WISHING 

ALL MALAYSIAN

A 

MERRY AND HAPPY

NEW YEAR 2012

Warmest Regards and Best Wishes

MalaysianKidneySPA

The Scribner shunt: 50 years later

Joseph B Lockridge¹ and Sindhu Chandran²

1. ¹Division of Nephrology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA
2. ²Division of Nephrology, Kidney Transplant Unit, Department of Medicine, University of California, San Francisco, San Francisco, California, USA
3. 
   
4. http://www.nature.com/ki/journal/v81/n1/full/ki2011344a.html

A 49-year-old male with end-stage renal disease returned to the United States 6 months following a repeat renal transplant in the Philippines that had failed 1 month after surgery. He presented with no records of his surgery or hospitalization, and stated that he had been on hemodialysis for 5 months. A Scribner shunt in the left arm (Figure 1) was identified by the nephrology service about 24 h following admission, with the connecting segment visible about 0.5 cm between the shunt lines (Figure 2). The arm was immediately covered with a dressing to minimize the risk of avulsion or interruption of the tubing, arterial clamps were made available at the bedside, and the device was removed 3 days later by a vascular surgeon. The ‘simplified’ or ‘poor-man's’ Scribner shunt (as it was known in the United Kingdom because it was inserted by the renal senior house officer rather than the surgeon) was developed in 1964 and consists of a simple loop of Teflon, which connects indwelling cannulae in the artery and vein. The connecting segment allows the artery and vein extensions to be attached to the dialyzer during dialysis and to be re-connected to each other after the treatment is completed. These shunts were prone to thrombosis, infection, and dislodgement and disappeared from most countries in the late 1970s and early 1980s, as venous catheters became widely adopted for temporary hemodialysis access. Many younger nephrologists in the United States have never seen a Scribner shunt. Prompt visual recognition is essential to avoid inadvertent manipulation or cannulation of the shunt, which can result in catastrophic bleeding.

Wishing 

All Christian Brothers and Sisters

A Merry & Blessed

Christmas

&

A Happy New Year

Best Wishes and Warmest Regards

MalaysianKidneySPA

Dietary salt influences postprandial plasma sodium concentration and systolic blood pressure

Rebecca J Suckling¹, Feng J He², Nirmala D Markandu² and Graham A MacGregor²

1. ¹Department of Cardiovascular Medicine, St George's University of London, London, UK
2. ²Barts and The London School of Medicine & Dentistry, Wolfson Institute of Preventive Medicine, London, UK

Kidney International advance online publication 2 November 2011; doi: 10.1038/ki.2011.369

Abstract:

The plasma sodium concentration has a direct effect on blood pressure in addition to its effects on extracellular volume regulated through changes in the endothelium. The mechanism for elevated blood pressure seen with habitually increased salt intake is unclear, especially the effect of salt in a single meal on plasma sodium concentration and blood pressure. To resolve this we compared the effect of soup with or without 6 g of salt (an amount similar to that in a single meal) on the plasma sodium concentration and blood pressure in 10 normotensive volunteers using a randomized, crossover design. The plasma sodium concentration was significantly increased by 3.13±0.75 mmol/l with salted compared with unsalted soup. Blood pressure increased in volunteers ingesting soup with added salt, and there was a significant positive correlation between plasma sodium concentration and systolic blood pressure. A 1-mmol/l increase in plasma sodium was associated with a 1.91-mm Hg increase in systolic blood pressure by linear regression. Thus, changes in plasma sodium concentration occur each time a meal containing salt is consumed. A potential mechanism for the changes in blood pressure seen with salt intake may be through its effects on plasma sodium concentration.

Dietary acid reduction with fruits and vegetables or bicarbonate attenuates kidney injury in patients with a moderately reduced glomerular filtration rate due to hypertensive nephropathy

Nimrit Goraya^1,2, Jan Simoni³, Chanhee Jo⁴ and Donald E Wesson^1,4

1. ¹Department of Internal Medicine, Texas A&M College of Medicine, Temple, Texas, USA
2. ²Department of Internal Medicine, Scott and White Healthcare, Temple, Texas, USA
3. ³Department of Surgery, Texas Tech University Health Sciences Center, Lubbock, Texas, USA
4. ⁴Department of Biostatistics, Scott and White Healthcare, Temple, Texas, 
5. 
   
6. USAKidney International (2012) 81, 86–93; doi:10.1038/ki.2011.313; published online 31 August 2011

Abstract

The neutralization of dietary acid with sodium bicarbonate decreases kidney injury and slows the decline of the glomerular filtration rate (GFR) in animals and patients with chronic kidney disease. The sodium intake, however, could be problematic in patients with reduced GFR. As alkali-induced dietary protein decreased kidney injury in animals, we compared the efficacy of alkali-inducing fruits and vegetables with oral sodium bicarbonate to diminish kidney injury in patients with hypertensive nephropathy at stage 1 or 2 estimated GFR. All patients were evaluated 30 days after no intervention; daily oral sodium bicarbonate; or fruits and vegetables in amounts calculated to reduce dietary acid by half. All patients had 6 months of antihypertensive control by angiotensin-converting enzyme inhibition before and during these studies, and otherwise ate ad lib. Indices of kidney injury were not changed in the stage 1 group. By contrast, each treatment of stage 2 patients decreased urinary albumin, N-acetyl β-d-glucosaminidase, and transforming growth factor β from the controls to a similar extent. Thus, a reduction in dietary acid decreased kidney injury in patients with moderately reduced eGFR due to hypertensive nephropathy and that with fruits and vegetables was comparable to sodium bicarbonate. Fruits and vegetables appear to be an effective kidney protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition in hypertensive and possibly other nephropathies.

Chronic renal failure from lead: myth or evidence-based fact?

Evans M, Elinder CG

Nephrology Unit, Department of Clinical Sciences Intervention and Technology, Karolinska Institute, Stockholm, Sweden. marie.evans@ki.se

Kidney Int. 2011 Feb;79(3):272-9. Epub 2010 Oct 13.

Abstract

In this mini review, we would like to challenge the well-established 'fact' that lead exposure causes chronic renal failure (CRF). Even though only scarce evidence exists of the relationship between lead and renal failure, a World Health Organization Environmental Health Criteria document summarizes that 'Lead has been a very common cause of acute or chronic renal failure'. It is also written and cited in textbooks and numerous publications that chronic lead nephropathy causes a slowly progressive interstitial nephritis manifested by a reduced glomerular filtration rate, and that there is a growing consensus that lead contributes to hypertension in the general population. We will argue that, when published reports are carefully scrutinized, such statements on lead and CRF are not evidence based but are rather founded on a few narrative reports on lead-exposed individuals and statistical associations between lead and serum creatinine (or urea) in a few population studies. We will, however, not argue that lead is not toxic and that lead does not cause other types of severe health effects where the evidence is unquestionable, but we do not believe that the kidneys are an early victim after lead exposure.

Daulat Tuanku!

Daulat Tuanku!

Daulat Tuanku!

The deleterious effect of metabolic acidosis on nutritional status of hemodialysis patients.

Soleymanian T, Ghods A.

Source

Division of Nephrology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Saudi J Kidney Dis Transpl. 2011 Nov;22(6):1149-54.

Abstract

One of the main causes of protein-energy malnutrition in patients on maintenance hemodialysis (MHD) is metabolic acidosis. The aim of this study was to evaluate the effect of metabolic acidosis on nutritional status in a group of MHD patients with adequately delivered dialysis treatment. Of 165 eligible anuric MHD outpatients with Kt/V ≥ 1 and no underlying inflammatory diseases, 47 subjects were enrolled. In order to evaluate the effect of different parameters on serum albumin, we measured the pre-dialysis serum albumin, blood pH, serum bicarbonate (HCO 3‾ ), Kt/V, normalized protein catabolic rate (nPCR) and body mass index (BMI) in these patients. The mean age of the study patients was 55 ± 13.8 years; there were 22 females and six diabetics. The average Kt/V was 1.22 ± 0.16, pH was 7.40 ± 0.15, serum HCO 3‾ was 23.18 ± 2.38 mEq/L, serum albumin was 4.03 ± 0.56 g/dL, nPCR was 1.00 ± 0.16 g/kg/day, post-dialysis body weight was 58.50 ± 11.50 kg and BMI was 23.47 ± 2.70 kg/m 2 . There was a statistically significant direct correlation between serum albumin and BMI (r = 0.415, P = 0.004), and between serum albumin and serum HCO 3 (r = 0.341, P = 0.019). On multiple regression analysis, the predictors of serum albumin were serum HCO3‾ and BMI (direct effect) and nPCR (inverse effect). In 17 patients on MHD with serum HCO3‾ <22 mEq/L, there was a significant inverse correlation between HCO 3 and nPCR (r = 0.492, P = 0.045), and these patients had significantly lower serum albumin compared with patients with serum HCO3‾ >22 mEq/L (P = 0.046). These data demonstrate that patients on MHD with metabolic acidosis had a lower serum albumin concentration despite adequate dialysis treatment. The inverse effect of nPCR on serum albumin concentration in acidotic MHD patients may be due to hypercatabolism in the setting of metabolic acidosis, leading to deleterious effects on the nutritional status of patients on MHD

Long interdialytic interval and mortality among patients receiving hemodialysis.

Robert N Foley, David T Gilbertson, Thomas Murray and Allan J Collins N Engl J Med 365(12):1099-107 (2011) PMID 21992122  DOI: 10.1056/NEJMoa1103313

Patients with end-stage renal disease requiring dialysis have limited tolerance of metabolic and volume-related deviations from normal ranges; in addition, the prevalence of cardiovascular disease is high among such patients. Given these problems, we hypothesized that a long interdialytic interval is associated with adverse events in patients receiving hemodialysis. We studied 32,065 participants in the End-Stage Renal Disease Clinical Performance Measures Project, a nationally representative sample of U.S. patients receiving hemodialysis three times weekly, at the end of calendar years 2004 through 2007. We compared rates of death and cardiovascular-related hospital admissions on the day after the long (2-day) interdialytic interval with rates on other days. The mean age of the cohort was 62.2 years; 24.2% of the patients had been receiving dialysis treatment for 1 year or less. Over a mean follow-up interval of 2.2 years, the following event rates were higher on the day after the long interval than on other days: all-cause mortality (22.1 vs. 18.0 deaths per 100 person-years, P<0.001), mortality from cardiac causes (10.2 vs. 7.5, P<0.001), infection-related mortality (2.5 vs. 2.1, P = 0.007), mortality from cardiac arrest (1.3 vs. 1.0, P = 0.004), mortality from myocardial infarction (6.3 vs. 4.4, P<0.001), and admissions for myocardial infarction (6.3 vs. 3.9, P<0.001), congestive heart failure (29.9 vs. 16.9, P<0.001), stroke (4.7 vs. 3.1, P<0.001), dysrhythmia (20.9 vs. 11.0, P<0.001), and any cardiovascular event (44.2 vs. 19.7, P<0.001). The long (2-day) interdialytic interval is a time of heightened risk among patients receiving hemodialysis. (Funded by the National Institutes of Health.). 

Hypercholesterolemia promotes early renal dysfunction in apolipoprotein E-deficient mice  

Camille M Balarini, Mariana ZT Oliveira, Thiago MC Pereira, Nyam F Silva, Elisardo C Vasquez, Silvana S Meyrelles andAgata L Gava

Published: 26 November 2011   Lipids in Health and Disease 2011, 10:22doi:10.1186/1476-511X-10-220

Abstract

Background

Aging and dyslipidemia are processes which can lead to deleterious consequences to renal function. Therefore, the aim of this study was to determine the effects of both hypercholesterolemia and aging on renal function in mice.

Methods

Male hypercholesterolemic apolipoprotein E-deficient mice (ApoE, n=13) and age-matched C57BL/6 control mice (C57, n=15) were studied at 2 (young) and 8 (adult) month-old. At each time point, animals were placed in metabolic cages for 24 hours to urine volume and urinary creatinine quantification. Blood samples were collected for serum cholesterol, urea and creatinine measurements. Glomerular filtration rate (GFR) was estimated through creatinine clearance determination. Mesangial expansion was evaluated by Periodic Acid Schiff staining, renal fibrosis was determined through Masson's trichrome staining and neuronal nitric oxide synthase (nNOS) expression in the kidney was performed by Western Blotting. To statistical analysis two- way ANOVA followed by Fisher's post hoc test was used.

Results

Total plasma cholesterol was increased about 5-fold in ApoE mice at both time points compared to C57 animals. At 2-month-old, GFR was already markedly reduced in ApoE compared to C57 mice (187 +/- 28 vs 358 +/- 92 uL/min, p<0.05). Adult C57 (-77%) and ApoE (-50%) mice also presented a significant reduction of GFR. In addition, serum urea was significantly increased in young ApoE animals compared to C57 mice (11 +/- 1.3 vs 7 +/- 0.9 mmol/L, p<0.01). A significant mesangial expansion was observed at 2-month old ApoE mice compared to C57 mice (35 +/- 0.6 vs 30 +/- 0.9 %, respectively, p<0.05), which was aggravated at 8-month old animals (40 +/- 3 and 35 +/- 3 %, respectively). Tubulointersticial fibrosis was augmented at both young (17 +/- 2%, p<0.05) and adult (20 +/- 1 %, p<0.05) ApoE mice compared to respective C57 age controls (8 +/- 1 and 12 +/- 2%, respectively). The expression of nNOS was markedly reduced in a time-dependent manner in both strains.

Conclusions

These data show that both hypercholesterolemia and aging contribute to the loss of renal function in mice.

Uric acid is a strong independent predictor of renal dysfunction in patients with rheumatoid arthritis

Dimitrios Daoussis¹, Vasileios Panoulas¹, Tracey Toms¹, Holly John¹, Ioannis Antonopoulos¹, Peter Nightingale², Karen MJ Douglas¹, Rainer Klocke¹ and George D Kitas^1,3*

¹Department of Rheumatology, Dudley Group of Hospitals NHS Trust, Russells Hall Hospital, Pensnett Road, Dudley, West Midlands, DY1 2HQ, UK

²Wolfson Laboratory, Department of Medical Statistics, School of Medicine, University of Birmingham, Queen Elizabeth Medical Centre, Edgbaston, Birmingham, B15 2TH, UK

Arthritis Research & Therapy 2009, 11:R116 doi:10.1186/ar2775


Introduction


Arthritis Research Campaign Epidemiology Unit, University of Manchester, Oxford Road, Stopford Building, Manchester, M13 9PT, UKRecent evidence suggests that uric acid (UA), regardless of crystal deposition, may play a direct pathogenic role in renal disease. We have shown that UA is an independent predictor of hypertension and cardiovascular disease (CVD), and that CVD risk factors associate with renal dysfunction, in patients with rheumatoid arthritis (RA). In this study we investigated whether UA associates with renal dysfunction in patients with RA and whether such an association is independent or mediated through other comorbidities or risk factors for renal impairment.

Methods

Renal function was assessed in 350 consecutive RA patients by estimated glomerular filtration rate (GFR) using the six-variable Modification of Diet in Renal Disease equation. Risk factors for renal dysfunction were recorded or measured in all participants. Linear regression was used to test the independence of the association between GFR and UA.

Results

Univariable analysis revealed significant associations between GFR and age, systolic blood pressure, total cholesterol, triglycerides, RA duration and UA. UA had the most powerful association with renal dysfunction (r = -0.45, P < 0.001). A basic model was created, incorporating all of the above parameters along with body mass index and gender. UA ranked as the first correlate of GFR (P < 0.001) followed by age. Adjustments for the use of medications (diuretics, low-dose aspirin, cyclooxygenase II inhibitors and nonsteroidal anti-inflammatory drugs) and further adjustment for markers of inflammation and insulin resistance did not change the results.

Conclusions

UA is a strong correlate of renal dysfunction in RA patients. Further studies are needed to address the exact causes and clinical implications of this new finding. RA patients with elevated UA may require screening for renal dysfunction and appropriate management

The Effect of High-Flux Hemodialysis on Hemoglobin Concentrations in Patients with CKD: Results of the MINOXIS Study.

Schneider A, Drechsler C, Krane V, Krieter DH, Scharnagl H, Schneider MP, Wanner C; for the MINOXIS Study Investigators.

Source

Division of Nephrology, University Hospital Würzburg, Würzburg, Germany;

Abstract

Background and objectivesHemodialysis treatment induces markers of inflammation and oxidative stress, which could affect hemoglobin levels and the response to erythropoietin use. This study sought to determine whether high-flux dialysis would help improve markers of renal anemia, inflammation, and oxidative stress compared with low-flux dialysis.Design, settings, participants, &amp; measurementsIn a prospective, controlled study, 221 patients undergoing maintenance hemodialysis and receiving darbepoetin-alfa treatment (mean age, 66 years; 55% male) from 19 centers were screened in a 20-week run-in period of low-flux hemodialysis with a synthetic dialysis membrane. Thereafter, 166 patients were enrolled and randomly assigned to receive a synthetic high-flux membrane or to continue on low-flux dialysis for 52 weeks. Data on myeloperoxidase, oxidized LDL, high-sensitivity C-reactive protein, and the Malnutrition Inflammation Score were collected at baseline and after 52 weeks; routine laboratory data, such as hemoglobin, ferritin, and albumin, and the use of darbepoetin-alfa, were also measured in the run-in period.

Results. After 52 weeks, the low-flux and the high-flux groups did not differ with respect to hemoglobin (mean ± SD, 11.7±0.9 g/dl versus 11.7±1.1 g/dl; P=0.62) or use of darbepoetin-alfa (mean dosage ± SD, 29.8±24.8 μg/wk versus 26.0±31.1 μg/wk; P=0.85). Markers of inflammation, oxidative stress, or nutritional status also did not differ between groups.

Conclusion. Over 1 year, high-flux dialysis had no superior effects on hemoglobin levels or markers of inflammation, oxidative stress, and nutritional status. These data do not support the hypothesis that enhanced convective toxin removal would improve patient outcome.

Clin J Am Soc Nephrol. 2011 Nov 17. [Epub ahead of print]: http://www.ncbi.nlm.nih.gov/pubmed/22096040