACKGROUND/AIMS: Metabolic syndrome (MS) as a risk factor for contrast-induced nephropathy (CIN) has not been studied. The aim of the present study was to assess the influence of MS on the development of CIN in patients undergoing coronary angiography. METHODS: This was a prospective cohort study. A total of 219 non-diabetic patients with reduced kidney function and age >or=60 years were divided into two groups (MS, n = 107 and non-MS, n = 112). CIN was defined as an increase of >or=25% in creatinine over the baseline value within 48 h of angiography. RESULTS: CIN occurred in 14% of the MS group and 3.6% of the non-MS group (p = 0.006). Serum creatinine increased from 1.06 +/- 0.17 to 1.12 +/- 0.27 mg/dl in the MS group and from 1.03 +/- 0.17 to 1.09 +/- 0.23 mg/dl in the non-MS group (p < 0.001). MS was a risk indicator of CIN [odds ratio (OR) 4.26; 95% confidence interval (95% CI) 1.19-15.25; p = 0.026). Impaired fasting glucose (OR 4.72; 95% CI 1.53-14.56; p = 0.007), high triglyceride (OR 4.06; 95% CI 1.22-13.44; p = 0.022), and multivessel involvement (OR 3.14; 95% CI 1.07-9.82; p = 0.038) in the MS group were predictors of CIN. CONCLUSION: Our data support the hypothesis that patients with MS are at risk of developing CIN.

Hyperuricemia as a risk factor for contrast-induced nephropathy in patients with chronic kidney disease.

OBJECTIVES: Hyperuricemia as a risk factor for contrast-induced nephropathy (CIN) has not been studied. BACKGROUND: The aim of the present study was to assess the influence of hyperuricemia on the development of CIN in patients undergoing coronary angiography. METHODS: This was a prospective cohort study. A total of 266 patients with a mean age of 58.33 +/- 7.85 years and serum creatinine > or = 1.2 mg/dl were divided into two groups (hyperuricemic, n = 126, and normouricemic, n = 140). CIN was defined as an increase of > or = 25% in creatinine over baseline within 48 hr of angiography, and hyperuricemia as serum uric acid > or = 7 mg/dl in males and > or = 6.5 mg/dl in females. RESULTS: CIN occurred in 15.1% of the hyperuricemic group and 2.9% of the normouricemic group (P < 0.001). Serum creatinine increased from 1.45 +/- 0.20 to 1.67 +/- 0.45 mg/dl in the hyperuricemic group and from 1.42 +/- 0.16 to 1.56 +/- 0.23 mg/dl in the normouricemic group (P < 0.001). Hyperuricemia [odds ratio (OR) 4.71; 95% confidence interval (95% CI) 1.29-17.21; P = 0.019] and a high incidence of multi-vessel coronary involvement (OR 3.59; 95% CI 1.12-11.48; P = 0.032) in the hyperuricemic group were predictors of CIN. Hypoalbuminemia (P = 0.001) and age > or = 70 years (P = 0.023) were other risk indicators of CIN. Length of hospital stay (P < 0.001) and CIN requiring renal replacement therapy (P = 0.017) were significantly higher in hyperuricemic group. Serum uric acid level > or = 7 mg/dl in males and > or = 5.9 mg/dl in females were found to be the best cut-off value for prediction of CIN. CONCLUSION: Our data support the hypothesis that patients with hyperuricemia are at risk of developing CIN.

[The effect of pre-procedural captopril on contrast-induced nephropathy in patients who underwent coronary angiography]. / Koroner anjiyografi yapilan Hastalarda islem oncesi verilen kaptoprilin kontrast madde nefropatisi uzerine etkisinin arastirilmasi.

OBJECTIVE: Contrast media induced nephropathy (CIN) is diagnosed as the acute renal failure developed following intravenous contrast media usage when all other causes of renal failure are excluded. In this study, we investigated the effects of captopril given before coronary angiography (CA) on CIN development. METHODS: A total of 80 patients, 43 males and 37 females, mean age: 58 +/- 8 years (range: 18-80), with serum creatinine level below 2 mg/dl, who underwent coronary angiography in Cardiology Clinic of Izmir Atatürk Training and Research Hospital between October 2000- February 2002, were included into the study. Captopril was administered in 48 patients 8 hours and an hour before CA (Captopril group). Remaining 32 patients had no captopril treatment (Control group). There were no significant differences between the groups by means of clinical and biochemical parameters. The levels of serum creatinine and serum urea and creatinine clearance in 24 hours urine were measured before CA application and 48 hours after the procedure. RESULTS: Five patients (8.3%) in the Captopril group and 1 patient (3%) in Control group developed CIN and this difference was statistically significant (p=0.02). CONCLUSION: Captopril is a risk factor for development of contrast media induced nephropathy.