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.).