Current Issue : October - December Volume : 2014 Issue Number : 4 Articles : 7 Articles
Background: Renal handling of sodium and water is abnormal in chronic kidney disease (CKD). The aim of this\nstudy was to test the hypothesis that abnormal activity of the aquaporin-2 water channels (AQP2), the\nsodium-potassium-2chloride transporter (NKCC2) and/or the epithelial sodium channels (ENaC) contribute to this\nphenomenon.\nMethods: 23 patients with CKD and 24 healthy controls at baseline and after 3% saline infusion were compared.\nThe following measurements were performed: urinary concentrations of AQP2 (u-AQP2), NKCC2 (u-NKCC2), ENaC\n(u-ENaC?), glomerular filtration rate (GFR) estimated by 51Cr-EDTA clearance, free water clearance (CH2O), urinary\noutput (UO), fractional excretion of sodium (FENa), plasma concentrations of AVP, renin (PRC), Angiotensin II (ANG II),\nAldosterone (Aldo) and body fluid volumes.\nResults: At baseline, GFR was 34 ml/min in CKD patients and 89 ml/ml in controls. There were no significant\ndifferences in u-AQP2, u-NKCC2 or u-ENaC?, but FENa, p-Aldo and p-AVP were higher in CKD patients than controls.\nIn response to hypertonic saline, patients with CKD had an attenuated decrease in CH2O and UO. A greater increase\nin U-AQP2 was observed in CKD patients compared to controls. Furthermore, u-NKCC2 increased in CKD patients,\nwhereas u-NKCC2 decreased in controls. Body fluid volumes did not significantly differ.\nConclusions: In response to hypertonic saline, u-NKCC2 increased, suggesting an increased sodium reabsorption\nvia NKCC2 in patients with CKD. U-AQP2 increased more in CKD patients, despite an attenuated decrease in CH2O.\nThus, though high levels of p-AVP and p-Aldo, the kidneys can only partly compensate and counteract acute\nvolume expansion due to a defective tubular response....
Background: HS219 (40 mg chitosan-loaded chewing gum) is designed to bind salivary phosphorus as an add-on\nto available phosphorus binders. We performed a randomized, placebo-controlled, double-blind study to evaluate\nthe efficacy and safety of HS219 in hemodialysis (HD) patients with hyperphosphatemia as an add-on to\nphosphorus binders.\nMethods: Sixty-eight HD patients who were maintained on calcium carbonate (n = 33) or sevelamer\nhydrochloride (n = 35) were enrolled. The primary end point was a change in serum phosphorus levels. Secondary\nend points included changes in levels of salivary phosphorus, serum calcium, parathyroid hormone (PTH), and\nintact fibroblast growth factor (iFGF) 23.\nResults: Sixty-three patients chewed either HS219 (n = 35) or placebo (n = 28) for 30 min, three times a day, for\n3 weeks. HS219 was well tolerated and safe. However, HS219 was not superior to placebo with additional\nreduction of serum phosphorus with respect to phosphorus binders at the end of the chewing period. There were\nno significant effects of HS219 on reduction of salivary phosphorus, serum calcium, iPTH, or iFGF23 levels.\nConclusions: The chitosan-loaded chewing gum HS219 does not affect serum and salivary phosphorus levels in\nJapanese HD patients with hyperphosphatemia. Our findings do not support previous findings that 20 mg of\nchitosan-loaded chewing gum reduces serum and salivary phosphorus levels....
Background: Tolvaptan is a selective vasopressin receptor antagonist (V2R) that increases free water excretion. We\nwanted to test the hypotheses that tolvaptan changes both renal handling of water and sodium and systemic\nhemodynamics during basal conditions and during nitric oxide (NO)-inhibition with L-NG-monomethyl-arginine\n(L-NMMA).\nMethods: Nineteen healthy subjects were enrolled in a randomized, placebo-controlled, double-blind, crossover\nstudy of two examination days. Tolvaptan 15 mg or placebo was given in the morning. L-NMMA was given as a\nbolus followed by continuous infusion during 60 minutes. We measured urine output(UO), free water clearance\n(CH2O), fractional excretion of sodium (FENa), urinary aquaporin-2 channels (u-AQP2) and epithelial sodium channels\n(u-ENaC?), plasma vasopressin (p-AVP), central and brachial blood pressure(cBP, bBP).\nResults: During baseline conditions, tolvaptan caused a significant increase in UO, CH2O and p-AVP, and FENa was\nunchanged. During L-NMMA infusion, UO and CH2O decreased more pronounced after tolvaptan than after\nplacebo (?54 vs.-42% and ?34 vs.-9% respectively). U-AQP2 decreased during both treatments, whereas u-ENaC?\ndecreased after placebo and increased after tolvaptan. CBP and bBP were unchanged.\nConclusion: During baseline conditions, tolvaptan increased renal water excretion. During NO-inhibition, the more\npronounced reduction in renal water excretion after tolvaptan indicates that NO promotes water excretion in the principal\ncells, at least partly, via an AVP-dependent mechanism. The lack of decrease in u-AQP2 by tolvaptan could be explained\nby a counteracting effect of increased plasma vasopressin. The antagonizing effect of NO-inhibition on u-ENaC suggests\nthat NO interferes with the transport via ENaC by an AVP-dependent mechanism....
Background: In developing countries, accessibility to specialists, and physician to patient contact time is limited. In\nThailand, A unique community health service is provided by subdistrict health care officers and Village Health\nVolunteers (VHVs). If the personnel were trained on proper chronic kidney disease (CKD) care, CKD progression\nwould be delayed.\nMethods/Design: We conducted a community-based, cluster randomized controlled trial at Kamphaeng Phet\nProvince, located about 400 kilometers north of Bangkok. Two out of eleven districts of the province were randomly\nselected. Approximatly 500 stage 3ââ?¬â??4 CKD patients from 2 districts were enrolled. Patients in both groups will be\ntreated with standard guidelines. The patients in intervention group were provided the additional treatments by\nmultidisciplinary team in conjunction with community CKD care network (subdistrict health care officers and VHVs)\nwhich will provide group counseling during each hospital visit and quarterly home visits to monitor dietary protein\nand sodium intake, blood pressure measurement and drug compliance. Duration of the study is 2 years. The\nprimary outcome is the difference of rate of eGFR decline. The secondary outcomes are laboratory parameters and\nincidence of clinical endpoints such as mortality rate and cardiovascular events, end-stage renal disease (ESRD), etc.\nInsights of this study may set forth a new standard of community-based CKD care....
Background: The long-term prognosis of clinically early IgA nephropathy (IgAN) patients remains to be clarified.\nWe investigated the long-term outcomes of IgAN patients with an apparently benign presentation and evaluated\nprognostic factors for renal survival.\nMethods: We included patients with biopsy-proven IgAN who had estimated glomerular filtration rates\n(eGFR) ?60 mL/min/1.73 m2, normal blood pressure, and proteinuria <0.5 g/day at the time of biopsy. The primary\noutcome was progression to end-stage renal disease (ESRD). The secondary outcome was a 50% increase in serum\ncreatinine level or an increase in proteinuria to >1 g/day.\nResults: The analysis included 153 patients who met the inclusion criteria. At diagnosis, their median systolic\nblood pressure was 120 (110ââ?¬â??130) mmHg, eGFR was 85.9 (74.9ââ?¬â??100.1) mL/min/1.73 m2, and proteinuria was\n0.25 (0.13ââ?¬â??0.38) g/day. Of these, 4 patients died and 6 reached ESRD. The 30-year renal survival rate was 85.5%.\nThree patients had increased serum creatinine levels and 11 developed proteinuria. Remission was observed in\n35 (22.9%) patients. A moderate or severe degree of interstitial fibrosis (adjusted odd ratio [OR] 5.93, 95%\nconfidence interval [CI] 1.44ââ?¬â??24.45, P = 0.014) and hypoalbuminemia (adjusted OR 6.18, 95% CI 1.20ââ?¬â??31.79, P = 0.029)\nwere independent predictors of the secondary outcome.\nConclusions: This study showed that the prognosis of early IgAN was not always favorable, even resulting in\nprogression to ESRD in some cases. Hypoalbuminemia and interstitial fibrosis should also be considered\nimportant prognostic factors in clinically early IgAN patients....
Background: Although percutaneous renal biopsy remains an essential tool in the diagnosis and treatment of renal\ndiseases, in recent times the traditional procedure of nephrologists has been performed by non-nephrologists\nrather than nephrologists at many institutions. The present study assessed the safety and adequacy of tissue yield\nduring percutaneous renal biopsy according to practitioners and techniques based on ultrasound.\nMethods: This study included 658 native renal biopsies performed from 2005 to 2010 at a single centre. The\nbiopsies were performed by nephrologists or expert ultrasound radiologists using the ultrasound-marked blind or\nreal-time ultrasound-guided techniques.\nResults: A total of 271 ultrasound-marked blind biopsies were performed by nephrologists, 170 real-time\nultrasound-guided biopsies were performed by nephrologists, and 217 real-time ultrasound-guided biopsies were\nperformed by radiologists during the study period. No differences in post-biopsy complications such as haematoma,\nneed for transfusion and intervention, gross haematuria, pain, or infection were observed among groups. Glomerular\nnumbers of renal specimens from biopsies performed by nephrologists without reference to any technique were\nhigher than those obtained from real-time ultrasound-guided biopsies performed by expert ultrasound radiologists.\nConclusions: Percutaneous renal biopsy performed by nephrologists was not inferior to that performed by expert\nultrasound radiologists as related to specimen yield and post-biopsy complications....
Background: Acute kidney injury (AKI) is a common clinical problem. Studies have documented the incidence of\nAKI in a variety of populations but to date we do not believe the real incidence of AKI has been accurately\ndocumented in a district general hospital setting.\nThe aim here was to describe the detected incidence of AKI in a typical general hospital setting in an unselected\npopulation, and describe associated short and long-term outcomes.\nMethods: A retrospective observational database study from secondary care in East Kent (adult catchment\npopulation of 582,300). All adult patients (18 years or over) admitted between 1st February 2009 and 31st July 2009,\nwere included. Patients receiving chronic renal replacement therapy (RRT), maternity and day case admissions were\nexcluded. AKI was defined by the acute kidney injury network (AKIN) criteria. A time dependent risk analysis with\nlogistic regression and Cox regression was used for the analysis of in-hospital mortality and survival.\nResults: The incidence of AKI in the 6 month period was 15,325 pmp/yr (adults) (69% AKIN1, 18% AKIN2 and 13%\nAKIN3). In-hospital mortality, length of stay and ITU utilisation all increased with severity of AKI. Patients with AKI\nhad an increase in care on discharge and an increase in hospital readmission within 30 days.\nConclusions: This data comes closer to the real incidence and outcomes of AKI managed in-hospital than any\nstudy published in the literature to date. Fifteen percent of all admissions sustained an episode of AKI with\nincreased subsequent short and long term morbidity and mortality, even in those with AKIN1. This confers\nan increased burden and cost to the healthcare economy, which can now be quantified. These results will\nfurnish a baseline for quality improvement projects aimed at early identification, improved management, and\nwhere possible prevention, of AKI....
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