Search

Retroperitoneal fibrosis (RPF), a disease with a severe outcome due to the complications it causes, can be associated with the processes of atherosclerosis with a massive and extensive fibrosis. In this paper we present a patient with retroperitoneal fibrosis in which we noticed estrogen receptors at the level of the periaortic fibrous tissue and we obtained a regression of this process under treatment with tamoxifen. [ABSTRACT FROM AUTHOR]

Introduction. Patients with breast cancer are treated after surgery by radiation and chemotherapy, potentially nephrotoxic. Patients with tumor estrogen-positive receptors are then treated with Tamoxifen with a possible renoprotective effect. Aim. To assess the effects of radiation and chemotherapy and of Tamoxifen on renal function in patients with breast cancer. Patients and Methods. We undertook a retrospective observational study on 76 breast cancer patients during 2002-2006. Depending on the estrogen receptor status of the tumour they were divided into group A (estrogen positive) with 50 patients, mean age: 57.64±9.34, treated with Tamoxifen and group B (estrogen negative), 26 patients, mean age: 50±9.83 who did not receive Tamoxifen. Both groups underwent surgical tumor resection, radiation and chemotherapy. The TNM status of the tumours was similar in both groups. (2/3 stages I and II and 1/3 stages III and IV). We followed up the GFR (MDRD 4) before radiation and chemotherapy and after this treatment. Thereafter, we followed up the GFR in group A at 1, 2 and 3 years of Tamoxifen and in group B at 1, 2 and 3 years of radiation and chemotherapy. Statistical analysis was performed using OpenEpi 2.3. software. Results. In group A the GFR declined not significantly after radiation and chemotherapy and at 1 year of Tamoxifen. At 2 ys of Tamoxifen, in the 18 surviving patients the GFR increased from 61.13±17.53 mL/min to 66.56±16.3 mL/min (p=0.009). At 3 y of Tamoxifen, the 12 surviving patients showed a preservation of the GFR. In group B the GFR declined from 88.14±14.63 mL/min (baseline) to 80.01±20.62 mL/min (p=0.0001) after radiation and chemotherapy. At 1 y after radiation and chemotherapy the GFR declined to 78.21±17.65 mL/min (p<0.001). At 2 y after radiation and chemotherapy in the 18 surviving patients the GFR declined to 70.94±13.39 mL/min (p<0.001 as compared to baseline). At 3 y in the 8 surviving patients the GFR declined to 61.36±9.17 mL/min (p=0.001 as compared to baseline). Conclusions. Patients undergoing treatment with Tamoxifen (group A) showed a preservation of their renal function. In patients undergoing radiation and chemotherapy alone (group B) we noticed a decline of the Glomerular Filtration Rate. [ABSTRACT FROM AUTHOR]

AIM: The renal and cerebral protective effects of pioglitazone were assessed in normoalbuminuric patients with type 2 diabetes mellitus (DM). METHODS: A total of 68 normoalbuminuric type 2 DM patients were enrolled in a one-year open-label randomized controlled trial: 34 patients (pioglitazone-metformin) vs. 34 patients (glimepiride-metformin). All patients were assessed concerning urinary albumin: creatinine ratio (UACR), urinary alpha1-microglobulin, urinary beta2-microglobulin, plasma asymmetric dymethyl-arginine (ADMA), GFR, hsC-reactive protein, fibrinogen, HbA1c; pulsatility index, resistance index in the internal carotid artery and middle cerebral artery, intima-media thickness in the common carotid artery; cerebrovascular reactivity was evaluated through the breath-holding test. RESULTS: At 1 year there were differences between groups regarding ADMA, urinary beta2-microglobulin, urinary alpha1-microglobulin, parameters of inflammation, serum creatinine, GFR, UACR, the cerebral haemodynamic indices. Significant correlations were found between alpha 1-microglobulin-UACR (R(2)=0.143; P=0.001) and GFR (R(2)=0.081; P=0.01); beta2-microglobulin-UACR (R(2)=0.241; P=0.0001) and GFR (R(2)=0.064; P=0.036); ADMA-GFR (R(2)=0.338; P=0.0001), parameters of inflammation, HbA1c, duration of DM, cerebral indices. There were no correlations between ADMA-UACR, urinary alpha1-microglobulin and beta2-microglobulin. CONCLUSION: Proximal tubule (PT) dysfunction precedes albuminuria and is dissociated from endothelial dysfunction in patients with type 2 DM. Pioglitazone delays PT dysfunction and improves cerebral vessels endothelial dysfunction in normoalbuminuric patients with type 2 DM. Key words: proximal tubule; endothelial dysfunction, albuminuria; pioglitazone. [ABSTRACT FROM AUTHOR]

Immune mechanisms play an important role in the pathogenesis of glomerulonephritis (GN), with autoimmunity being the main underlying pathogenetic process of both primary and secondary GN. We present three autoimmune diseases mediated by different autoimmune mechanisms: glomerulonephritis in vasculitis mediated by anti-neutrophil cytoplasmic antibodies (ANCAs), glomerulonephritis mediated by anti-glomerular basement membrane antibodies (anti-GBM antibodies), and immune complex-mediated glomerulonephritis. Some of these diseases represent a common clinical and histopathologic scenario, namely rapidly progressive crescentic glomerulonephritis. This is a severe illness requiring complex therapy, with the main role being played by therapy aimed at targeting immune mechanisms. In the absence of immune therapy, the crescents, the characteristic histopathologic lesions of this common presentation, progress toward fibrosis, which is accompanied by end-stage renal disease (ESRD). The fact that three diseases mediated by different immunopathologic mechanisms have a common clinical and histopathologic picture reveals the complexity of the relationship between immunopathologic mechanisms and their clinical expression. Whereas most glomerular diseases progress by a slow process of sclerosis and fibrosis, the glomerular diseases accompanied by glomerular crescent formation can progress, if untreated, in a couple of months into whole-nephron glomerulosclerosis and fibrosis. The outcome of different immune processes in a common clinical and histopathologic phenotype reveals the complexity of the relationship of the kidney with the immune system. The aim of this review is to present different immune processes that lead to a common clinical and histopathologic phenotype, such as rapidly progressive crescentic glomerulonephritis.

(1) Introduction and Aims: Little is known about the relationship between renal pathology and gallbladder pathology, although the two organs (the gallbladder and the right kidney) are in close proximity to one another. If a renal abscess disseminates, the gallbladder would be one of the secondary organs involved. As the bile provides a favorable environment for the development of pathogenic germs, it allows for the development of acute cholecystitis, even if calculi are absent, thus resulting in the development of acute acalculous cholecystitis. The aim of our study was to analyze the association between acute acalculous cholecystitis (AAC) and renal abscesses. (2) Methods: A department-wide retrospective cohort observational study including 67 patients with renal abscesses, with a mean age of 34.5+/-16.21 years and with five males and 62 females, was conducted. All of the patients were examined by an abdominal ultrasound. The lab tests included CBC with differential liver enzymes and serum bilirubin (in order to assess alterations in the liver function which can be associated with AAC) and serum creatinine (in order to assess the renal function). Blood culture and urine culture tests were also performed. (3) Results: Of the 67 patients with renal abscesses, eight (11.94%) were associated with acute cholecystitis: four cases (5.97%) of acalculous cholecystitis and four cases (5.97%) of calculous cholecystitis, two of which presented biliary sludge (acute micro-calculous cholecystitis). All four cases of acute acalculous cholecystitis presented with sepsis, and there was one case of septic shock at onset. We did not observe an impairment in renal function in the patients presenting with acute acalculous cholecystitis, and hepatic impairment was inconstant and moderate. All of the cases had a favorable outcome after a prompt initiation of intensive antibiotic therapy; both the renal abscess and the acute acalculous cholecystitis receded without further complications. (4) Conclusions: The association of acute acalculous cholecystitis with renal abscesses could be related to the possibility of germ dissemination from the infectious focus. In the case of a renal abscess, careful clinical, lab, and imaging exams of the gallbladder are recommended in order to ensure early therapeutic intervention in the event of an association with acute acalculous cholecystitis.

Aims: Long noncoding RNAs (lncRNAs) play key roles in the pathophysiology of DKD involving actions of microRNAs (miRNAs). The aims of the study were to establish the involvement of selected lncRNAs in the epigenetic mechanisms of podocyte damage and tubular injury in DKD of type 2 diabetes mellitus (DM) patients in relation to a particular miRNAs profile. Methods: A total of 136 patients with type 2 DM and 25 healthy subjects were assessed in a cross-sectional study concerning urinary albumin: creatinine ratio (UACR), eGFR, biomarkers of podocyte damage (synaptopodin, podocalyxin) and of proximal tubule (PT) dysfunction (Kidney injury molecule-1-KIM-1, N-acetyl-D-glucosaminidase-NAG), urinary lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), nuclear-enriched abundant transcript 1 (NEAT1), myocardial infarction-associated transcript (MIAT), taurine-upregulated gene 1 (TUG1), urinary miRNA21, 124, 93, 29a. Results: Multivariable regression analysis showed that urinary lncMALAT1 correlated directly with urinary synaptopodin, podocalyxin, KIM-1, NAG, miRNA21, 124, UACR, and negatively with eGFR, miRNA93, 29a (p<0.0001; R 2 =0.727); urinary lncNEAT1 correlated directly with synaptopodin, KIM-1, NAG, miRNA21, 124, and negatively with eGFR, miRNA93, 29a (p<0.0001; R 2 =0.702); urinary lncMIAT correlated directly with miRNA93 and 29a, eGFR (p<0.0001; R 2 =0.671) and negatively with synaptopodin, KIM-1, NAG, UACR, miRNA21, 124 (p<0.0001; R 2 =0.654); urinary lncTUG1 correlated directly with eGFR, miRNA93, 29a, and negatively with synaptopodin, podocalyxin, NAG, miRNA21, 124 (p<0.0001; R 2 =0.748). Conclusions: In patients with type 2 DM lncRNAs exert either deleterious or protective functions within glomeruli and PT. LncRNAs may contribute to DKD through modulating miRNAs expression and activities. This observation holds true independently of albuminuria and DKD stage., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Aim: An advanced proteomics platform for protein biomarker discovery in diabetic chronic kidney disease (DKD) was developed, validated and implemented. Materials & methods: Three Type 2 diabetes mellitus patients and three control subjects were enrolled. Urinary peptides were extracted, samples were analyzed on a hybrid LTQ-Orbitrap Velos Pro instrument. Raw data were searched using the SEQUEST algorithm and integrated into Proteome Discoverer platform. Results & discussion: Unique peptide sequences, resulted sequence coverage, scoring of peptide spectrum matches were reported to albuminuria and databases. Five proteins that can be associated with early DKD were found: apolipoprotein AI, neutrophil gelatinase-associated lipocalin, cytidine deaminase, S100-A8 and hemoglobin subunit delta. Conclusion: Urinary proteome analysis could be used to evaluate mechanisms of pathogenesis of DKD.

Aims: To evaluate if there is a link between inflammation (expressed by inflammatory cytokines) and the early stage of diabetic kidney disease (DKD), as shown by markers of podocyte damage and proximal tubular (PT) dysfunction., Methods: In this study were enrolled 117 type 2 DM patients (36-normoalbuminuria, 42-microalbuminuria, 39- macroalbuminuria), and 11 healthy subjects. Serum and urinary IL-1 alpha, IL-8, IL-18, urinary albumin:creatinine ratio (UACR), eGFR, biomarkers of podocyte damage (podocalyxin, synaptopodin, nephrin) and of PT dysfunction (KIM-1, NAG) were assessed., Results: In multivariable regression urinary Il-1 alpha correlated positively with podocalyxin and NAG (p < 0.0001, R 2 = 0.57); urinary IL-8 correlated directly with synaptopodin, NAG, nephrin, and KIM-1 (p < 0.0001, R 2  = 0.67); urinary IL-18 correlated directly with synaptopodin, NAG, and nephrin (p < 0.0001, R 2  = 0.59). Serum IL-1 alpha correlated positively with nephrin, synaptopodin, NAG (P < 0.0001, R 2  = 0.68); serum IL-8 correlated directly with synaptopodin and NAG (p < 0.0001, R 2  = 0.66); serum IL-18 correlated directly with NAG, KIM-1, and podocalyxin (p < 0.0001, R 2 =0.647)., Conclusions: Pro-inflammatory interleukins are associated with podocyte injury and PT dysfunction in early DKD. These could exert a key role in the pathogenesis of early DKD, before the development of albuminuria., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background : The association of vascular remodeling in the kidney and the brain with a particular microRNAs (miRNA) profile is not well studied. Methods : Seventy-six patients with Type 2 diabetes and 11 healthy subjects were assessed concerning urine albumin: creatinine ratio (UACR), biomarkers of podocyte injury and of proximal tubule (PT) dysfunction. MiRNA were quantified in blood and urine by a real-time PCR System. Cerebrovascular ultrasound measurements were performed in the carotid and middle cerebral arteries. Results : MiRNA21 and miRNA124 correlated positively with nephrin, podocalyxin, synaptopodin, urinary N-acetyl-D-glucosaminidase (NAG), urinary kidney-injury molecule-1 (KIM-1), UACR, and negatively with eGFR; miRNA125a, 126, 146a, 192 correlated negatively with nephrin, podocalyxin, synaptopodin, urinary NAG, urinary KIM-1, UACR, and directly with eGFR. Plasma miRNA-21 and miRNA192 correlated directly with cerebral hemodynamics parameters of atherosclerosis and arteriosclerosis. MiRNA-124, 125a, 126, 146a showed negative correlations with the same parameters. Conclusions : In Type 2 diabetes patients there is an association of vascular remodeling in the brain and the kidney with a specific miRNAs pattern. Cerebrovascular changes occur even in normoalbuminuric patients, with 'high-to-normal' levels of podocyte injury and PT dysfunction biomarkers. These phenomena may be explained by the variability of miRNA expression within the two organs in early DKD.

Aim: The involvement of proinflammatory interleukins (IL) in diabetic kidney disease of Type 2 diabetes mellitus (DM) patients was studied in relation to a particular miRNA profile. Materials & methods: A total of 117 patients with Type 2 DM and 11 controls were enrolled in a case series study. Serum and urinary ILs and miRNAs were assessed. Results: IL-1α correlated with miRNA21, 124, estimated glomerular filtration rate (eGFR) and negatively with miRNA125a and 192; IL-8 with miRNA21, 124, eGFR and negatively with miRNA125a, 126 and 146a; IL-18 with miRNA21, 124 and negatively with miRNA146a, 192, eGFR. Conclusion: There is an association between specific serum and urinary ILs and serum and urinary miRNAs profiles in the inflammatory response in Type 2 DM patients with diabetic kidney disease.

MicroRNAs (miRNAs) are short non-coding RNA species that are important post-transcriptional regulators of gene expression. The aim of the study was to establish a potential explanation of podocyte damage and proximal tubule (PT) dysfunction induced by deregulated miRNAs expression in the course of type 2 diabetes mellitus (DM). A total of 68 patients with type 2 DM and 11 healthy subjects were enrolled in a cross-sectional study and assessed concerning urinary albumin:creatinine ratio (UACR), urinary N -acetyl-β-D-glucosamininidase (NAG), urinary kidney injury molecule-1, urinary nephrin, podocalyxin, synaptopodin, estimated glomerular filtration rate (eGFR), urinary miRNA21, miRNA124, and miRNA192. In univariable regression analysis, miRNA21, miRNA124, and miRNA192 correlated with urinary nephrin, synaptopodin, podocalyxin, NAG, KIM-1, UACR, and eGFR. Multivariable regression analysis yielded models in which miRNA192 correlated with synaptopodin, uNAG, and eGFR (R 2 =0.902; P<0.0001), miRNA124 correlated with synaptopodin, uNAG, UACR, and eGFR (R 2 =0.881; P<0.0001), whereas miRNA21 correlated with podocalyxin, uNAG, UACR, and eGFR (R 2 =0.882; P<0.0001). Urinary miRNA192 expression was downregulated, while urinary miRNA21 and miRNA124 expressions were upregulated. In patients with type 2 DM, there is an association between podocyte injury and PT dysfunction, and miRNA excretion, even in the normoalbuminuria stage. This observation documents a potential role of the urinary profiles of miRNA21, miRNA124, and miRNA192 in early DN. Despite their variability across the segments of the nephron, urinary miRNAs may be considered as a reliable tool for the identification of novel biomarkers in order to characterize the genetic pattern of podocyte damage and PT dysfunction in early DN of type 2 DM., Competing Interests: Competing interests: None declared., (© American Federation for Medical Research (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Background: Diabetic nephropathy is a severe complication of Type 2 diabetes. Tubular lesions may play an important role in its early stages. The aim of our study was to determine if atorvastatin protects the podocytes and the proximal tubule in patients with Type 2 diabetes., Methods: A total of 63 patients with Type 2 diabetes completed this 6-months prospective pilot study. They were randomized to continue rosuvastatin therapy (control group) or to be administered an equipotent dose of atorvastatin (intervention group), and were assessed regarding urinary podocytes, podocyte-associated molecules, and biomarkers of proximal tubule dysfunction., Results: The patients from the intervention group presented a significant reduction in podocyturia (from 7.0 to 4.0 cells/ml, p < .05), urinary nephrin (from 1.7 to 1.3 mg/g, p < .001), urinary vascular endothelial growth factor (from 262.8 to 256.9, p < .01), urinary alpha 1 -microglobulin (from 10.0 to 8.3 mg/g, p < .01), urinary kidney injury molecule-1 (from 139.5 to 136.3 ng/g, p < .001), and urinary advanced glycation end-products (from 112.6 to 101.3 pg/ml, p < .001). Podocyturia correlated directly with the podocyte damage biomarkers, proximal tubule dysfunction biomarkers, albumin to creatinine ratio, and advanced glycation end-products, and inversely with the glomerular filtration rate., Conclusions: In patients with Type 2 diabetes, atorvastatin exerts favorable effects on the kidney. There is a correlation between the evolution of the podocytes and of the proximal tubule biomarkers, supporting the hypothesis that the glomerular changes parallel proximal tubule dysfunction in the early stages of diabetic nephropathy.

Introduction: Acute kidney injury (AKI) increases the risk of death in acute ischemic stroke (AIS) patients. Intravenous thrombolytic therapy (iv. rt-PA) seems to be the most effective treatment for AIS patients. The effects of AKI on iv. rt-PA treated AIS cases is less studied. Our paper addresses this issue., Methods: 45 consecutive stroke patients treated with iv. rt-PA (median age = 64 years; 29 male) and 59 age and sex matched controls not eligible for iv. rt-PA have been enrolled in our study. Subjects were followed-up until hospital release or death (median follow up time = 12 days)., Results: The prevalence of AKI did not differ between iv. rt-PA treated patients and controls (35.5% vs. 33.89%). In both groups, AKI was associated with increased in-hospital mortality: 50.0% vs. 3.4% p<0.0001 (in the rt-PA treated), and 45% vs. 30.7% (in controls). AKI iv. rt-PA treated patients had a significantly higher risk of in hospital mortality as compared to the no-AKI iv. rt-PA treated (HR = 15.2 (95%CI [1.87 to 124.24]; P = 0.011). In a Cox-multivariate model, the presence of AKI after iv. rt-PA remained a significant factor (HR = 8.354; p = 0.041) influencing the in-hospital mortality even after correction for other confounding factors. The independent predictors for AKI were: decreased eGFR baseline and elevated serum levels of uric acid at admission, (the model explained 60.2% of the AKI development)., Conclusions: The risk of AKI was increased in AIS patients. Thrombolysis itself did not increase the risk of AKI. In the iv. rt-PA patients, as compared to non-AKI, those which developed AKI had a higher rate of in-hospital mortality. The baseline eGFR and the serum uric acid at admission were independent predictors for AKI development in the iv. rt-PA treated AIS patients.

Aims: Detection of podocytes in the urine of patients with type 2 diabetes may indicate severe injury to the podocytes. In the course of type 2 diabetes the proximal tubule is involved in urinary albumin processing. We studied the significance of podocyturia in relation with proximal tubule dysfunction in type 2 diabetes., Methods: A total of 86 patients with type 2 diabetes (34-normoalbuminuria; 30-microalbuminuria; 22-macroalbuminuria) and 28 healthy subjects were enrolled in the study and assessed concerning urinary podocytes, podocyte-associated molecules, and biomarkers of proximal tubule dysfunction. Urinary podocytes were examined in cell cultures by utilizing monoclonal antibodies against podocalyxin and synaptopodin., Results: Podocytes were detected in the urine of 10% of the healthy controls, 24% of the normoalbuminuric, 40% of the microalbuminuric, and 82% of the macroalbuminuric patients. In multivariate logistic regression analysis, urinary podocytes correlated with urinary albumin:creatinine ratio (p=0.006), urinary nephrin/creat (p=0.001), urinary vascular endothelial growth factor/creat (p=0.001), urinary kidney injury molecule-1/creat (p=0.003), cystatin C (p=0.001), urinary advanced glycation end-products (p=0.002), eGFR (p=0.001)., Conclusions: In patients with type 2 diabetes podocyturia parallels proximal tubule dysfunction independently of albuminuria and renal function decline. Advanced glycation end-products may impact the podocytes and the proximal tubule., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Aim: The study assessed mRNA expression of podocyte-associated molecules in urinary sediments of patients with type 2 diabetes mellitus (DM) in relation to urinary podocytes, biomarkers of podocyte injury and of proximal tubule (PT) dysfunction., Methods: A total of 76 patients with type 2 DM and 20 healthy subjects were enrolled in a cross-sectional study, and assessed concerning urinary podocytes, urinary mRNA of podocyte-associated genes, urinary biomarkers of podocyte damage and of PT dysfunction., Results: We found significant differences between urinary mRNA of podocyte-associated molecules in relation with albuminuria stage. In multivariable regression analysis, urinary mRNA of nephrin, podocin, alpha-actinin-4, CD2-associated protein, glomerular epithelial protein 1 (GLEPP1), ADAM 10, and NFκB correlated directly with urinary podocytes, albuminuria, urinary alpha 1 -microglobulin, urinary kidney-injury molecule-1, nephrinuria, urinary vascular endothelial growth factor, urinary advanced glycation end-products (AGE), and indirectly with eGFR (p < 0.0001, R 2  = 0.808; p < 0.0001, R 2  = 0.825; p < 0.0001, R 2  = 0.805; p < 0.0001, R 2  = 0.663; p < 0.0001, R 2  = 0.726; p < 0.0001, R 2  = 0.720; p < 0.0001, R 2  = 0.724)., Conclusions: In patients with type 2 DM there is an association between urinary mRNA of podocyte-associated molecules, biomarkers of podocyte damage, and of PT dysfunction. GLEPP1, ADAM10, and NFκB may be considered additional candidate molecules indicative of early diabetic nephropathy. AGE could be involved in this association.

Objectives: Due to the shortage of living kidney donors and the current diabetes mellitus (DM) pandemic, studying the association of solitary kidney (SK) with DM is of paramount importance. Our aim was to assess the significance of the association between SK and DM., Materials and Methods: Eighty-four patients with SK and DM (group A), with a mean age of 62.46±12.72 years, of whom 36 were males and 48 were females, were enrolled in the study. The control group (group B) comprised 84 SK patients without DM of similar age and duration of existence of a SK. Mean age: 61.58±8.22 years, 23 males and 61 females. Serum creatinine, GFR (CKD-EPI), glycaemia, cholesterol, triglycerides, uric acid, proteinuria/24h, systolic blood pressure (SBP), diastolic blood pressure (DBP) and BMI were assessed., Results: The group of patients with SK and DM (group A) had a higher BMI (p=0.0007), higher metabolic abnormalities (higher glycaemia [p<0.001], triglycerides [p=0.0004], uric acid [p=0.019] and proteinuria/24h [p=0.006]). The study group also had a higher prevalence of hypertension (p=0.003) and coronary artery disease (p=0.031)., Conclusions: We found a higher value of proteinuria in the study group, significant metabolic abnormalities, as well as a higher prevalence of hypertension and coronary artery disease. However, no differences with respect to GFR were found, which could have significant implications for transplantation., (Copyright © 2016 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

The solitary kidney (SK) undergoes adaptive phenomena of hyperfunction and hyperfiltration. These secondary adaptive phenomena can make it more vulnerable to potentially nephrotoxic therapies. Adverse reactions of the kidneys to ciprofloxacin are rare, but sometimes severe. Therefore, our study sought to assess the reactions to ciprofloxacin of patients with solitary kidney (SK) and urinary tract infection (UTI) by means of urinary biomarkers. We studied 19 patients with SK and urinary tract infection (UTI) who had been administered a 7-day treatment with intravenous ciprofloxacin. Urinary N-acetyl-beta-d-glucosaminidase, alpha 1-microglobulin, and estimated glomerular filtration rate (eGFR) of these patients were measured at the initiation and at the end of treatment. In 47.37% patients NAG diminished under ciprofloxacin treatment. This observation has the significance of favourable evolution of the tubulointerstitial lesions caused by UTI and lack of nephrotoxic effects; 52.63% cases presented an increase of urinary NAG, a fact that suggests a nephrotoxic effect of ciprofloxacin. The evolution of urinary alpha 1-microglobulin was similar to that one of urinary NAG. Only one of three cases with chronic kidney disease (CKD) stage 5 presented acute kidney injury, associated with increase in the tubular markers. In spite of the high variability of the urinary biomarkers, UTI evolved favourably in these cases; eGFR increased in 16 out of 19 patients, a fact which is indicative of a good outcome of renal function, even in patients with elevated levels of the tubular damage biomarkers. This observation supports the hypothesis that eGFR may be dissociated from the biomarkers which assess tubular injury. In SK patients the occurrence of AKI is not frequent, although the urinary biomarkers rise in some patients treated with ciprofloxacin. This is related not only to the nephrotoxic effect of the drug, but probably to the association of other factors (allergy, individual susceptibility). In SK patients, renal tubular biomarkers, especially NAG, allow monitoring of tubular injury and impose caution in prescribing ciprofloxacin treatment, mainly to patients at risk. Ciprofloxacin is relatively safe regarding its nephrotoxicity, while caution is required in vulnerable patients., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Chronic glomerulonephritis is related to focus infection. Odontogenic foci are frequently involved in glomerulonephritis. The relationship with the odontogenic focus infection can be demonstrated by the occurrence or aggravation of the symptoms of glomerulonephritis: proteinuria, haematuria, high blood pressure and oedema. Glomerular impairment in glomerulonephritis occurs together with inflammatory alterations of the tubulointerstitial compartment that can play an important part in the evolution of the disease. Tubular urinary markers can indicate the activation of this compartment during an infection of a focus, an odontogenic focus in our study.The paper aims at demonstrating the relationship between the odontogenic focus infection and tubulointerstitial lesions, assessed by a tubular urinary marker, N-acetyl beta-D glucosaminidase (NAG).We investigated the urinary N-acetyl beta-D glucosaminidase of 20 patients with chronic glomerulonephritis who presented odontogenic focus infections, comparing them with patients with chronic glomerulonephritis without odontogenic foci and of 20 controls, clinically healthy persons.Chronic glomerulonephritis patients with odontogenic focus infection presented clearly increased values as compared to clinically healthy control persons of urinary N-acetyl beta-D glucosaminidase.These patients underwent surgical intervention on the odontogenic focus under antibacterial prophylactic treatment. In 75% cases, the values of N-acetyl beta-D glucosaminidase diminished, indicating the favourable effect of the treatment of the odontogenic focus on the tubulointerstitial compartment in patients with chronic glomerulonephritis. In 25% cases this therapeutic treatment was associated with an increase of the values of urinary N-acetyl beta-D glucosaminidase, expressing its unfavourable effect on chronic glomerulonephritis.Urinary N-acetyl beta-D glucosaminidase indicated an etiopathogenetic relationship between the odontogenic focus and the tubulointerstitial compartment in chronic glomerulonephritis.

Diabetic nephropathy (DN) is a frequent and severe complication of diabetes mellitus (DM). Its diagnosis in incipient stages may allow prompt interventions and an improved prognosis. Towards this aim, biomarkers for detecting early DN can be used. Microalbuminuria has been proven a remarkably useful biomarker, being used for diagnosis of DN, for assessing its associated condition-mainly cardiovascular ones-and for monitoring its progression. New researches are pointing that some of these biomarkers (i.e., glomerular, tubular, inflammation markers, and biomarkers of oxidative stress) precede albuminuria in some patients. However, their usefulness is widely debated in the literature and has not yet led to the validation of a new "gold standard" biomarker for the early diagnosis of DN. Currently, microalbuminuria is an important biomarker for both glomerular and tubular injury. Other glomerular biomarkers (transferrin and ceruloplasmin) are under evaluation. Tubular biomarkers in DN seem to be of a paramount importance in the early diagnosis of DN since tubular lesions occur early. Additionally, biomarkers of inflammation, oxidative stress, podocyte biomarkers, and vascular biomarkers have been employed for assessing early DN. The purpose of this review is to provide an overview of the current biomarkers used for the diagnosis of early DN.

Background: Diabetic atherosclerosis and microangiopathy parallel diabetic nephropathy. The aim of our study was to evaluate the pattern of endothelial dysfunction in two vascular territories, the kidney and the brain, both affected by diabetic vasculopathic complications. The endothelial variability was evaluated in relation to advanced glycation end-products modified peptides., Methods: Seventy patients with type 2 diabetes mellitus and 11 healthy subjects were assessed concerning urine albumin: creatinine ratio, plasma and urinary advanced glycation end-products, plasma asymmetric dimethyl-arginine, serum cystatin C, intima-media thickness in the common carotid arteries, the pulsatility index, the resistance index in the internal carotid arteries and the middle cerebral arteries, the cerebrovascular reactivity through the breath-holding test., Results: The breath-holding index correlated with asymmetric dimethyl-arginine (R²=0.151; p<0.001), plasma advanced glycation end-products (R²=0.173; p<0.001), C-reactive protein (R²=0.587; p<0.001), duration of diabetes mellitus (R²=0.146; p=0.001), cystatin C (R²=0.220; p<0.001), estimated glomerular filtration rate (R²=0.237; p=0.001). Urine albumin: creatinine ratio correlated with urinary advanced glycation end-products (R²=0.257; p<0.001), but not with asymmetric dimethyl-arginine (R²=0.029; p=0.147)., Conclusions: In type 2 diabetic patients endothelial dysfunction in the cerebral vessels appears to be dissociated from glomerular endothelial dysfunction in early diabetic nephropathy. Advanced glycation end-products could impact both the cerebral vessels and the glomerular endothelium., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Introduction and Aims: Balkan endemic nephropathy (BEN), a regional tubulointerstitial kidney disease encountered in South-Eastern Europe, with still undefined etiology and inexorable evolution towards end stage renal disease, raises the question of the relative contribution of family and environmental factors in its etiology. In order to evaluate the intervention of these factors, markers of tubular injury have been assessed, this lesion being considered an early renal involvement in BEN., Methods: The paper studies relatives of BEN patients currently included in dialysis programmes (for involvement of the family factor) and their neighbors (for involvement of environmental factors) and analyzes them with regard to tubular injury by means of tubular biomarkers (N-acetyl-beta-d-glucosaminidase-NAG and alpha-1-microglobulin), and albuminuria. At the same time, glomerular filtration rate (GFR) (CKD-EPI) was measured. It is considered that, in order to acquire the disease, one should have lived for 20 years in the BEN area. The relatives have been classified according to this criterion., Results: More evident tubular injury was found in the neighbors of BEN patients living for more than 20 years in the endemic area, which argues in favor of environmental factors. Higher levels of urinary alpha-1-microglobulin and albumin in relatives of BEN patients who had been living for more than 20 years in the area than in relatives with a residence under 20 years, plead for the same hypothesis. GFR was lower in persons who had been living for more than 20 years in the BEN area (neighbors and relatives)., Conclusions: Environmental factors could be more important in BEN than family factors.

Background: Advanced glycation end-products have been involved in the pathogenesis of proximal tubule dysfunction which characterizes diabetic tubulopathy., Methods: A total of 76 Type 2 diabetes mellitus patients and 28 healthy controls were evaluated concerning a potential association of glycated peptides with proximal tubule dysfunction by assessing urine albumin:creatinine ratio, urinary alpha1-microglobulin, urinary neutrophil gelatinase-associated lipocalin, plasma and urinary advanced glycation end-products, plasma asymmetric dimethyl-arginine, serum cystatin C. Fully automated chip-nanoelectrospray ionization and high-capacity ion trap multistage mass spectrometry characterized the urinary proteomic profile., Results: The urinary glycated proteins displayed a molecular weight of 15,121.4 Da in normoalbuminuric patients and of 30,180.4 Da in microalbuminuric patients. Urinary alpha1-microglobulin and neutrophil gelatinase-associated lipocalin correlated with urinary advanced glycation end-products (R(2)=0.586; R(2)=0.415), urine albumin: creatinine ratio (R(2)=0.292; R(2)=0.116), estimated glomerular filtration rate (R(2)=0.172; R(2)=0.135), serum cystatin C (R(2)=0.146; R(2)=0.129), but not with asymmetric dimethyl-arginine. In multivariable regression analysis models, the correlations for urinary alpha1-microglobulin and neutrophil gelatinase-associated lipocalin remained significant with urine albumin: creatinine ratio, urinary advanced glycation end-products, estimated glomerular filtration rate (P<0.0001, R(2)=0.674; P<0.0001, R(2)=0.551; P<0.0001, R(2)=0.482)., Conclusions: In patients with Type 2 diabetes mellitus urinary glycated peptides are associated with proximal tubule dysfunction. The proteomic patterns of urinary glycated peptides could differentiate normo- from microalbuminuric patients and may explain a potential relation between the size and the glycation status of glycated peptides, and the extent of proximal tubule dysfunction. The lack of correlation between parameters of endothelial dysfunction and proximal tubule dysfunction cannot exclude glomerular involvement in early diabetic nephropathy.

Pregnancy is a physiological condition that requires immune tolerance to the product of conception. Systemic lupus erythematosus (SLE) is a disease with well-represented immune mechanisms that disturb immune tolerance. The association of pregnancy with systemic lupus erythematosus creates a particular immune environment in which the immune tolerance specific of pregnancy is required to coexist with alterations of the immune system caused by SLE. The main role is played by T regulatory (Treg) cells, which attempt to regulate and adapt the immune system of the mother to the new conditions of pregnancy. Other components of the immune system also participate to maintain maternal-fetal immune tolerance. If the immune system of pregnant women with SLE is not able to maintain maternal immune tolerance to the fetus, pregnancy complications (miscarriage, fetal hypotrophy, and preterm birth) or maternal complications (preeclampsia or activation of SLE, especially in conditions of lupus nephritis) may occur. In certain situations this can be responsible for neonatal lupus. At the same time, it must be noted that during pregnancy, the immune system is able to achieve immune tolerance while maintaining the anti-infectious immune capacity of the mother. Immunological monitoring of pregnancy during SLE, as well as of the mother's disease, is required. It is important to understand immune tolerance to grafts in transplant pathology.

The relationship between the kidney and other organs is notable. The best known is the relation with the cardiovascular system. Relationships with other organs are less studied, although their involvement sometimes dominates the clinical picture and the outcome of disease. The paper analyzes the kidney-liver relationship, namely chronic kidney disease and chronic liver disease from an immune viewpoint. The immune system operates as a unitary whole. There is an interdependence between the immune system of the liver, considered a lymphoid organ, and the kidney, whose participation in immune processes is well-known. The most important chronic liver diseases are viral hepatitis B and C. Infection with these viruses can lead to renal involvement, producing mainly glomerular disease. At the same time, secondary glomerulonephritis can cause an unfavorable outcome of the primary disease. The relationship between chronic liver disease and chronic kidney disease during chronic B and C hepatitis occurs via circulating immune complexes or complexes formed in situ. Cell-mediated immunity is also involved. The antiviral treatment of B and C hepatitis is also aimed at secondary glomerular disease. The participation of immune mechanisms raises the question of administering immunomodulating medication, a type of medication that influences viral replication--this is why it is associated with antiviral medication. Other two chronic liver diseases, namely liver cirrhosis, in which the main mechanism is a toxic one, and non-alcoholic steatohepatitis can produce via immune mechanisms glomerular involvement. In its turn, chronic kidney disease in advanced stages causes lipid metabolism disturbances with hypertriglyceridemia, which can influence fatty loading of the liver in the above-mentioned liver diseases. One can speak about a cross-talk between the liver and the kidney, in which immune mechanisms play an important role.

Background: There is an ongoing debate as to whether early diabetic nephropathy in Type 2 diabetes mellitus may be attributed to the glomerulus or to the proximal tubule. Urinary excretion of nephrin and vascular endothelial growth factor may increase even in the normoalbuminuria stage. In the course of diabetic nephropathy, the proximal tubule may be involved in the uptake of urinary nephrin and vascular endothelial growth factor., Materials and Methods: Two groups of consecutive Type 2 diabetes mellitus outpatients (38 normo-, 32 microalbuminuric) and 21 healthy subjects were enrolled in a cross-sectional study and evaluated concerning the relation of proximal tubule dysfunction with the podocyte biomarkers excretion, assessed by ELISA methods. The impact of advanced glycation end-products on this relation was also queried., Results: Urinary alpha1-microglobulin and kidney injury molecule-1 correlated with urinary albumin:creatinine ratio (R2 = 0.269; p < 0.001; R2 = 0.125; p < 0.001), nephrinuria (R2 = 0.529; p<0.001; R2 = 0.203; p < 0.001), urinary vascular endothelial growth factor (R2 = 0.709; p < 0.001; R2 = 0.360; p < 0.001), urinary advanced glycation end-products (R2 = 0.578; p < 0.001; R2 = 0.405; p < 0.001), serum cystatin C (R2 = 0.130; p < 0.001; R2 = 0.128; p<0.001), and glomerular filtration rate (R2 = 0.167; p < 0.001; R2 = 0.166; p < 0.001); nephrinuria and urinary vascular endothelial growth factor correlated with urinary albumin:creatinine ratio (R2 = 0.498; p < 0.001; R2 = 0.227; p<0.001), urinary advanced glycation end-products (R2 = 0.251; p < 0.001; R2 = 0.308; p < 0.001), serum cystatin C (R2 = 0.157; p < 0.001; R2 = 0.226; p < 0.001), and glomerular filtration rate (R2 = 0.087; p = 0.007; R2 = 0.218; p < 0.001)., Conclusions: In Type 2 diabetes mellitus there is an association of proximal tubule dysfunction with podocyte damage biomarkers, even in the normoalbuminuria stage. This observation suggests a potential role of the proximal tubule in urinary nephrin and urinary vascular endothelial growth factor processing in early diabetic nephropathy, a fact which could be related to advanced glycation end-products intervention. Podocyte damage and proximal tubule dysfunction biomarkers could be validated as a practical approach to the diagnosis of early diabetic nephropathy by further studies on larger cohorts.

Background and Aims: In order to assess the role played by tubular epithelial cells (TEC) and interstitial vascular endothelial cells (VEC) in interstitial fibrogenesis in human glomerulonephritis, we studied the expression of markers of activated fibroblasts (α-smooth muscle actin (αSMA) and vimentin (Vim)) and of the transforming growth factor β (TGFβ), at the level of these cells., Methods: We studied retrospectively 41 renal biopsies from patients with primary and secondary glomerulonephritis [24 males, 17 females, mean age 45.5 ± 12.9 years]. Immunohistochemistry using monoclonal antibodies (SMA, Vim, TGFβ) was assessed using a semiquantitative score, that was correlated with biological and histological data (quantified using a scoring system in order to assess active-inflammatory and chronic-sclerotic/fibrotic lesions)., Results: The presence of SMA and Vim as markers of myofibroblasts was found in TECs and VECs. TEC Vim expression correlated with interstitial Vim expression (r = 0.38; p = 0.008), interstitial infiltrate (r = 0.31; p = 0.027), interstitial fibrosis (R = 0.25; p = 0.042), GFR (r = -0.35; p = 0.016), SMA (r = -0.42; p = 0.015), TGFβ (r = 0.25; p = 0.046), and hemoglobin (r = -0.55; p < 0.001). VEC Vim expression showed indirect correlations with interstitial infiltrate (r = -0.32; p = 0.023) and interstitial fibrosis (r = -0.34; p = 0.017)., Conclusion: Our study reflects the complexity of the involvement of VEC and mainly of TEC in fibrosis. The expression of mesenchymal markers at the tubular cell level (especially Vim) correlates with histological interstitial changes, with the decrease of renal function and more strongly with anemia.

Introduction: The solitary kidney (SK) may present increased vulnerability to nephrotoxicity because of adaptive phenomena., Aims: Assessing the vulnerability of the SK with urinary tract infections (UTI) to gentamicin by means of urinary biomarkers (N-acetyl-beta-D-glucosaminidase (NAG) and urinary alpha-1-microglobulin), as well as glomerular filtration rate (GFR)., Methods: We studied 14 patients with SK with UTI (group A) (mean age 58.07 ± 13.61 years, mean duration of SK 13.55 ± 12.33 years) who were administered gentamicin for 7 days. Group B consisted by 17 patients with SK without any other associated renal pathology (average age 51.17 ± 9.39 years, average existence period of a single kidney 33.23 ± 21.73 years). We also included a third group (group C) represented by nine healthy individuals, with two kidneys., Results: Increased values of urinary NAG were found in group B as compared to group C and alpha-1 microglobulin in group A as compared to group B. During treatment with gentamicin, increased values of both NAG and alpha-1-microglobulin in group A were found on day 7 as compared to values before treatment (day 7 NAG=18.99 ± 14.07 U/g creat versus day 0, NAG=5.15 ± 6.54 U/g creat, p=0.004; day 7 alpha-1-microglobulin=20.88 ± 18.84 mg/g creat versus day 0, urinary alpha-1-microglobulin=4.96 ± 6.57 mg/g creat, p=0.003). No statistically significant alterations of GFR were noticed after 7 days of treatment., Conclusions: We found the nephrotoxic effects of gentamicin at tubular level, but not at glomerular level. The nephrotoxic potential of gentamicin in patients with a SK can be monitored by assessing urinary biomarkers during treatment of UTI.

The kidneys, as an integral part of the body, are in close functional relationship with other organs. Dysfunction of the relationship with one organ will affect the kidney. Chronic kidney disease (CKD) leads in time to alteration of the relationship of the kidney with other organs, sometimes with severe consequences. Thus, cardiovascular involvement in CKD leads to increased severity of CKD, with an increase in mortality rate. At present, the relationship between the kidney and the lung has been less studied. Many aspects of this relationship are still unknown. The objective of the present paper is to analyze the main situations of the alteration of the kidney-lung relationship in clinical pathology, with special reference to chronic kidney disease. The pulmonary-renal syndrome is at the forefront. This pathology--well known in practice--refers mainly to the kidney-lung relationship in vasculitis, systemic lupus erythematosus and Goodpasture's syndrome. The relationship between the kidney and the lung is not limited to this syndrome. Many systemic diseases like sarcoidosis and amyloidosis alter the lung-kidney binomial. Likewise, the association in some patients of an important disorder primarily affecting the lung, such as silicosis, with concomitant renal involvement, highlights the relationship between the lungs and kidneys in clinical pathology. It is very important to know heart-kidney relationships via the lung in pulmonary arterial hypertension. In-depth knowledge of the patient with chronic kidney disease also requires thorough analysis of the lung-kidney relationship. This relationship is very evident in haemodialysed patients, taking into consideration that the pulmonary circulation is influenced by the dialysis membranes, in patients on peritoneal dialysis and especially in transplanted patients whose kidney-lung relationship has a favorable outcome. Although little dealt with, the relationship between the kidneys and the lungs requires more attention, as it can have important consequences, and appropriate therapy.

Aims: End Stage Renal Disease (ESRD) represents a microinflammatory state accompanied by oxidative stress and an imbalance between pro- and antioxidants. Vitamin C is a highly effective antioxidant, acting to lessen oxidative stress. The aim of our study was to assess the Antioxidant Capacity of Water soluble substances (ACW) and the Antioxidant Capacity of Liposoluble substances (ACL) in patients with Balkan Endemic Nephropathy (BEN) on hemodialysis undergoing Vitamin C therapy as compared to healthy controls., Methods: Twenty-one patients with BEN on hemodialysis (HD), mean age: 63.33 +/- 5.42 years, 6 M and 15 F, were enrolled into the study. All patients received 10 vials of Vitamin C 750 mg/5 ml every 2 months. Eleven apparently healthy subjects, mean age: 63.73 +/- 5.21 years, 6 M and 5 F, served as controls. The photochemiluminescence assay was used to measure the antioxidant activity of plasma samples. The results are presented in equivalent concentration units of Vitamin C for water soluble antioxidants and in equivalent concentration units of Trolox (synthetic Vitamin E) for lipid soluble antioxidants. Both concentrations are expressed in micromols/L. Statistical analysis (non-parametric Wilcoxon test) was performed using NCSS., Results: Mean duration since BEN diagnosis was: 8.24 +/- 3.5 years. Mean duration since HD initiation was: 4.92 +/- 3.4 years. Smoking status was negative in all patients. Hypertension was present in 15 patients (71.42%), cardiovascular disease in 10 (47.61%), HCV infection in 13 (61.9%), 1 patient had HBV + HCV infection, 1 had renal tuberculosis, 1 had upper urinary tract cancer, 1 genital cancer, and I autoimmune thyroid disease. The Antioxidant Capacity of Water soluble substances (ACW) in patients with BEN was 477.6 +/- 177.63 micromols/L, significantly higher as compared to controls: 198.05 +/- 196.63 micromols/L; p = 0.01, whereas the Antioxidant Capacity of Liposoluble substances (ACL) in patients with BEN was 33.9 +/- 22.99 micromols/L, non-significantly different as compared to controls: 27.38 +/- 4.21 micromols/L; p = 0.22., Conclusions: We conclude that Vitamin C therapy in patients with BEN on HD significantly increases the Antioxidant Capacity of Water soluble substances (ACW) as compared to controls and could be used to counter oxidative stress in patients with ESRD.

Unlabelled: CKD patients present deficient elimination of potassium. Ambulatory treatment with hypotensors, mainly angiotensin-renin system inhibitors, can be associated in these patients with potassium retention and risk of hyperkalemia. In pre-dialysis stage-5 CKD patients, the use of medication accompanied by hyperkalemia increases risks of developing it. Using diuretics like spironolactone also increases this risk. Serum potassium can also increase in case of inappropriate consumption of potassium-rich food (bananas). Since ambulatory care does not always rigorously control hyperkalemia in CKD patients we consider it is useful to screen patients when they are referred to dialysis services. The screening can reflect the management of ambulatory CKD patients under treatment with ACE-I and ARB hypotensors. We remark that beta-blockers are attributed a (limited) role in increasing the values of serum K., Material and Method: We studied a group of 477 stage-5 CKD patients referred for dialysis to The Dialysis Centre of the Emergency County Hospital Timişoara. The average age of the patients was 57.41 +/- 14.26 years. 260 were males and 217 females. All were stage-5 CKD with GFR < 15 mL/min/1.73 m2, with a group average value of eGFR of 5.72 +/- 2.81 mL/min/1.73m2. Our investigations showed hypokalemia in 14 patients (2.93%). Hyperkalemia was found in 179 patients. Of these, 124 had mild hyperkalemia (5.5-6.4 mEq/L), 45 patients had medium hyperkalemia (6.5-7.5 mEq/L) and 10 (2.09%) had severe hyperkalemia (K > 7.5 mEq/L)., Discussion: Hyperkalemia was more frequent in patients who had been treated with blockers of the renin-angiotensin system than in patients who had used other hypotensors or who had not needed hypotensors and had not taken diuretics. Severe hyperkalemia (K > 7.5 mEq/L) was present both in patients treated with blockers of the renin-angiotensin system and in those treated with other hypotensors and in 1 case without hypotensor or diuretic treatment. 2 cases treated with blockers of the renin-angiotensin-aldosterone system with severe hyperpotassemia associated antialdosteronic diuretics, cumulating hyperpotassemic effects. Diuretic treatments with loop diuretics influenced the values of serum K of most patients. Hyperkalemia represents an important problem in nephrology because of the risks it induces in the treatment ofpre-dialysis CKD patients and it requires attentive monitoring.

Unlabelled: HCV is an important cause of renal disease. Taal and Brenner have identified risk factors for CKD and have suggested that these risk factors be incorporated into a renal risk score analogous to the Framingham cardiovascular score. Given the high HCV-renal disease comorbidity, we sought to assess risk factors for CKD in patients with HCV chronic hepatitis., Methods: One hundred-seventeen patients with HCV chronic hepatitis (mean age: 50.68 +/- 9.14 years; 86 female and 31 male) hospitalized in the Department of Hepatology during 2009 were enrolled into the study. All patients were assessed for the risk factors for CKD proposed by Taal and Brenner: albuminuria, diabetes mellitus, hypertension, obesity, anemia, hypercholesterolemia, hypertriglyceridemia, nephrotoxins, primary renal disease, associated urological disorder, cardiovascular disease and family history of CKD. Renal function (GFR-CKD-Epi) was also evaluated., Statistical Analysis: Pearson's correlation coefficient and Odds Ratio (OR) was performed using SPSS17 and Epi 3.2.2., Results: The prevalence of albuminuria was 21.36%, of hypertension was 20.51%, of obesity was 21.36%, and hypercholesterolemia was present in 41.02% of the cases. Renal function was as follows: 10.25% (12/117) of the patients had a GFR < 60 mL/min/1.73 sqm.; 64.95% (76/117) of the patients had a GFR between 60-89 mL/min/1.73 sqm.; and 24.78% (29/117) had a GFR > or = 90 mL/min/1.73 sqm., Conclusions: Our study shows that HCV chronic hepatitis is associated with renal function impairment in a high percentage of patients. Prominent risk factors for CKD are present in these patients, such as albuminuria, hypertension, obesity, and hypercholesterolemia, which need to be actively searched and addressed therapeutically.