Clinical nephrology Journal Impact Factor & Information

Publisher: Dustri-Verlag

Journal description

Clinical Nephrology appears monthly and publishes manuscripts containing original material with emphasis on the following topics: prophylaxis, pathophysiology, immunology, diagnosis, therapy, experimental approaches and dialysis and transplantation.

Current impact factor: 1.23

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.232
2012 Impact Factor 1.288
2011 Impact Factor 1.171
2010 Impact Factor 1.058
2009 Impact Factor 1.373
2008 Impact Factor 1.413
2007 Impact Factor 1.32
2006 Impact Factor 1.418
2005 Impact Factor 1.543
2004 Impact Factor 1.316
2003 Impact Factor 1.341
2002 Impact Factor 1.341
2001 Impact Factor 1.531
2000 Impact Factor 1.638
1999 Impact Factor 1.553
1998 Impact Factor 1.323
1997 Impact Factor 1.437
1996 Impact Factor 1.643
1995 Impact Factor 1.441
1994 Impact Factor 1.339
1993 Impact Factor 1.575
1992 Impact Factor 1.456

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.19
Cited half-life 9.80
Immediacy index 0.27
Eigenfactor 0.00
Article influence 0.34
Website Clinical Nephrology website
Other titles Clinical nephrology
ISSN 0301-0430
OCLC 1747233
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Dustri-Verlag

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Archiving status unclear
  • Conditions
    • We have contacted this publisher on multiple occasions, and have not been able to obtain a response to our enquiries. If you have any information on this publisher's policy, please submit an update using the form below.
  • Classification
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Publications in this journal

  • Clinical nephrology 09/2015; 84 (2015)(3):127-129.
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    ABSTRACT: Dent disease (DD) is a rare X-linked tubulopathy characterized by a proximal tubular dysfunction leading to nephrocalcinosis/nephrolithiasis and progressive renal failure. The disease is associated with a mutation either in CLCN5 or OCRL genes. We aim to define clinical and genetic disease characteristics and summarize treatments of Polish patients with DD. The study cohort consists of 10 boys (aged 5 - 16.5 years) whose data were collected through POLtube Registry. All of the patients had tubular proteinuria, hypercalciuria, and nephrocalcinosis/nephrolithiasis. Renal impairment and growth deficiency were found in 3 patients and rickets in 2 patients. In total, 9 of 10 patients carried a mutation in the CLCN5 gene. Five of 9 detected mutations were novel. In 1 patient with a clinical phenotype of DD, no mutations in either CLCN5 or OCRL were discovered. Therapy consisted of thiazides in 7 patients, and phosphate supplements and enalapril in 3 cases. Growth hormone therapy was initiated in 3 patients and resulted in improved growth rate. We report clinical and molecular characterization of Polish children with DD. Our study suggests that this tubulopathy may be generally under-diagnosed in Poland. The study revealed variable treatments, demonstrating a need for therapeutic guidelines.
    Clinical nephrology 08/2015; DOI:10.5414/CN108522
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    ABSTRACT: Aminoglycosides are a major weapon against serious Gram-negative rod infections, yet aminoglycoside usage is limited by the risk of nephrotoxicity. The risk of toxicity is reduced by extended-interval dosing of aminoglycosides, defined as 5 - 7 mg/kg given intravenously in intervals of 24 hours or greater based on serum drug concentrations. In critically ill patients undergoing continuous venovenous hemofiltration, there are few published reports of the pharmacokinetics of extended-interval dosing of aminoglycosides. We evaluated the pharmacokinetics of extended-interval dosing of gentamicin and tobramycin in 9 critically ill patients on continuous venovenous hemofiltration at Dartmouth-Hitchcock Medical Center between April 2007 and September 2011. Aminoglycoside elimination half-life values were highly variable (median 7 hours, range 3 - 26 hours) and did not correlate with total body weight or estimated creatinine clearance derived from the dose of continuous venovenous hemofiltration. Five of 9 patients cleared infection, but only 4 patients survived to hospital discharge, 2 of whom were dialysis-dependent. Extended interval aminoglycoside dosing during continuous venovenous hemofiltration yields unpredictable half-lives and drug levels among high-risk critically ill patients. Close monitoring of serum aminoglycoside levels is required.
    Clinical nephrology 08/2015; DOI:10.5414/CN108559
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    ABSTRACT: Podocyte depletion is a characteristic feature of progressive renal failure. We hypothesize that studying the podocyte mRNA level in urinary sediment may provide diagnostic and prognostic information in adult nephrotic syndrome. We studied 25 patients with minimal change nephropathy (MCN), 25 with focal segmental glomerulosclerosis (FSGS), and 17 healthy controls. The mRNA levels of nephrin, podocin, and synaptopodin in urinary sediment were quantified. There were significant differences in the urinary sediment nephrin and podocin, but not synaptopodin, mRNA levels between diagnosis groups. Post-hoc analysis further showed that urinary nephrin mRNA levels of the MCN group were lower than those in the control and FSGS groups, although the difference between MCN and FSGS groups did not reach statistical significance. The degree of proteinuria inversely correlated with urinary nephrin mRNA levels in the MCN (r = -0.526, p = 0.007) as well as in the FSGS group (r = -0.521, p = 0.008). For the FSGS group, the rate of renal function decline significantly correlated with baseline urinary synaptopodin mRNA levels (r = -0.496, p = 0.012). Urinary nephrin and podocin mRNA levels were reduced in patients with MCN and probably FSGS, and the magnitude of reduction correlated with the degree of proteinuria. Urinary synaptopodin mRNA levels correlated with the subsequent rate of renal function decline in patients with FSGS. Our result indicates that urine sediment podocyte mRNA levels provide novel insights in the pathophysiology of nephrotic syndrome and could be useful for risk stratification.
    Clinical nephrology 08/2015; DOI:10.5414/CN108607
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    ABSTRACT: Amyloidosis results from the pathologic deposition of beta pleated sheet fibrils within various organs including the kidney. Most often, the deposition is composed of the well-known monoclonal immunoglobulin light chains (AL) or serum amyloid A protein (AA). Recently, a new type of amyloidogenic protein was discovered, leukocyte chemotactic factor 2 (LECT2). This type of amyloid tends to have an affinity to kidney and liver and is recognized as a distinct clinico-pathologic type of amyloidosis, presenting with varying degrees of impaired kidney function and proteinuria. Herein, a case of this uncommon novel amyloidosis is presented with a brief review of the literature.
    Clinical nephrology 08/2015; DOI:10.5414/CN108549
  • John M Burkart · Anne C Beaubrun · Kurt A Olson · Grace S Park · Susan V Yue · Robert J Rubin
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    ABSTRACT: The impact of the United States Prospective Payment System (PPS) "bundle payment system" on anemia management within small dialysis organizations (SDOs) was studied to evaluate the financia burden on SDOs. Facilities enrolled in the original study on SDOs were grouped into three hemoglobin (Hb) categories by subject-months: > 25% of subjectmonths with Hb < 10 g/dL (sub-10); > 25% of subject-months with Hb > 12 g/dL (super-12); remaining facilities (10 - 12 group). Subjectlevel data aggregated to facility level for Hb concentration, intravenous (IV) epoetin α (EA) dose per administration, dose titration, and EA administration frequency during the baseline and follow-up periods were described. Baseline demographic characteristics were imbalanced between the sub-10 (n = 7) and super-12 facilities (n = 5). Mean (SD) Hb concentrations were similar for sub-10 (11.1 (3.0) g/dL) and super-12 (11.6 (2.2) g/dL) facilities during the baseline period, but differed during the follow-up period (10.4 (2.7) vs. 11.4 (2.3) g/dL). The median (Q1, Q3) EA IV dose per administration during follow-up was 3,726 (3,467, 3,961) and 5,712 (4,816, 7,324) units in the sub-10 and super-12 facilities, respectively. A small trend toward upward titration was seen. Results suggest a difference in anemia management between sub-10 and super-12 facilities during the first year of PPS implementation. Future analyses evaluating patterns of reimbursement and shifts in clinical practice guidelines are warranted globally.
    Clinical nephrology 08/2015; DOI:10.5414/CN108573
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    ABSTRACT: Colchicine is an approved agent in the management and prophylaxis of gout and familial Mediterranean fever but its therapeutic value is limited by its narrow therapeutic index. Multisystem toxicity is uncommonly reported; and is often associated with renal impairment and/or specific drug interactions. We report two cases of colchicine toxicity marked by severe neuromyopathy in a diabetic with stage 4 chronic kidney disease (CKD) and a renal transplant recipient. Both patients presented with diarrhea, acute on chronic kidney injury and progressive muscle weakness while on colchicine for several weeks or longer. In addition to kidney disease, risk factors for colchicine toxicity included maintenance therapy with simvastatin in the first patient and cyclosporine in the second. Creatine phosphokinase (CPK) was elevated in both cases at presentation and neurophysiologic studies showed a pattern of severe myopathy with axonal sensorimotor neuropathy. The first patient recovered from neurological weakness in a few weeks, but the second patient suffered an extraordinarily protracted and severe neuromuscular disability for a year. The two cases reinforce the need for extra vigilance in prescribing and monitoring colchicine therapy in renal patients with specific attention to drug interactions known to increase the risk of toxicity, thus avoiding such combinations in patients with renal impairment.
    Clinical nephrology 08/2015; DOI:10.5414/CN108343
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    ABSTRACT: A 60-year-old female with an extensive history of stone disease and shock wave lithotripsy presents with recurrent and increasingly severe renal colic. Work-up reveals obstruction with translucent debris that is found to be composed of keratin. Her history of chronic irritation of the collecting system has resulted in keratinizing squamous metaplasia (KSM) with hyperkeratosis that has sloughed from the upper urinary tract and has become lodged in the ureter. Because of the worsening of her symptoms on conservative management, the patient elected for a nephrectomy and her symptoms have since resolved. KSM of the renal pelvis is a relatively rare phenomenon and most often presents with irritative symptoms. It is thought to result from chronic irritation of the urothelium. KSM has been found to be coincident with squamous cell cancers of the urinary tract, though clear data implicating KSM as a premalignant lesion is lacking. We present a case of recurrent renal colic secondary to sloughing keratin debris from KSM.
    Clinical nephrology 08/2015; DOI:10.5414/CN108581
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    ABSTRACT: There are few reports of IgA nephropathy (IgAN) with antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. The authors report the clinical and pathological findings in 14 patients with IgAN and ANCA seropositivity. These retrospective cases consisted of 4 men and 10 women with a mean age of 44.4 ± 12.7 years. ANCA-positivity was documented by EUROBlot kits and indirect immunofluorescence in all patients. The results of EUROBlot kits were positive in 14 patients (12 MPO-ANCA, 2 PR3-ANCA). Indirect immunofluorescence was positive in 14 patients (12 P-ANCA, 2 C-ANCA). Three of 14 IgAN with ANCA-positive patients showed severe clinical manifestations with crescents involving a mean of 56% glomeruli, including heavy proteinuria (mean 24-hour urine protein: 3.8 g/d), hematuria and acute renal failure (mean creatinine: 4.5 ± 3.7 mg/dL). The remaining 11 patients with no crescents showed various degrees of proteinuria (mean 24-hour urine protein: 2.4 ± 2.4 g/d), hematuria and serum creatinine levels (median creatinine: 0.9 (IQR, 0.5 - 1.4) mg/dL). The follow-up period for 10 patients had an average length of 14.0 ± 11.2 months. Among the three patients with crescents who had been treated with steroids and cyclophosphamide, one patient became dialysis dependent at the time of biopsy and remained on dialysis after treatment, another died of acute heart failure, and the last one showed improvement in renal function after treatment and did not develop end-stage renal disease (ESRD) 26 months after renal biopsy. The remaining 7 patients with no crescents were treated with steroids, cyclophosphamide, renin-angiotensin system inhibitors, and/or Traditional Chinese Medicine; 6 had stabilized or improved renal function and one progressed to ESRD with worsening renal function. These findings suggest not all ANCAs are involved in the pathology of IgAN. In patients with IgAN and ANCAs, identification of pathogenic vs. non-pathogenic ANCAs is recommended.
    Clinical nephrology 08/2015; DOI:10.5414/CN108571
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    ABSTRACT: BK virus is ubiquitous worldwide, with infection usually occurring in early childhood. BK virus replicates prolifically under immunosuppressive conditions, causing inflammation along the genitourinary tract and progressing clinically to hemorrhagic cystitis, ureteral stenosis, and tubulointerstitial nephritis. Most BK virusassociated nephropathy occurs in renal allograft patients after kidney transplantation, although some case reports have described BK virus-associated nephropathy in the native kidney, particularly in patients with human immunodeficiency virus infection. Here we present the case of a 49-year-old male with acquired immunodeficiency syndrome (AIDS) and renal dysfunction with hydronephrosis. The renal biopsy showed tubulointerstitial nephritis with lymphoplasmacytic infiltrates and intranuclear inclusions in the tubular epithelium, which are typical findings for BK virus-associated nephropathy. In addition, immunohistochemical staining revealed that the SV40 large T antigen exhibited a nuclear localization in tubular cells. To the best of our knowledge, this is the first case report of BK virus-associated nephropathy combined with hydronephrosis that was diagnosed by biopsy in a patient with AIDS.
    Clinical nephrology 08/2015; DOI:10.5414/CN108482
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    ABSTRACT: Low-protein diet (LPD) together with supplementation with ketoanalogs (KA) is associated with slower decline of estimated glomerular filtration rate (eGFR) in chronic kidney disease (CKD). We compared potential clinical and economic outcomes of KA supplement initiation at eGFR 15 - 29 mL/min/1.73 m2 vs. eGFR < 15 mL/min/1.73 m2 in CKD patients on LPD from the healthcare payer's perspective. Markov model was designed to simulate outcomes of adult patients with eGFR 15 - 29 mL/min/1.73 m2 on two strategies LPD with KA supplementation; watchfulwaiting on LPD alone and KA initiation when eGFR declined to < 15 mL/min/1.73 m2. Medical cost and quality-adjusted life-years (QALYs) were calculated over 10 years. Results The early-initiation group gained higher QALYs (3.926 QALYs vs. 3.787 QALYs) with lower cost (USD 564,637 vs. USD 914,236) (USD 1 = NTD 30) when compared with the watchful-waiting group in base-case analysis. Sensitivity analysis indicated that early KA initiation at eGFR at 17 - 29 mL/min/1.73 m2 would be the preferred cost-effective option, if relative reduction of eGFR decline associated with LPD plus KA was > 4%. 10,000 Monte Carlo simulations showed the early-initiation group to be less costly with higher QALYs gained than the watchful-waiting group by USD 343,665 (95% CI 342,139 - 345,191) and 0.160 QALYs (95% CI 0.140 - 0.180), respectively. Early KA supplementation with LPD in CKD patients appeared to be cost-saving and gained higher QALYs in Taiwan. Acceptance of early supplemented LPD as cost-effective depended upon the reduction of eGFR decline associated with KA plus LPD and eGFR level to initiate KA supplementation.
    Clinical nephrology 08/2015; DOI:10.5414/CN108560
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    ABSTRACT: Fibrillary glomerulonephritis (FGN) is a rare disorder with poor renal prognosis. It is a heterogeneous disease associated with significant risk of end-stage renal disease (ESRD). Its etiology and pathogenesis have not been clearly identified. We report a case of a patient presenting with hypertensive crisis, nephrotic range proteinuria, and rapidly progressive glomerulonephritis (RPGN). The kidney biopsy demonstrates crescentic GN on light microscopy (LM) and strong pseudo-linear/globular glomerular basement membrane (GBM) staining for immunoglobulin G on immunofluorescence (IF), suggestive of anti-GBM disease. However, circulating anti-GBM antibodies were negative. Electron microscopy (EM) revealed fibrillary deposits in the GBM, confirming the diagnosis of FGN. Review of the literature revealed very few reported similar cases. It appears that severe hypertension and heavy proteinuria, while uncommon in anti-GBM disease, are consistent findings in RPGN form of FGN.
    Clinical nephrology 08/2015; DOI:10.5414/CN108508
  • Clinical nephrology 08/2015; 84 (2015)(2):118-119. DOI:10.5414/CN108440
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    ABSTRACT: Chronic kidney disease (CKD) is a major health problem worldwide with dramatically increasing incidence and prevalence. Serum cystatin C (sCysC) has been clarified by many studies as a relatively accurate marker to evaluate renal function. Meta-analysis of diagnostic test studies. Various clinical settings of CKD, including adult patients with diabetes, renal transplant patients, and so on. A computerized search of PubMed, Cochrane clinical trial database, and Current Contents (from inception until June 16, 2014) was performed to identify potentially relevant articles. Increased sCysC concentration. The measured glomerular filtration rate measured by nuclear medicine techniques such as 99Tc-diethylene triamine pentacaetic acid (99Tc-DTPA) or 51Cr-ethylenediamine tetra-acetic acid (51Cr-EDTA), or calculated by Cockcroft-Gault (CG) or Modification of Diet in Renal Disease (MDRD) formula or 24 hours creatinine clearance rate. In total 19 studies were included in this study. Across all settings, the diagnostic odds ratio (DOR) of sCysC in predicting CKD was 40 (95% CI, 26 - 61) when sensitivity and specificity was 0.85 (95% CI, 0.81 - 0.89) and 0.87 (95% CI, 0.84 - 0.90), respectively. The area under the curve for the receiver-operating characteristic (AUROC) of sCysC to predict CKD was 0.92 (95% CI, 0.90 - 0.94). For the diagnostic value of sCysC in diabetics with CKD, the DOR was 51 (95% CI, 22 - 122), with sensitivity and specificity of 0.89 and 0.87, respectively. Subgroup analysis showed that sCysC was of better diagnostic value in the West than in Asia, and the diagnostic value of sCysC assayed by particle-enhanced nephelometric immunoassay (PENIA) was higher than sCysC assayed by particle-enhanced turbidimetric immunoassay (PETIA). SCysC appears to be a good biomarker in the definition of CKD. However, its performance is different in subgroups restricted by clinical settings, race, and sCysC assay.
    Clinical nephrology 08/2015; 84 (2015)(2):86-94. DOI:10.5414/CN108525
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    ABSTRACT: Although IgA nephropathy (IgAN) is the leading cause of glomerulonephritis worldwide, there are few large cohorts representative of U.S. Prognosis remains challenging, particularly as more patients are treated with RAAS blockade and immunosuppression. We analyzed a retrospective cohort of IgAN patients followed at Columbia University Medical Center from 1980 to 2010. We evaluated two outcomes - halving of eGFR and ESRD - using three proportional hazards models: 1) a model with only clinical parameters, 2) a model with only histopathologic parameters, and 3) a model combining clinical and histopathologic parameters. Of 154 patients with biopsy-proven IgAN, 126 had follow-up data available and 93 had biopsy slides re-read. Median follow-up was 47 months. The cohort was 64% male, 60% white, and the average age was 34 years at diagnosis. Median (IQR) eGFR and proteinuria at diagnosis were 64.1 (38.0 - 88.7) mL/min/1.73 m2 and 2.7 (1.3 - 4.5) g/day. Over 90% of subjects were treated with RAAS blockade, and over 66% received immunosuppression. In the clinical parameters-only model, baseline eGFR and African-American race predicted both halving of eGFR and ESRD. In the histopathologic parameters-only model, no parameter significantly predicted outcome. In the combined model, baseline eGFR remained the strongest predictor of both halving of eGFR (p = 0.03) and ESRD (p = 0.001), while the presence of IgG by immunofluorescence microscopy also predicted progression to ESRD. In this diverse U.S. IgAN cohort in which the majority of patients received RAAS blockade and immunosuppression, baseline eGFR, African-American race, and co-staining of IgG predicted poor outcome.
    Clinical nephrology 07/2015; DOI:10.5414/CN108556
  • Clinical nephrology 07/2015; DOI:10.5414/CN108513
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    ABSTRACT: Acute interstitial nephritis (AIN) presents with acute kidney injury, with evidence of interstitial inflammation and tubulitis on histology, and the presence of fever, rash, and eosinophiluria. Although the pathogenesis of this disease is not well understood, cell-mediated immunity is thought to play a major role. We hypothesized that IgE mediated mast cell activation is also involved in the pathogenesis of renal injury in AIN. 28 patients, with biopsy proven AIN over a 5-year period, were included in this study. Clinical data, including renal outcomes and the etiologies of AIN, were evaluated in all patients. Available tissues (renal biopsy) from 26 of the patients were stained for β-tryptase (marker for mast cell degranulation), IgE, IL-16, and CD3. A negative control for immunostaining was included. Samples from all 26 individuals stained positive for β-tryptase (mean of 11.16 cells/high power field), IgE (mean average of 0.68 cells/HPF), IL-16 (28% of the interstitium), and CD3 (33% of the interstitium). Acute interstitial nephritis was due to medication in 73%, systemic disease in 15%, and unknown (idiopathic) in 12% of the cases. 86% of patients were treated with corticosteroids. 18% required acute inpatient dialysis, with 7% remaining on dialysis longterm. Our study suggests that IgE and mast cell activation may play a role in the pathogenesis of AIN.
    Clinical nephrology 07/2015; DOI:10.5414/CN108254
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    ABSTRACT: Lymphomatous processes have been shown to involve the kidney by direct and paraneoplastic mechanisms. Direct injury can manifest by effacement of typical parenchymal architecture by the lymphomatous infiltrate, and indirect, paraneoplastic mechanisms have been associated with a variety of glomerular lesions. Mantle cell lymphoma (MCL) has rarely been reported to be associated with both direct infiltration and/ or paraneoplastic glomerular lesions. We describe a patient with rapidly progressive glomerulonephritis whose renal biopsy showed effacement of the renal parenchyma by MCL and a membranoproliferative pattern of glomerular injury. The patient's bone marrow was also involved by MCL, and serology revealed small M-spikes and a positive rheumatoid factor. The clinicopathologic findings were consistent with a membranoproliferative pattern of glomerular injury secondary to MCL with infiltrative destruction of renal parenchyma. This case is unusual in that MCL was diagnosed on renal biopsy, that there was a two-pronged mechanism of renal injury, and that there were two separate monoclonal immunoglobulins elaborated by the lymphoma that could be associated with the glomerular injury. Although it is uncommon to make an initial diagnosis of lymphoma from a renal biopsy, it should be recognized that patients with lymphoma might develop clinically significant renal sequelae econdary to both direct and indirect mechanisms of lymphoma-mediated nephropathy.
    Clinical nephrology 07/2015; DOI:10.5414/CN108462
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    ABSTRACT: Calcineurin inhibitors are critical-dose drugs with a narrow therapeutic range and optimal monitoring strategies are discussed in terms of safety and efficacy. A new pharmacodynamic monitoring tool - assessing the expression of nuclear factor of activated T-cells (NFAT)-regulated genes - has been established to directly measure the functional effect of cyclosporine A (CsA) in an individual patient. Until now, only sparse data on NFAT-regulated gene expression within the early post-transplant period have been available. Altogether 80 de novo renal transplant patients were enrolled in this non-interventional cohort-study. Immunosuppression consisted of interleukin (IL)-2 receptor antagonist induction, CsA, mycophenolic acid and steroids. Expression of NFAT-regulated genes (IL-2, granulocyte-macrophage colony stimulating-factor (GM-CSF), interferon-γ (IFN-γ)) was determined by qRT-PCR (real-time reverse transcription-PCR) at CsA C0 (prior to CsA intake) and C2 (2 hours after CsA intake) at regular follow-up visits within 6 months after transplantation. The median age of all patients was 47.9 ± 13.7 years (54 male). Residual NFAT-regulated gene expression showed a high interindividual variability. Inversely to reduction of CsA doses, NFAT-regulated genes increased from 1.78 ± 1.33% to 8.04 ± 7.36% in month 1 to month 6. Despite comparable CsA C0 levels, NFAT-regulated gene expression was significantly less inhibited in patients with treated biopsy-proven acute rejections (2.9 ± 2.2% vs. 2.0 ± 1.7%, p = 0.047). Patients with very low residual expression of NFAT-regulated genes were at an increased risk for early infectious episodes. Residual expression of IFN-γ and GM-CSF genes correlated significantly with clinical outcomes. NFAT-regulated gene expression is highly inhibited in the early post-transplant period in renal allograft recipients on CsA treatment. High residual NFAT-regulated gene expression was related to acute rejection episodes and low residual expression with infectious complications. Thus, NFAT-monitoring has the potential to support pharmacokinetic monitoring during the early post-transplant period.
    Clinical nephrology 07/2015; DOI:10.5414/CN108623