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Nephron Clinical Practice
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ISSN (Print) 1660-2110 - ISSN (Online) 1660-2110
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Contents Vol. 128, 2014
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  Abstract:
  Nephron Clin Pract 2014;128:I-VI
  PubDate: Tue, 27 Jan 2015 00:00:00 +010
Chronic Kidney Disease in Disadvantaged Populations
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  Abstract:
  Nephron Clin Pract 2014;128:292-296
  PubDate: Fri, 16 Jan 2015 00:00:00 +010
Association of de novo Dipstick Albuminuria with Severe Acute Kidney
Injury in Critically Ill Septic Patients
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  Abstract: Background: Acute kidney injury (AKI) occurs frequently in septic patients. Albuminuria may play a role as an early marker of septic AKI. The potential association between de novo dipstick albuminuria (DA) and septic AKI has not been examined. Methods: We conducted a single-center observational cohort study of 423 critically ill septic patients without chronic kidney disease (CKD) or prior positive DA within 3 months before admission. The association between de novo DA within the first 24 h of presentation and AKI at 72 h was examined. Results: AKI was identified in 268/423 (63%) patients and 20/423 (4.7%) required dialysis. De novo DA was associated with AKI (univariate OR 1.91; 95% CI 1.27-2.86, p = 0.002). The association persisted in a multivariate logistic regression model adjusted for demographics, baseline kidney function, comorbidities, critical illness parameters, and exposure to nephrotoxins (adjusted OR 1.87; 95% CI 1.21-2.89, p = 0.005). The association between de novo DA and AKI was stronger for severe AKI, i.e. Acute Kidney Injury Network (AKIN) stage 3 (adjusted OR 2.99; 95% CI 1.52-5.85, p = 0.001) and AKIN stage 2 (adjusted OR 1.79; 95% CI 1.002-3.21, p = 0.049) but not AKIN stage 1 (adjusted OR 1.41; 95% CI 0.87-2.29, p = 0.16). Conclusions: De novo DA within the first 24 h of admission was independently associated with severe AKI in critically ill septic patients. Future studies are required to fully elucidate the utility of DA testing in the early detection and stratification of AKI.
  Nephron Clin Pract 2014;128:373-380
  PubDate: Tue, 13 Jan 2015 00:00:00 +010
Differential Membrane Expression of Toll-Like Receptors and Intracellular
Cytokine Induction in Peripheral Blood Monocytes of Patients with Chronic
Kidney Disease and Diabetic Nephropathy
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  Abstract: Background: Toll-like receptors (TLRs) are key players in the innate immune system whose activation leads to an inflammatory response. Inflammation plays an important role in the pathogenesis of chronic kidney disease (CKD) and diabetes mellitus. The aim of our study was to assess the proinflammatory state of nondialysis CKD patients by evaluating the membrane expression of TLR2 and TLR4 and the intracellular IL-1β and IL-6 production in response to the ligand Pam3Cys-Ser-(Lys)4 (Pam3CSK4). Methods: 85 nondialysis CKD patients [mean estimated glomerular filtration rate: 34 (17-90) ml/min/1.73 m2] were divided in 2 groups: 55 nondiabetic CKD patients (CKD group) and 30 patients with diabetic nephropathy (DN group). The two groups were compared with 36 healthy subjects (control group). TLR2 and TLR4 membrane expression in monocytes and Pam3CSK4-induced intracellular production of IL-1β and IL-6 were assessed by flow cytometry. Results: Both patient groups showed increased TLR2 membrane expression compared with the control group, both at baseline (p < 0.05 for both) and after Pam3CSK4 stimulation (p < 0.05 for both). The DN group exhibited significantly higher TLR4 expression at baseline compared to the CKD and control groups (p < 0.04 and p < 0.02, respectively). Intracellular IL-1β and IL-6 levels at baseline were significantly lower in CKD patients compared to the DN and control groups. After Pam3CSK4 stimulation, intracellular IL-1β and IL-6 increased in all groups, but were lower in the CKD group versus the control group or DN group, which exhibited higher levels than the controls. Conclusions: Nondialysis CKD patients showed significant alterations in TLR2 and TLR4 membrane expression, and impaired Pam3CSK4-induced cytokine production in monocytes, a phenomenon that is markedly influenced by the presence of diabetes.
  Nephron Clin Pract 2014;128:399-406
  PubDate: Sat, 10 Jan 2015 00:00:00 +010
Correction of Hyper- and Hyponatraemia during Continuous Renal Replacement
Therapy
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  Abstract: Background: Severe hyper- and hyponatraemia is associated with significant risks, yet its correction can also have serious consequences when implemented too fast or inadequately. The safe correction of serum sodium levels is particularly challenging when renal replacement therapy (RRT) is required. Methods: Using 2 case scenarios, we aim to illustrate a simple method of correcting hyper- and hyponatraemia safely by step-wise manipulation of the dialysate/replacement fluid. Results: During continuous RRT, hypernatraemia can be corrected effectively and safely by adding small pre-calculated amounts of 30% NaCl to the dialysate/replacement fluid bags aiming for a [Na+] in the fluid that allows safe equilibration and correction of the serum [Na+]. To correct hyponatraemia safely, pre-calculated amounts of sterile water can be added in a step-wise manner to achieve a fluid [Na+] that equals the desired target serum [Na+]. Conclusion: During continuous RRT, the step-wise adjustment of [Na+] of dialysate/replacement fluids offers a safe and reliable method to correct sodium disorders.
  Nephron Clin Pract 2014;128:394-398
  PubDate: Sat, 10 Jan 2015 00:00:00 +010
Ectopic Expression of Fatty Acid-Binding Protein 4 in the Glomerulus Is
Associated with Proteinuria and Renal Dysfunction
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  Abstract: Background/Aims: Fatty acid-binding proteins (FABPs) are a family of intracellular lipid chaperones. Among FABPs, FABP1 (liver FABP) is expressed in proximal tubular epithelial cells in the kidney, and urinary FABP1 has been reported to reflect damage of proximal tubular epithelial cells. However, roles of other FABP isoforms in renal pathologies have not been reported. Recently, FABP4 (adipocyte FABP/aP2) was reported to be expressed in peritubular capillaries (PTCs), but not in glomerular capillaries in the normal kidney. We examined the hypothesis that pathological conditions alter the level and localization of FABP4 expression in the kidney, which mediates renal dysfunction. Methods: A total of 112 consecutive patients who underwent renal biopsy were retrospectively enrolled. Expression of FABP4 protein and mRNA in the kidney was examined by immunohistochemistry and in situ hybridization, respectively. The ratio of FABP4-positive area to total area within glomeruli (G-FABP4-Area), urinary protein level (U-Protein), and change in estimated glomerular filtration rate (eGFR) 1 year after biopsy were examined. Results: FABP4 protein and mRNA were expressed not only in PTCs, but also in endothelial cells and macrophages in the glomerulus. G-FABP4-Area was correlated with U-Protein (r = 0.497, p < 0.001). As a subanalysis, in patients with IgA nephropathy (n = 34), G-FABP4-Area was significantly larger in cases with an endocapillary proliferative lesion, and change in eGFR was negatively correlated with G-FABP4-Area at baseline (r = -0.537, p = 0.008). Conclusion: Ectopic FABP4 expression in the glomerulus is induced by renal diseases and is closely associated with proteinuria and renal dysfunction.
  Nephron Clin Pract 2014;128:345-351
  PubDate: Fri, 09 Jan 2015 00:00:00 +010
The 99mTc-DTPA Urinary Clearance Method May Be Preferable to the Plasma
Disappearance Method for Assessing Glomerular Filtration Rate in Diabetic
Nephropathy
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  Abstract: Background: Isotopic glomerular filtration rate (iGFR) measurement is comparable to the inulin method. In this study, we compared urinary and plasma iGFR methodologies in patients with diabetic nephropathy. Methods: A total of 147 patients from 3 sites in the Diabetic Intervention with Vitamins to Improve Nephropathy (DIVINe) trial provided 213 sets of urine and blood collections, at baseline, 18 and 36 months. Results: The mean (with standard deviation) plasma iGFR of 60.7 (24.9) ml/min/1.73 m2 compared to urinary iGFR of 52.0 (28.0) ml/min/1.73 m2 was statistically significant (p value
  PubDate: Thu, 08 Jan 2015 00:00:00 +010
Compared Decline of Residual Kidney Function in Patients Treated with
Automated Peritoneal Dialysis and Continuous Ambulatory Peritoneal
Dialysis: A Multicenter Study
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  Abstract: Background: There is controversy concerning the compared rates of decline of residual kidney function (RKF) in patients treated with continuous ambulatory peritoneal dialysis (CAPD) and automated peritoneal dialysis (APD). Objectives and Method: Following an observational, multicenter design, we studied 493 patients initiating peritoneal dialysis (PD) in four different Spanish units. We explored the effect of the PD modality on the rate of decline of RKF and the probability of anuria during follow-up. We applied logistic regression for intention-to-treat analyses, and linear mixed models to explore time-dependent variables, excluding those affected by indication bias. Main Results: Patients started on APD were younger and less comorbid than those initiated on CAPD. Baseline RKF was similar in both groups (p = 0.50). Eighty-seven patients changed their PD modality during follow-up. The following variables predicted a faster decline of RKF: higher (rate of decline) or lower (anuria) baseline RKF, younger age, proteinuria, nonprimary PD, use of PD solutions rich in glucose degradation products, higher blood pressure, and suffering peritonitis or cardiovascular events during follow-up. Overall, APD was not associated with a fast decline of RKF, but stratified analysis disclosed that patients with lower baseline RKF had an increased risk for this outcome when treated with this technique (HR: 2.26, 95% CI: 1.09-4.82, p = 0.023). Moreover, the probability of anuria during follow-up was overtly higher in APD patients (HR: 3.22, 95% CI: 1.25-6.69, p = 0.002). Conclusions: Starting PD patients directly on APD is associated with a faster decline of RKF and a higher risk of developing anuria than doing so on CAPD. This detrimental effect is more marked in patients initiating PD with lower levels of RKF.
  Nephron Clin Pract 2014;128:352-360
  PubDate: Thu, 08 Jan 2015 00:00:00 +010
Effects of Sleepiness on Survival in Japanese Hemodialysis Patients:
J-DOPPS Study
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  Abstract: Sleep disorder and poor sleep quality are common in chronic hemodialysis (HD) patients. They have been claimed as a cause of morbidity and mortality. The relationship between the degree of sleepiness and survival has not been studied. We studied the degree of sleepiness in 1,252 adult HD patients (age ≥20 years) recruited into the Dialysis Outcomes Practice Pattern Study in Japan (J-DOPPS III), using the Japanese version of the Epworth Sleepiness Scale (JESS) questionnaire. Demographic data were presented for three subgroups: low, intermediate, and high JESS score. Cox proportional hazard regression analysis was performed to estimate the independent effect of several variables on survival. The hazard ratio for mortality was 2.312 (95% CI 1.267-4.220; p = 0.006) for those with a high JESS score (vs. those with a low JESS score) after adjusting for age, vintage (length of time on HD), sex, diabetes, body mass index, cardiovascular disease, HD treatment regimen (time, frequency, and single-pool Kt/V), laboratory data (serum albumin, creatinine, and total cholesterol), and medication (antihypertensive drugs, erythropoietin, vitamin D, and phosphate binders). Patients ≥70 years of age with comorbid conditions (congestive heart failure, stroke, and diabetes) showed a significantly higher JESS score (≥16). The JESS score did not show interaction by age. Results showed that the degree of sleepiness is related to survival in Japanese HD patients, particularly in elderly patients.
  Nephron Clin Pract 2014;128:333-340
  PubDate: Thu, 08 Jan 2015 00:00:00 +010
Therapeutic Advances in the Treatment of Polycystic Kidney Disease
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  Abstract: The spectrum of polycystic kidney disease (PKD) comprises a family of inherited syndromes defined by renal cyst formation and growth, progressive renal function loss and variable extrarenal manifestations. The most common form, autosomal-dominant PKD is caused by mutations in one of two genes, PKD1 or PKD2. Recent developments in genomic and proteomic medicine have resulted in the discovery of novel genes implicated in the wide variety of less frequent, recessive PKD syndromes. Cysts are the disease, and overall cystic burden, measured by MRI as total kidney volume, is being established as the best available biomarker of disease progression. Current state-of-the-art therapy is aimed at quality treatment for chronic renal insufficiency and cyst-related complications. Recent therapeutic studies have focused on mechanisms reducing intracellular cyclic AMP levels, blocking the renin-angiotensin-aldosterone system and inhibiting the mTOR-signaling pathway. PKD therapies with vasopressin antagonists and somatostatin analogues result in the reduction of intracellular cAMP levels and have shown limited clinical success, but side effects are prominent. Similarly, mTOR pathway inhibition has not shown significant therapeutic benefits. While the HALT-PKD study will answer questions by the end of 2014 about the utility of renin-angiotensin-aldosterone system blockade and aggressive blood pressure control, the next generation of PKD therapy studies targeting proliferative mechanisms of cyst expansion are already under way. Advances in research on the molecular mechanisms of cystogenesis will help design novel targeted PKD therapies in the future.
  Nephron Clin Pract 2014;128:297-302
  PubDate: Tue, 06 Jan 2015 00:00:00 +010

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