Mild Kidney Dysfunction Research Articles

Plasma Levels of Uric Acid, Urea and Creatinine in Diabetics Who Visit the Clinical Analysis Laboratory (CAn-Lab) at Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.

Diabetes mellitus is one of the most common metabolic diseases worldwide. This metabolic disorder contributes greatly to the significant proportion of the burden of renal damage and dysfunction. The aim of the study was to investigate the renal function of the diabetic patients who visit the Clinical Analysis Laboratory (CAn-Lab) at the Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana. Demographic data as well as medical history were obtained through the administration of a questionnaire. Anthro-pometric measurements were taken and blood samples were analysed for glucose, uric acid, urea and creatinine. Data collected were analysed using SPSS version 16.0. A total of 34 diabetic patients, aged from 40-77 y were recruited, 22 (64.7%) of them were males with mean age of 57.40 ± 11.8 y (±SD), while 12 (35.3%) were females with mean age of 58.17 ± 7.47 y. There was a statistically significant difference between the mean duration of the disease, as the females had longer duration, 12.50 ± 6.95 y, as compared to 7.32 ± 4.48 y in males (p=0.033). The mean plasma creatinine level in the females was 84.17 ± 54.73 μmol/l. In the diabetic population, there was a positive correlation between age and plasma creatinine level, (r=0.375, p=0.029). In the female diabetics, there was a positive correlation between fasting blood sugar (FBS) and the measured metabolic end products (r>0.5, p<0.05), a positive correlation between body mass index (BMI) and uric acid (r=0.576, p=0.005) and a positive correlation between BMI and FBS (r= 0.625, p= 0.030). Our results on the parameters measured; show that the diabetic population was experiencing mild kidney dysfunction, compared to non-diabetic controls.

Level of galectin-3 and ST2 in ischemic chronic heart failure depending on the functional state of kidneys

Aim. The aim of the study was to investigate the characteristics of level markers of fibrosis galectin-3 (Gal-3), ST2 in patients with ischemic chronic heart failure (CHF) depending on the glomerular filtration rate.Methods and results. The study involved 113 patients with ischemic CHF. Depending on glomerular filtration patients were divided into 3 groups: those with normal function (≥90 ml/min/1.73 m2), mild (60-89 ml/min/1.73 m2) and moderate (30-59 ml/min/1.73 m2) kidney dysfunction. It is established that in patients with ischemic CHF with moderate renal dysfunction level of Gal-3 is higher as compared with mild dysfunction and normal renal function (7.1 % and 53.6 %, respectively). The level of ST2 had about the same value in the groups of moderate and mild dysfunction, but was higher than in the group of normal renal function (11.7 % and 12.1 %, respectively). In the group of patients with ischemic CHF with moderate renal dysfunction correlation analysis showing that only Gal-3 revealed interrelationships of NT-proBNP (r=0,77; p=0,04), cystatin C (r=0,91; p=0.002).Conclusion. In patients with ischemic CHF with normal renal function revealed a strong correlation interrelationships between Gal-3, ST2 and the parameters of the structural remodeling of the left ventricle.

Apoptotic cell administration is detrimental in murine renal ischaemia reperfusion injury.

BackgroundAcute kidney injury induced by renal ischaemia reperfusion injury (IRI) is characterised by renal failure, acute tubular necrosis (ATN), inflammation and microvascular congestion. The administration of apoptotic cells (ACs) has been shown to reduce inflammation in various organs including the liver and kidney. This study explored whether AC administration prior to the induction of renal IRI was protective.FindingsRenal IRI was induced in Balb/c mice by clamping the renal blood vessels for either 20, 24 or 25 minutes to induce mild, moderate or severe kidney dysfunction respectively. Renal function and injury was determined 24 hours following IRI by measurement of plasma creatinine and ATN scoring respectively. ACs were generated from Balb/c thymocytes and classified as either predominantly early or late apoptotic by Annexin-V and propidium iodide staining. Early AC administration prior to severe IRI had no influence on plasma creatinine or ATN severity. In contrast, administration of early or late ACs significantly worsened renal function in mice with mild or moderate renal IRI, respectively, compared to PBS treated controls, though ATN scores were comparable. Despite ACs exerting pro-coagulant effects, the worsening of renal function was not secondary to increased microvascular congestion, inferred by fibrin and platelet (CD41) deposition, or inflammation, assessed by neutrophil infiltration.ConclusionsDespite the AC-derived protection demonstrated in other organs, ACs do not protect mice from renal IRI. ACs may in fact further impair renal function depending on injury severity. These data suggest that AC-derived protection is not translationally relevant for patients with acute kidney injury induced by ischaemic injury.Electronic supplementary materialThe online version of this article (doi:10.1186/s12950-014-0031-6) contains supplementary material, which is available to authorized users.

Safety, efficacy and renal effect of febuxostat in patients with moderate-to-severe kidney dysfunction.

Hyperuricemia (HU) is common in patients with chronic kidney disease (CKD), and accumulating evidence suggests it has a pathogenic role in the progression of the disease. However, a major challenge in treating patients with HU is the adverse effects caused by urate-lowering drugs used to treat CKD. Because of these untoward effects, doses need to be reduced, which leads to suboptimal efficacy. Febuxostat has been shown to be highly efficacious in reducing serum uric acid (sUA) and is well tolerated in patients with mild kidney dysfunction. However, its safety and efficacy have not been well studied in more advanced cases of CKD. We studied the safety and efficacy of escalating doses of febuxostat over a 24-week period in 70 patients with CKD stages 3b, 4 and 5, and we also observed the changes in blood pressure, estimated glomerular filtration rate (eGFR) and proteinuria following the reduction of sUA. Drug-related adverse events (AEs) occurred in only 5 out of 70 patients. All but one of the events were mild, and all five patients fully recovered. By 24 weeks, the reduction of sUA levels was >40% in CKD stage 3b and >50% in CKD stages 4 and 5. More than 70% of patients achieved target sUA levels of 6 mg dl(-1) or less. Multivariate analysis showed that a greater reduction in sUA with febuxostat was associated with an increase in eGFR and a tendency toward decreased proteinuria. Febuxostat was safe and efficacious in the treatment of CKD stages 3b-5.

Statins Against Drug-Induced Nephrotoxicity

Drug-induced nephrotoxicity (DIN) accounts for up to 60% of hospital acquired acute kidney injury with considerable morbidity and mortality. Several efforts have been made to reduce drug-induced nephrotoxicity; however, DIN remains a matter of concern. Statins with their antioxidant, anti-inflammatory and anti-apoptotic effects may have the potential to protect kidney against DIN. The present review evaluated all of the available in vitro and in vivo studies that examined the use of statins as renoprotective agents against nephrotoxic drugs. Materials for this review were obtained by searching Medline, PubMed, Scopus, Cochrane central register of controlled trials, and Cochrane database of systematic reviews. Key words used as search terms included "statin", "3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, "HMG-CoA reductase inhibitors", "nephroprotective", "renoprotective", "drug-induced renal diseases", "drug-induced nephrotoxicity", "drug-induced renal toxicity", "drug-induced nephropathy", "drug-induced renal side effects", and "contrast-induced nephropathy". This search was performed without time limitation. Only English language articles were included in this review. This review concluded that chronic statin user may be less prone to contrast-induced nephropathy (CIN) compared with statin non-users. Short-term high dose statin administration may also reduce the incidence of CIN in statin naïve patients. This renoprotective effect of statins against CIN is seen in low risk patients with normal kidney function or mild kidney dysfunction, but probably not in patients with moderate to severe renal dysfunction. Based on available animal data, statins may protect kidney against gentamicin-, cisplatin- and cyclosporine-induced nephrotoxicity, however, theses animal results have not yet been confirmed by human data. This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.

Prevalence of acute kidney injury in intensive care units: The “COrte de prevalencia de disFunción RenAl y DEpuración en críticos” point-prevalence multicenter study

PurposeThis study aimed to measure the point prevalence of kidney dysfunction (KD) in the intensive care setting. Materials and MethodsA point-prevalence, single-day, prospective study was conducted. Of 919 patients present in 42 Intensive care units (ICUs) for 2 specific days (September 2009 and March 2010), 832 cases were included. Mild KD was defined as a measured creatinine clearance of 90 to 60 mL min−1 1.73 m−2, and severe KD was defined as a creatinine clearance less than 60 mL min−1 1.73 m−2. ResultsPrevalence of mild KD was 15.9/100 patients/d (13.5-18.5), and severe KD was 42.4/100 patients/d (39.1-45.8). We considered as having a low probability of experiencing KD those patients without chronic kidney disease, acute kidney injury network stage 0, and a serum creatinine less than 1.2 mg/dL, but among them (557 patients), 18.1% (15.2%-21.6%) had mild KD and 24.2% (20.9%-28%) had severe KD.ICU mortality was 10.6% (7.81%-14.4%) for patients without dysfunction, 16.6% (11.2%-24%) for patients with mild KD, and 29.7% (25.2%-34.7%; P < .001) for patients with severe KD, with a relative risk for severe KD vs no KD of 2.54 (1.90-3.40).In 54.3% patients, at least 1 renal insult was reported. One nephrotoxic drug was administered to 34.4% and 2 or more to 14.9% patients, with a lower frequency among those with chronic kidney disease (30.6% vs 50.8%; P < .05). ConclusionsEach day of study, more that half of the patients admitted to the ICU showed some derangement in kidney function. More than 25% of patients not fulfilling the KD criteria by serum creatinine or acute kidney injury network showed, in fact, a severe KD, and this finding was associated with higher mortality. More than 50% of the patients admitted to the ICU were subjected to at least 1 renal insult.

Hyperuricemia may be related to contrast-induced nephropathy after percutaneous coronary intervention

Dear Editor, We have read with great interest the recently published article titled, “The relationship between hyperuricemia and the risk of contrast-induced nephropathy after percutaneous coronary intervention in patients with relatively normal serum creatinine”, by Yong Liu et al. (1). In that well-presented paper, the authors investigated the value of hyperuricemia in predicting the risk of contrast-induced nephropathy (CIN) in patients with relatively normal serum creatinine who are undergoing CIN. They demonstrated that CIN might develop in patients with normal creatinine levels. Hyperuricemia is a significant and independent predictor of CIN after percutaneous coronary intervention (PCI) and results in significantly increased in-hospital mortality and CIN incidence, which requires renal replacement therapy after PCI. Thus, despite having normal baseline creatinine levels, patients with hyperuricemia, an intra-aortic balloon pump, emergent PCI, or older age should receive more comprehensive renal prophylaxis to reduce the occurrence of CIN. CIN has been recognized as a serious complication of PCI and may cause increased morbidity and mortality. CIN is one of the most important reasons for hospital-acquired renal failure and can cause prolonged hospitalization, increased cost and incidence of renal and cardiovascular events, and mortality. Elderly patients have a higher risk of CIN because of decreased renal reserve. In addition, some factors, such as an estimated glomerular filtration rate (eGFR) of 200 mL have been identified as risk factors for CIN after PCI (2). Additionally, alcohol consumption and the arterial blood pressure level before contrast exposure may be associated with CIN. Hypertriglyceridemia, metabolic syndrome, an impaired fasting glucose level, and multivessel disease may also be associated with a higher incidence of CIN (3). Some medications, including renin-angiotensin-aldosterone system medications, may also be related to CIN (4). It would have been interesting for the authors to provide information about these factors in this study. Finally, the authors used the Cockcroft-Gault equation to measure eGFR. The Cockcroft-Gault equation may underestimate eGFR in younger age groups and may overestimate eGFR in older individuals compared with the Modification of Diet in Renal Disease (MDRD) formula (5). Although the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently published an equation for eGFR using the same variables (serum creatinine level, age, sex, and race) as the MDRD formula, the CKD-EPI equation more accurately categorized individuals with respect to long-term clinical risk (6). In addition, even mild chronic kidney dysfunction, defined as an eGFR <90 mL/min, and dehydration were risk factors for CIN. For this reason, it may be useful to include the results using the CKD-EPI equation and accounting for mild chronic kidney dysfunction and dehydration as risk factors for CIN.

Neutrophil-to-Lymphocyte Ratio May Predict Contrast-Induced Nephropathy

We read with interest the article ‘‘Neutrophil-to-lymphocyte ratio predicts contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention’’ by Kaya et al. They investigated the relationship between neutrophilto-lymphocyte (N/L) ratio and contrast-induced nephropathy (CIN) in patients with ST-segment elevation myocardial infarction (STEMI). They demonstrated a relationship between N/L ratio and CIN development in patients with STEMI undergoing primary percutaneous coronary intervention. They also demonstrated an independent association between N/L ratio and CIN development in patients with STEMI undergoing coronary angiography. A full blood count is a cheap method that provides information about red and white cells, platelets, count and dimensions of subgroups of cells, and parameters like red cell distribution width, platelet cell distribution width, and mean platelet volume. Routine peripheral blood counts may be useful in risk stratification of patients with CIN. The white blood cell (WBC) count is one of the inflammatory biomarkers. Although the WBC may be within the normal range, subtypes of WBC, as expressed by the N/L ratio, may predict all-cause mortality. The N/L ratio is an easy, cheap, noninvasive, and widely available laboratory marker used to evaluate systemic inflammation. The N/L ratio has received increased attention due to its role as an independent prognostic factor for coronary artery disease (CAD), hypertension, chronic kidney disease, diabetes, heart failure, cerebrovascular disease, peripheral arterial disease, and malignancy. It can also be affected by atherosclerotic risk factors such as smoking, alcohol consumption, hypercholesterolemia, metabolic syndrome, nonalcoholic liver disease, abnormal thyroid function tests, and older age. Furthermore, acute bacterial and viral infections may change the N/L ratio. Additionally, medications such as antihypertensive therapy including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, b-blockers, and statins may influence the N/L ratio. It would be useful and the results might be different, if the authors described these factors. The CIN is a serious complication of PCI. The CIN is one of the most important reasons of hospital-acquired renal failure. The CIN can cause prolonged hospitalization, increased cost and incidence of renal and cardiovascular events, and mortality. Elderly patients are at greater risk of CIN because of decreased renal reserve. In addition, some factors like glomerular filtration rate (GFR) 200 mL were identified as risk factors for CIN after PCI. Alcohol consumption and arterial blood pressure before contrast exposure may be associated with increased risk of CIN in patients. Hypertriglyceridemia, metabolic syndrome, impaired fasting glucose, and multivessel disease may also be associated with the higher incidence of CIN. Also, some medications including a renin–angiotensin–aldosterone system medications may be related to CIN. Finally, they used the Cockcroft-Gault equation to calculate the GFR. The modification of diet in renal disease (MDRD) is another method for calculating the GFR. However, the Cockcroft-Gault equation may estimate lower GFR in younger age groups compared with the MDRD formula, but it can measure higher GFR in older individuals compared with the MDRD formula. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently published an equation for GFR using the same variables (serum creatinine level, age, sex, and race) as the MDRD formula. However, the CKD-EPI equation more accurately categorized individuals with respect to longterm clinical risk of incident end-stage renal disease, all-cause mortality, coronary heart disease, and stroke compared with the MDRD formula. In addition, even mild chronic kidney dysfunction such as a GFR <90 mL/min and dehydration was also a risk factor for CIN. In conclusion, these findings will enlighten further studies about N/L ratio as a surrogate marker of risk stratification in

β-Trace Protein

β-Trace protein, also known as Lipocalin type prostaglandin D synthase, is a low-molecular mass glycoprotein (between 23,000 and 29,000 Da depending on the degree of glycosylation) that converts prostaglandin H2 into prostaglandin D2. β-Trace protein was initially isolated from cerebrospinal fluid and served as a marker of cerebrospinal fluid leakage; however, its cDNA and gene have been isolated in numerous human body tissues, including central nervous system, retina, melanocytes, heart, and male genital organs. In recent years, β-trace protein has emerged as a promising novel endogenous marker of GFR, representing a more sensitive marker for mild kidney dysfunction than serum creatinine. In this regard, β-trace protein has been proposed as an alternative marker to Cystatin C for measuring kidney function. Beyond its role for estimating renal function, β-trace protein is also emerging as a novel biomarker in cardiovascular risk. It has been associated with several cardiovascular disorders, playing a potential role for prognostic stratification in patients with acutely decompensated heart failure and acute coronary syndromes and being advocated as a novel marker for cardiovascular risk prediction.

CKD, Plasma Lipids, and Common Carotid Intima-Media Thickness

Altered levels of atherogenic lipoproteins have been shown to be common in mild kidney dysfunction. This study sought to determine the associations between plasma lipids (including LDL particle distribution) and subclinical atherosclerosis measured by the common carotid intima-media thickness (IMT) across levels of estimated GFR (eGFR) and to assess whether inflammation modifies these associations. Cross-sectional analyses of 6572 participants in the Multi-Ethnic Study of Atherosclerosis enrolled from 2000 to 2002 were performed. CKD, defined as eGFR <60 ml/min per 1.73 m(2), was present in 853 individuals (13.0%). Associations of total cholesterol and LDL cholesterol (LDL-C) with IMT were J shaped, particularly among participants with CKD (P value for interaction, P=0.01). HDL cholesterol (HDL-C) and small-dense LDL-C were consistently and linearly associated with IMT across levels of eGFR. The results showed differences in IMT of -21.41 (95% confidence interval, -41.00, -1.57) in eGFR ≥60 and -58.49 (-126.61, 9.63) in eGFR <60 per unit difference in log-transformed HDL-C, and 4.83 (3.16, 6.50) in eGFR ≥60 and 7.48 (1.45, 13.50) in eGFR <60 per 100 nmol/L difference in small-dense LDL. Among participants with CKD, inflammation significantly modified the associations of total cholesterol and LDL-C with IMT (P values for interaction, P<0.01 and P<0.001, respectively). Compared with total cholesterol and LDL-C, abnormalities in HDL-C and small-dense LDL-C are more strongly and consistently associated with subclinical atherosclerosis in CKD. Inflammation modifies the association between total cholesterol and LDL-C with IMT.

Fibrinogen, Hematocrit, and Platelets in Mild Kidney Dysfunction and the Role of Uric Acid: An Italian Male Population Study

Fibrinogen, Hematocrit, and Platelets in Mild Kidney Dysfunction and the Role of Uric Acid: An Italian Male Population Study

Glomeruloid haemangiomas associated with generalized oedema in a patient with atypical POEMS syndrome.

A 55-year-old woman was admitted for evaluation of progressive generalized oedema and mild kidney dysfunction (serum creatinine 1.12 mg/dL; blood urea nitrogen 45 mg/dL). On admission, generalized oedema, transudative pleural effusion, collapsed inferior vena cava and low fractional excretion of sodium (0.14%) suggested severe volume depletion due to plasma extravasation; however, its aetiology could not be attributed to decreased colloid osmotic pressure (serum total protein 6.4 g/dL). Further examination of the patient revealed hepatosplenomegaly, slowing of nerve conduction velocities, albuminocytological dissociation in the cerebrospinal fluid, and multiple cherry-red papules on the neck and chest (Figure 1). These features were suggestive of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome, also called osteosclerotic myeloma or Crow–Fukase syndrome. However, this case did not entirely fulfil the diagnostic criteria because monoclonal plasma cell disorders were not detected [1]. The skin biopsy revealed lesions consistent with glomeruloid haemangiomas (Figure 2), which is considered to be a specific marker for POEMS syndrome [2]. Furthermore, the serum level of vascular endothelial growth factor (VEGF), which is involved in the pathogenesis of POEMS syndrome [1], was extremely elevated to 16 300 pg/mL. These findings led us to make a diagnosis of atypical POEMS syndrome and speculate that microvascular hyperpermeability induced by excess VEGF resulted in generalized oedema and effusions associated with severe volume depletion [3,4]. In patients with oedema and effusions of unknown cause, one should consider the possibility of disorders associated with VEGF overproduction including POEMS syndrome. Fig. 1 Multiple eruptive cherry-red papules on the neck. Fig. 2 (a) Dermal lesions showing vascular structures with capillary loops, resembling renal glomeruli (haematoxylin–eosin stain). (b) Endothelial cells stained for CD 31.

5 ASSOCIATION BETWEEN RENAL FUNCTION AND CANCER INCIDENCE IN A LARGE, POPULATION-BASED COHORT

You have accessJournal of UrologyGeneral & Epidemiological Trends & Socioeconomics: Evidence-based Medicine & Outcomes I1 Apr 20105 ASSOCIATION BETWEEN RENAL FUNCTION AND CANCER INCIDENCE IN A LARGE, POPULATION-BASED COHORT Anders Christensson, Caroline Savage, Angel Cronin, M. Frank O'Brien, Peter Nilsson, Jonas Manjer, Andrew Vickers, Paul Russo, and Hans Lilja Anders ChristenssonAnders Christensson Malmo, Sweden More articles by this author , Caroline SavageCaroline Savage New York, NY More articles by this author , Angel CroninAngel Cronin New York, NY More articles by this author , M. Frank O'BrienM. Frank O'Brien New York, NY More articles by this author , Peter NilssonPeter Nilsson Malmo, Sweden More articles by this author , Jonas ManjerJonas Manjer Malmo, Sweden More articles by this author , Andrew VickersAndrew Vickers New York, NY More articles by this author , Paul RussoPaul Russo New York, NY More articles by this author , and Hans LiljaHans Lilja New York, NY More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.048AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES There are reports that impaired renal function increases the risk of several types of cancer. We evaluated whether moderately impaired renal function influenced risk of developing cancer in a large, population-based cohort. METHODS We used data from Malmö Preventative Medicine Project, a large, population-based cohort (74% participation) containing demographic data and blood samples collected from 33,346 persons aged 33-50 during 1974-86 in Malmö, Sweden. Incident cancers were identified from the Swedish Cancer Registry, updated to 12/31/2006. Glomerular filtration rate (GFR) was estimated using the Modified Diet and Renal Disease formula. Patients were classified as having normal kidney function (GFR≥90 mL/min/1.73m2), mild kidney disease (GFR 60-89 mL/min/1.73m2) or moderate kidney dysfunction (GFR<60 mL/min/1.73m2). We calculated the risk of being diagnosed with cancer using the cumulative incidence function in the presence of a competing risk (death without cancer diagnosis). RESULTS 7,577 patients were diagnosed with cancer and 4,588 died with no cancer diagnosis. The median age at baseline was 47 (IQR 40, 49). 22,183 (69%) participants were male; prostate cancer was the most common cancer diagnosis (n=1,579). Most subjects had mild kidney disease (n=22,336; 70%); 3% (n=1,015) had moderate renal dysfunction and 27% (n=8,621) had normal renal function. The cumulative incidence of cancer was highest for those with the most severely impaired renal function: 20-year cumulative incidence of cancer was 17.3% (95% CI: 15.1%, 19.8%) for those with GFR<60 versus 13.5% (95% CI: 13.0%, 13.9%) and 11.6% (95% CI: 10.9%, 12.3%) for those with GFR 60-89, and ≥90 mL/min/1.73m2, respectively (p<0.001; Figure). This association remained significant after adjustment for age (p<0.001). CONCLUSIONS The mechanism by which cancer risk is associated with renal impairment is unclear but could be due to changes in the accumulation of low molecular mass substances due to decreased GFR. It will be critical to determine which types of cancer are elevated with renal dysfunction. © 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e2-e3 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Anders Christensson Malmo, Sweden More articles by this author Caroline Savage New York, NY More articles by this author Angel Cronin New York, NY More articles by this author M. Frank O'Brien New York, NY More articles by this author Peter Nilsson Malmo, Sweden More articles by this author Jonas Manjer Malmo, Sweden More articles by this author Andrew Vickers New York, NY More articles by this author Paul Russo New York, NY More articles by this author Hans Lilja New York, NY More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Association between serum uric acid and early kidney damage in middle-aged and elderly

To investigate the association between serum uric acid (UA) and early kidney damage and the prevalence of early kidney damage [89 >or= GFR >or= 60 ml * min(-1) * (1.73m(2))(-1)] in the middle-aged and elders with normal serum creatinine. A survey of cardiovascular risk factors, including serum UA and estimated glomerular filtration rate (eGFR) [according to MDRD (modification of diet in renal disease) equation], was carried out in a local general population of Chengdu. A total of 1023 subjects with normal serum creatinine [mean age: (63 +/- 6) years; male: female = 52.7%: 47.3%] were recruited by random sampling method. The subjects were divided into 4 groups (A, B, C, D) according to the quartiles of serum UA levels (A: UA < 282 micromol/L, B: 282 micromol/L <or= UA < 331 micromol/L, C: 331 micromol/L <or= UA < 379 micromol/L, D:UA >or= 379 micromol/L). In the group, the prevalence of early kidney damage was 28.1% (men: 35.8% > women: 19.5%, P < 0.01). In men and women, serum UA and mild kidney dysfunction were negatively correlated, and the prevalence of early kidney damage significantly increased with the elevated level of serum UA. The prevalence of early kidney damage was higher in men than women (P < 0.01). According to the logistic regression analysis adjusting for age, gender, waist, body mass index, triglyceride, HDL-C, total cholesterol, history of hypertension and diabetes type 2, the odds ratio of the prevalence of early kidney damage were 1.0 [B: 1.740 (P = 0.151), C: 3.599 (P = 0.01) and D: 5.488 (P < 0.01) respectively]. In the middle-aged and elders with normal serum creatinine, serum UA and eGFR are negatively correlated. And serum UA level is independently associated with early kidney damage.

Fibrinogen, Hematocrit, Platelets in Mild Kidney Dysfunction and the Role of Uric Acid: An Italian Male Population Study

To examine the relationship between some blood parameters and mild kidney dysfunction. A total of 719 Italian men aged 42 to 74 years from a population-based survey carried out in the town of Bollate (Milan). General linear models were used to examine the variations in plasma fibrinogen, hematocrit, platelet counts, mean platelet volume, and uric acid across levels of kidney function (estimated on the basis of glomerular filtration rate [GFR]), adjusting for age, education, smoking, alcohol consumption, physical activity (evaluated as TV watching, engaging in sport practice, and walking/cycling), waist circumference, arm muscle area, high-density lipoprotein (HDL)-cholesterol, triglycerides, hypertension, diabetes, cardiovascular disease history, and nonsteroid anti-inflammatory, diuretic, and antihypertensive drug use. Plasma fibrinogen and hematocrit levels increased, and platelet counts and mean platelet volume significantly decreased as GFR fell to <80 or <70 mL/min per 1.73 m(2); stratified analysis revealed an association with serum uric acid levels. Alterations compatible with an increased cardiovascular risk were particularly evident among the participants with higher uric acid levels, whereas those indicative of platelet dysfunction were found among participants with lower levels. Parameters affecting hemostasis and blood viscosity are altered when kidney function is only slightly reduced, and the patterns of these relationships seem to be influenced by the levels of serum uric acid, whose easy and inexpensive measurement could have prognostic value.

Effect of chronic kidney disease on individual and population medical expenditures in the Japanese population

Chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease (CVD), and may also lead to an increase in medical expenditures. The effect of CKD on individual and population medical expenditures was examined in a Japanese cohort study. The participants included 4026 Japanese National Health Insurance beneficiaries aged 40-74 years living in one city, who had no history of major CVD. They were classified into three categories according to their glomerular filtration rate (GFR) at the baseline survey, and their total medical expenditures were followed-up for 3 years. The arithmetic and geometric means of the cumulative medical expenditures were calculated for each category. The geometric mean was also expressed after adjusting for several confounding factors using analysis of covariance. The CKD-related medical expenditures attributable to the participants with mild (60 < or = GFR < 90) or moderate (30 < or = GFR < 60) kidney dysfunction were compared with those of participants with normal (GFR > or = 90) kidney function. There was a negative correlation between the GFR category and the arithmetic and geometric means of personal medical expenditures (adjusted geometric mean: GFR > or = 90, 167,879 yen; 60 < or = GFR < 90, 210,660 yen; and 30 < or = GFR < 60, 330,050 yen). The CKD-related medical expenditures accounted for 11.5 and 6.5% of the total medical expenditures for the participants with mild and moderate kidney dysfunction, respectively. The prevention of mild CKD is very important for containing medical expenditures. Appropriate strategies, such as regular creatinine measurement, are needed for early detection of CKD.

Mild chronic kidney dysfunction and treatment strategies for stable coronary artery disease

Our objective was to evaluate the association of chronic kidney dysfunction in patients with multivessel chronic coronary artery disease, preserved left ventricular function, and the possible interaction between received treatment and cardiovascular events. The glomerular filtration rate was determined at baseline on 611 patients who were randomized into three treatment groups: medical treatment, percutaneous coronary intervention, and coronary artery bypass surgery. Incidence of myocardial infarction, angina requiring a new revascularization procedure, and death were analyzed during 5 years in each group. Of 611 patients, 112 (18%) were classified as having normal renal function, 349 (57%) were classified as having mild dysfunction, and 150 (25%) were classified as having moderate dysfunction. There were significant differences among the cumulative overall mortality curves among the three renal function groups. Death was observed more frequently in the moderate dysfunction group than the other two groups (P < .001). Interestingly, in patients with mild chronic kidney dysfunction, we observed that coronary artery bypass treatment presented a statistically higher percentage of event-free survival and lower percentage of mortality than did percutaneous coronary intervention or medical treatment Our results confirm that coronary artery disease accompanied by chronic kidney dysfunction has a worse prognosis, regardless of the therapeutic strategy for coronary artery disease, when renal function is at least mildly impaired. Additionally, our data suggest that the different treatment strategies available for stable coronary artery disease may have differential beneficial effects according to the range of glomerular filtration rate strata.

Podagra, Uric Acid, and Cardiovascular Disease

Hippocrates would not be surprised to read that persons with gout had higher mortality, and particularly cardiovascular-related mortality, than persons without gout.1 On the other hand, he might well have been bemused, nearly 2500 years after he described the syndrome, that this made news. Article p 894 He should not have been. All too often, rigorous examination debunks conventional wisdom. Reassuringly, in this case, Drs Choi and Curhan found evidence to support long-standing belief. These dedicated and productive students of the pathogenesis and natural history of gout have here reported empiric data from the 51 000 male nonphysician health professionals who participated in the Health Professions Follow-up Study. From initial examination in 1986 through nearly 600 000 person-years of follow-up, 5825 deaths occurred, of which 2132 were cardiovascular and 1576 were ascribed to coronary heart disease, rates that attest to the generally good health of the group. The ≈6% prevalence of gout, at baseline, in men in their mid-50s, who mirror the general US population in body mass index, reported history of hypertension, hypercholesterolemia, and diabetes mellitus, was higher than expected. Interim biennial questionnaires identified incident cases of gout. Participants with gout were both more likely to report coronary heart disease (CHD) at baseline and, regardless of CHD status, more likely than gout-free persons to have cardiovascular disease (CVD) risk factors. Results were presented after stratification by CHD status at baseline. As expected, the incidence of all-cause and CHD mortality was much greater in those with than in those without prevalent CHD. The adjusted increased relative risk of those with gout (compared with those without) for all-cause, CVD, and CHD mortality was ≈25%. The single exception was a near doubling of increased relative risk of CHD mortality among those free of CHD at baseline. Neither the inclusion of incident …

Association between 25-hydroxyvitamin D deficiency and cardiovascular disease in type 2 diabetic patients with mild kidney dysfunction

A potentially modifiable and underestimated risk factor for cardiovascular disease (CVD) in subjects with kidney dysfunction is 25-hydroxyvitamin D deficiency, although the relationship between inadequate vitamin D status and manifest CVD in type 2 diabetic subjects with mild kidney impairment has not been extensively examined. We evaluated the relationship between serum 25-hydroxyvitamin D concentrations, baseline kidney function (estimated using the modification of diet in renal disease equation) and manifest CVD (myocardial infarction, angina, ischaemic stroke, coronary revascularization or carotid endarterectomy) among 462 consecutive patients with type 2 diabetes. In the whole population, the mean age was 62+/-7 years, 64% were men, 76.3% had hypertension and the mean estimated glomerular filtration rate (GFR) was 94+/-33 ml/min/1.73 m(2). Kidney function was strongly and inversely associated with CVD. In multivariate logistic regression analysis, there was an inverse association between serum 25-hydroxyvitamin D concentrations and prevalent CVD [odds ratio 0.95 (95% CI 0.92-0.98; P=0.001)] in the whole population independent of baseline kidney function and other known risk factors. Additionally, the association between serum 25-hydroxyvitamin concentrations and CVD [odds ratio 0.97 (95% CI 0.94-0.99; P=0.045)] remained statistically significant in participants in the lowest estimated GFR tertile after adjustment for potential confounders. Decreased 25-hydroxyvitamin D concentrations are independently associated with prevalent CVD in type 2 diabetic patients with mild kidney dysfunction.

One-Year Mortality in Critically Ill Patients by Severity of Kidney Dysfunction: A Population-Based Assessment

Kidney dysfunction in the intensive care unit (ICU) results in increased morbidity, mortality, and health care costs; however, long-term mortality has not been described across strata of severity in kidney dysfunction. The primary objective is to describe and assess factors associated with 1-year mortality in critically ill patients stratified by severity of kidney dysfunction during admission to the ICU. Kidney dysfunction is defined by peak serum creatinine values and stratified by: (1) no dysfunction (creatinine < 1.7 mg/dL [<150 micromol/L]), (2) mild dysfunction (creatinine, 1.7 to 3.4 mg/dL [150 to 299 micromol/L]), (3) moderate dysfunction (creatinine >or= 3.4 mg/dL [>or= 300 micromol/L]), (4) severe acute dysfunction requiring renal replacement therapy (acute renal failure), or (5) preexisting end-stage kidney disease. Population-based surveillance was of adult residents of the Calgary Health Region (population, 1 million) admitted to any multidisciplinary ICU and a cardiovascular surgery ICU from May 1, 1999, to April 30, 2002. Of 5,693 admissions, 62% were men, median age was 64.9 years (interquartile range, 50.6 to 74.5 years), and mean Acute Physiology and Chronic Health Evaluation (APACHE) II score was 24.9 +/- 8.7 (SD). Case fatality rates stratified by renal dysfunction were 17% (763 of 4,411), 47% (370 of 790), 48% (77 of 160), 64% (153 of 240), and 40% (37 of 92) for no, mild, and moderate dysfunction; severe acute renal failure; and end-stage kidney disease, respectively. By means of multivariate analysis, 1-year mortality was associated independently with advancing age, medical diagnosis, higher APACHE II score, and presence and severity of kidney dysfunction, although no difference was evident comparing those with mild to moderate dysfunction. End-stage kidney disease was not associated independently with 1-year mortality. Severity of kidney dysfunction in patients in the ICU is associated with an incremental increase in long-term mortality. Although patients classified with either mild or moderate kidney dysfunction had an increased risk for death, use of serum creatinine level alone was poor at discriminating long-term outcome, suggesting this measure alone should not be used for defining long-term prognosis.