Publications by authors named "Steven G Achinger"

22 Publications

  • Page 1 of 1

Chronicity of Uncorrected Hyponatremia and Clinical Outcomes in Older Patients Undergoing Hip Fracture Repair.

Front Med (Lausanne) 2020 30;7:263. Epub 2020 Jun 30.

Instituto de Investigaciones Metabólicas, Universidad del Salvador, Buenos Aires, Argentina.

Chronic hyponatremia is a risk factor for hip fracture but remains uncorrected in most patients. This study evaluated if preoperative chronicity of uncorrected hyponatremia influences outcomes after hip fracture repair. Evaluated were older patients hospitalized for hip fracture repair between 2007 and 2012 with plasma sodium measured at admission and ≥1 preadmission outpatient measurement. Patients were classified as being normonatremic (NN; plasma sodium 135-145 mmol/L), chronic prolonged hyponatremia (CPH; ≥2 consecutive plasma sodium values <135 mmol/L over >90 days), or recent hyponatremia (one plasma sodium <135 mmol/L within 30 days before admission with previously normal plasma sodium). Length of hospital stay, in-hospital death, post-operative complications, 30-day readmission, and long-term mortality were the evaluated outcomes. Multivariable Cox regression was used to evaluate the association of hyponatremia status with outcomes. Among 1,571 eligible patients, 76.7% were NN, 14% had CPH, and 9.1% had RH. Compared with NN patients, CHN patients were older and had more prior heart failure, alcoholism, and anticonvulsant drug use. In multivariable analyses, neither CPH or RH was associated with hospital length of stay, in-hospital or 30-day death, or 30-day readmission, while RH was associated with post-operative sepsis [adjusted odds ratio (aOR) 1.84, 95% CI: 1.01-3.35). Only CPH was independently associated with long-term all-cause death (OR 1.53, 95% CI: 1.12-2.09). Hyponatremia affects nearly 25% of patients undergoing hip fracture repair. Preoperative chronic untreated hyponatremia is associated with increased post-operative mortality following surgical repair of a hip fracture in older patients. Future studies should evaluate if correction of hyponatremia could decrease long-term mortality after hip fracture repair.
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http://dx.doi.org/10.3389/fmed.2020.00263DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338672PMC
June 2020

Use of Desmopressin in Hyponatremia: Foe and Friend.

Kidney Med 2019 Mar-Apr;1(2):65-70. Epub 2019 Mar 14.

Renal Consultants of Houston, Houston, TX.

Use of desmopressin (1-deamino-8-d-arginine vasopressin; DDAVP), a synthetic vasopressin receptor agonist, has expanded in recent years. Desmopressin leads to renal water retention, and iatrogenic hyponatremia may result if fluid intake is not appropriately restricted. It is common practice to stop a medication that is causing toxicity, and this advice is promulgated in Micromedex, which suggests withholding desmopressin if hyponatremia occurs. If intravenous saline solution is administered and desmopressin is withheld at the same time, rapid changes in serum sodium levels may result, which puts the patient at risk for demyelinating lesions. In the management of desmopressin-associated hyponatremia with neurologic symptoms, the drug should not be withheld despite the presence of hyponatremia. The medication should be continued while administering intravenous hypertonic saline solution. Desmopressin is also used to minimize water excretion during the correction of hyponatremia during water diuresis. When treating hyponatremia, clinicians should monitor closely to avoid free-water diuresis. To prevent ongoing water losses in urine and overly rapid "autocorrection" of serum sodium level, desmopressin can be given to reduce free-water losses. These treatment recommendations are the authors' perspective from previously published work and personal clinical experience.
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http://dx.doi.org/10.1016/j.xkme.2019.02.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7380358PMC
March 2019

When the source of inflammation is hiding in plain sight: Failed kidney transplants, clotted arteriovenous grafts, and central venous catheters.

Semin Dial 2019 01 22;32(1):15-21. Epub 2018 Jul 22.

Renal Consultants of Houston, Houston, TX, USA.

Cardiovascular mortality accounts for most deaths among hemodialysis patients and far exceeds the cardiovascular mortality rate of the general population. One important aspect of cardiovascular risk among dialysis patients is chronic inflammation. Iatrogenic sources of chronic inflammation in the form of failed renal allografts, old clotted arteriovenous grafts, and hemodialysis catheters play important, sometimes, unrecognized roles in this inflammatory state. There is ample observational evidence that these sources of inflammation are associated with hypoalbuminemia, erythropoetin-resistant anemia, and increased markers of chronic inflammation. In dialysis patients with chronic inflammation from potentially modifiable sources, causes should be sought and correction undertaken if possible. Allograft nephrectomy should be offered to patients with a chronic inflammatory state and a failed renal transplant. Unused, clotted AV grafts should be considered a likely source of chronic inflammation as well as infection and should be removed when evidence of infection is present on indium scanning. Catheter rates ought to be kept to a minimum for the many well-recognized reasons for their undesirability as well as for their potential to produce chronic inflammation with all of its ill effects.
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http://dx.doi.org/10.1111/sdi.12739DOI Listing
January 2019

Electrolyte Disturbances in Chronic Alcohol-Use Disorder.

N Engl J Med 2018 01;378(2):202-3

Renal Consultants of Houston, Houston, TX

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http://dx.doi.org/10.1056/NEJMc1714331DOI Listing
January 2018

The authors reply.

Crit Care Med 2018 01;46(1):e100-e101

Department of Nephrology, Watson Clinic LLP, Lakeland, FL; Department of Research, Renal Consultants of Houston, Houston, TX, Department of Nephrology, Hospital Italiano, Buenos Aires, Argentina, Department of Nephrology, Hospital Austral, Austral University, Buenos Aires, Argentina, and Department of Nephrology, University of California, Irvine, CA.

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http://dx.doi.org/10.1097/CCM.0000000000002784DOI Listing
January 2018

Treatment of Hyponatremic Encephalopathy in the Critically Ill.

Crit Care Med 2017 Oct;45(10):1762-1771

1Department of Nephrology, Watson Clinic LLP, Lakeland, FL. 2Renal Consultants of Houston, Department of Research, Houston, TX. 3Department of Nephrology, Hospital Italiano, Buenos Aires, Argentina. 4Department of Nephrology, Hospital Austral, Austral University, Buenos Aires, Argentina. 5Department of Nephrology, University of California, Irvine, CA.

Objectives: Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency and often encountered in the ICU setting. This article provides a critical appraisal and review of the literature on identification of high-risk patients and the treatment of this life-threatening disorder.

Data Sources, Study Selection, And Data Extraction: Online search of the PubMed database and manual review of articles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopathy in critical illness.

Data Synthesis: Hyponatremic encephalopathy is a frequently encountered problem in the ICU. Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes. Manifestations are varied, depending on the extent of CNS's adaptation to the hypoosmolar state. The absolute change in serum sodium alone is a poor predictor of clinical symptoms. However, certain patient specific risks factors are predictive of a poor outcome and are important to identify. Gender (premenopausal and postmenopausal females), age (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are more predictive of poor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodium.

Conclusions: In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% saline, given over 10 minutes, should be promptly administered. The goal of this initial bolus is to quickly treat cerebral edema. If signs persist, the bolus should be repeated in order to achieve clinical remission. However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-2 hours and 15-20 mEq/L in the first 48 hours of treatment. It has recently been demonstrated in a prospective fashion that 500 mL of 3% saline at an infusion rate of 100 mL per hour can be given safely. It is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and intervene with IV 3% sodium chloride as this is the time to intervene rather than waiting until more severe symptoms develop. Cerebral demyelination is a rare complication of overly rapid correction of hyponatremia. The principal risk factors for cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of therapy, correction past the point of 140 mEq/L, chronic liver disease, and hypoxic/anoxic episode.
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http://dx.doi.org/10.1097/CCM.0000000000002595DOI Listing
October 2017

Getting it Straight: Avoiding Blunders While Criticizing a Peer's Work.

Int J Epidemiol 2016 06 14;45(3):619-20. Epub 2015 Aug 14.

Renal Consultants of Houston - Houston, TX, USA and Senior Consultant in Nephrology and Medicine, Hospital Italiano - Buenos Aires, Argentina.

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http://dx.doi.org/10.1093/ije/dyv154DOI Listing
June 2016

Disorders of plasma sodium.

N Engl J Med 2015 03;372(13):1267-8

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http://dx.doi.org/10.1056/NEJMc1501342DOI Listing
March 2015

Desmopressin acetate (DDAVP)-associated hyponatremia and brain damage: a case series.

Nephrol Dial Transplant 2014 Dec 8;29(12):2310-5. Epub 2014 Aug 8.

Renal Consultants of Houston, Houston, TX, USA Hospital Italiano, Buenos Aires, Argentina.

Background: Desmopressin (DDAVP) is typically prescribed for central diabetes insipidus, von Willebrands disease and for enuresis. DDAVP-associated hyponatremia is a known complication of DDAVP therapy. The currently recommended treatment for this condition calls for discontinuing DDAVP as part of the initial therapy. This recommendation could lead to a water diuresis and potentially over-correction of the serum sodium.

Methods: The 15 patients in this case series developed symptomatic DDAVP-associated hyponatremia and were admitted to acute care hospitals. Thirty-eight percent presented with symptomatic hyponatremia and 62% developed symptomatic hyponatremia due to concomitant DDAVP and hypotonic intravenous fluid administration during a hospital stay. Group 1 patients (n = 13) were treated by withholding DDAVP and providing intravenous saline. Group 2 patients (n = 2) were treated by continuing DDAVP and providing DDAVP and intravenous hypertonic saline.

Results: Among Group 1 patients, in whom DDAVP was withheld as initial management of DDAVP-associated hyponatremia (n = 13), the mean change in serum sodium in the first 2 days of treatment was 37.1 ± 8.1 mEq/L. The ultimate outcome in this group was death in 23%, severe brain damage in 69% and moderate brain damage in 8%. In Group 2 patients, in whom DDAVP was continued (n = 2) as part of the initial management strategy, the mean change in serum sodium was 11.0 ± 0 mEq/L in the first 2 days. The ultimate outcome was survival without neurological sequelae in both cases.

Conclusions: Discontinuing DDAVP in a patient with symptomatic DDAVP-associated hyponatremia can lead to rapid correction of the serum sodium and resultant severe neurological injury. In contrast, continuing the medication while correcting DDAVP-associated hyponatremia may lead to better outcomes by avoiding over-correction of the serum sodium. Thus, an alternative approach that we propose is to continue DDAVP as part of the initial management of this disorder.
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http://dx.doi.org/10.1093/ndt/gfu263DOI Listing
December 2014

Inflammation from dialysis, can it be removed?

Nephrol Dial Transplant 2013 Apr 28;28(4):770-3. Epub 2012 Oct 28.

Department of Nephrology, Watson Clinic, LLP – Lakeland, FL, USA.

Mortality among hemodialysis patients remains unacceptably high in the USA, especially among newly diagnosed end-stage renal disease patients. Chronic inflammation is a risk factor for cardiovascular disease among HD patients. It has been shown that complications of the arteriovenous (AV) access are not just limited to overt infectious complications but they may also pose a threat as a haven for occult infection and can aggravate the chronic inflammatory state. This inflammatory state is characterized by failure to thrive, erythropoietin-resistant anemia, hypoalbuminemia, elevated plasma C-reactive protein levels, which are well-known risk factors for increased morbidity and mortality on dialysis. In this issue, Wasse et al. presents a paper that demonstrates in a large cohort that failed AV grafts are associated with increased chronic inflammatory markers. They have provided a mechanistic insight into the causes of the chronic inflammatory state among dialysis patients. Along this line, it has also been demonstrated that failed renal allografts are also harbors of a chronic inflammatory state and that the removal of a failed renal allograft will lead to resolution of both overt inflammation and subclinical inflammatory states. This suggests that in select dialysis patients the surgical removal of foci of chronic inflammation can have an impact on the overall inflammatory state and perhaps survival.
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http://dx.doi.org/10.1093/ndt/gfs480DOI Listing
April 2013

Long-term effects of daily hemodialysis on vascular access outcomes: a prospective controlled study.

Hemodial Int 2013 Apr 28;17(2):208-15. Epub 2012 Sep 28.

Department of Nephrology, Watson Clinic, LLP-Lakeland, FL, USA.

Daily hemodialysis has been associated with surrogate markers of improved survival among hemodialysis patients. A potential disadvantage of daily hemodialysis is that frequent vascular access cannulations may affect long-term vascular access patency. The study design was a 4-year, nonrandomized, contemporary control, prospective study of 77 subjects in either 3-h daily hemodialysis (six 3-h dialysis treatments weekly; n = 26) or conventional dialysis (three 4-h dialysis treatments weekly; n = 51). Outcomes of interest were vascular access procedures (fistulagram, thrombectomy and access revision). Total access procedures (fistulagram, thrombectomy and access revision) were 543.2 (95% confidence interval [CI]: 432.9, 673.0) per 1000 person-years in the conventional dialysis group vs. 400.8 (95% CI: 270.2, 572.4) per 1000 person-years in the daily hemodialysis dialysis group (incidence rate ratio = 0.74 with 95% CI: from 0.40 to 1.36, P = 0.33), after adjusting for age, gender, diabetes status, serum phosphorus, hemoglobin level and erythropoietin dose, there was no significant differences in incidence rate of total access procedures (P-value > 0.05). There was no difference in time to first access revision between the daily dialysis and the conventional dialysis groups after adjustment for covariates (hazard ratio = 0.99 95% CI: 0.42, 2.36, P = 0.96). Daily hemodialysis is not associated with increased vascular access complications, or increased vascular access failure rates.
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http://dx.doi.org/10.1111/j.1542-4758.2012.00756.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4108201PMC
April 2013

Use of 3-hour daily hemodialysis and paricalcitol in patients with severe secondary hyperparathyroidism: A case series.

Hemodial Int 2010 Apr 10;14(2):193-9. Epub 2010 Mar 10.

Physicians Clinical Research, San Antonio, Texas, USA.

Patients with poor metabolic control receiving conventional hemodialysis are at risk for developing severe secondary hyperparathyroidism. We postulated that daily hemodialysis may be effective at controlling parathyroid hormone (PTH) in the setting of severe secondary hyperparathyroidism by improving the control of hyperphosphatemia and allowing increased use of vitamin D analogs. We present 5 patients with severe secondary hyperparathyroidism (median iPTH=1783 pg/mL) who were treated with 3-hour daily hemodialysis (3 hours x 6 times a week). Daily hemodialysis, at 1 year, was associated with a 70.4% reduction in median PTH (1783 pg/mL [interquartile range: 1321-1983]-472 pg/mL [334, 704], P<0.001). Additionally, there was an increase in paricalcitol dose from 0 mcg/d to 10.8 (2.00, 11.7) mcg/d, a 39% reduction in calcium x phosphorus product (80.3 +/- 26.8-48.9 +/- 14.0, P<0.01), a 52% reduction in serum phosphorus (9.90 +/- 2.34-4.75 +/- 0.79 mg/dL, P<0.0001), and a 17.6% increase in serum calcium (8.18 +/- 2.04-9.62 +/- 0.93 mg/dL, P<0.01). Three-hour daily hemodialysis with the use of high-dose paricalcitol is associated with improved control of severe secondary hyperparathyroidism.
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http://dx.doi.org/10.1111/j.1542-4758.2009.00424.xDOI Listing
April 2010

Transplant nephrectomy improves survival following a failed renal allograft.

J Am Soc Nephrol 2010 Feb 29;21(2):374-80. Epub 2009 Oct 29.

Department of Clinical Research, Renal Consultants of Houston, 2412 Westgate Street, Houston, TX, USA.

There is a growing number of patients returning to dialysis after a failed kidney transplant, and there is increasing evidence of higher mortality among this population. Whether removal of the failed renal allograft affects survival while receiving long-term dialysis is not well understood. We identified all adults who received a kidney transplant and returned to long-term dialysis after renal allograft failure between January 1994 and December 2004 from the US Renal Data System. Among 10,951 transplant recipients who returned to long-term dialysis, 3451 (31.5%) received an allograft nephrectomy during follow-up. Overall, 34.6% of these patients died during follow-up. Receiving an allograft nephrectomy associated with a 32% lower adjusted relative risk for all-cause death (adjusted hazard ratio 0.68; 95% confidence interval 0.63 to 0.74) after adjustment for sociodemographic characteristics, comorbidity burden, donor characteristics, interim clinical conditions associated with receiving allograft nephrectomy, and propensity to receive an allograft nephrectomy. In conclusion, within a large, nationally representative sample of high-risk patients returning to long-term dialysis after failed kidney transplant, receipt of allograft nephrectomy independently associated with improved survival.
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http://dx.doi.org/10.1681/ASN.2009050480DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834539PMC
February 2010

Brain cell volume regulation in hyponatremia: role of sex, age, vasopressin, and hypoxia.

Am J Physiol Renal Physiol 2008 Sep 30;295(3):F619-24. Epub 2008 Apr 30.

Renal Consultants of Houston, 2412 Westgate Street, Houston, TX 77019, USA.

Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors--discrepancy between skull size and brain size--are important in the genesis of brain damage. In adults, certain hormones--estrogen and vasopressin (usually elevated in cases of hyponatremia)--have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na(+)-K(+)-ATPase system to extrude cellular Na(+). In menstruant women, estrogen + vasopressin inhibits the Na(+)-K(+)-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po(2) and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones.
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http://dx.doi.org/10.1152/ajprenal.00502.2007DOI Listing
September 2008

Left ventricular hypertrophy: is hyperphosphatemia among dialysis patients a risk factor?

J Am Soc Nephrol 2006 Dec;17(12 Suppl 3):S255-61

Dialysis Service, Texas Diabetes Institute, Bextar County Hospital District, San Antonio, TX 78201, USA.

Cardiovascular disease occurs in ESRD patients at rates that are far higher than is seen in the general population, and cardiovascular deaths account for the majority of deaths among dialysis patients. Abnormal mineral metabolism is a novel cardiovascular risk factor among dialysis patients. Recently published results demonstrated that even with good control of BP and anemia, conventional hemodialysis is associated with significant left ventricular hypertrophy (LVH); however, daily hemodialysis was associated with a significant reduction in LV mass index (LVMI). Furthermore, it was shown that control of serum phosphorus correlates with the reduction in LVMI. These data suggest a novel mechanism for the deleterious effect of elevated serum phosphorus on cardiovascular outcomes among hemodialysis patients: LVH. Other investigators have noted an association of hyperphosphatemia and LVH; however, this study was the first to demonstrate that improvement in serum phosphorus is associated with reduction in LVM. In addition, it is shown that daily hemodialysis is an effective modality in improving serum phosphorus through significantly improved phosphorus removal. Elevated serum phosphorus leads to vascular calcification, which can lead to LVH by decreasing vascular compliance. However, our study showed an improvement in LVMI during a 12-mo period. Because vascular calcification is unlikely to remit over this time period, it is proposed that serum phosphorus has a reversible, cardiotoxic effect that leads to LVH that can be reversed successfully with good control of serum phosphorus.
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http://dx.doi.org/10.1681/ASN.2006080923DOI Listing
December 2006

Dysnatremias: why are patients still dying?

South Med J 2006 Apr;99(4):353-62; quiz 363-4

Division of Nephrology, Department of Medicine, University of Texas Health Science Center San Antonio, San Antonio, TX, USA.

Dysnatremias are a common clinical entity that are often associated with poor outcomes. This review takes a case study approach to understand how dysnatremias can result in devastating neurologic consequences. Concrete guidelines are provided for prevention, early recognition and treatment along with a discussion of how urinary electrolytes and osmolality can be used to guide therapy. Case studies in hyponatremic encephalopathy include the post-operative state, thiazide diuretics, extreme exercise and DDAVP use. Reasons to avoid using hypotonic parenteral fluids, risk factors for hyponatremic encephalopathy such as age, gender, and hypoxia, and the appropriate use of 3% sodium chloride are discussed. Case studies in hypernatremia include hypernatremia in the ICU setting and the emerging condition of breastfeeding-associated hypernatremia in infants.
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http://dx.doi.org/10.1097/01.smj.0000209351.55330.76DOI Listing
April 2006

Effects of short daily versus conventional hemodialysis on left ventricular hypertrophy and inflammatory markers: a prospective, controlled study.

J Am Soc Nephrol 2005 Sep 20;16(9):2778-88. Epub 2005 Jul 20.

Division of Nephrology, Texas Diabetes Institute, University of Texas Health Science Center San Antonio, San Antonio, TX 78229-3900, USA.

Left ventricular hypertrophy (LVH) and inflammation independently increase risk for death in people who receive hemodialysis. A nonrandomized, controlled trial was conducted of the effect of short daily (6 sessions/wk of 3 h each) or conventional (three sessions/wk of 4 h each) hemodialysis on LVH and inflammatory factors. A total of 26 short daily hemodialysis and 51 matched conventional hemodialysis patients were enrolled, and baseline and 12-mo measures of echocardiographic left ventricular mass index (LVMI), serum C-reactive protein (CRP), serum calcium and phosphorus, and erythropoietin resistance index were collected. Baseline characteristics were similar between groups except that hemoglobin and serum calcium were lower and serum phosphorus was higher in the short daily hemodialysis group. At 12-mo follow-up, short daily hemodialysis patients experienced a 30% decrease in LVMI (154 +/- 33 to 108 +/- 25; P < 0.0001). After adjustment for potential confounders, short daily hemodialysis (beta = -41.63, P = 0.03) and percentage decrease in serum phosphorus (beta = -0.12, P = 0.04) predicted a 12-mo decrease in LVMI. Among short daily hemodialysis patients, there were significant reductions in median CRP levels [1.22 interquartile range (IQR) (0.37 to 3.70) to 0.05 IQR (0.05 to 1.17); P < 0.01] and erythropoietin resistance index [19.5 IQR (8.6 to 37.6) to 10.5 IQR (5.5 to 14.6); P < 0.001]. There were no significant changes in LVMI, CRP, or erythropoietin resistance index in the conventional hemodialysis group. Short daily hemodialysis is associated with improved fluid and phosphorus management and a reduction in LVH and inflammatory factors compared with conventional hemodialysis. Future trials are needed to determine whether short daily hemodialysis can reduce morbidity and mortality in this high-risk population.
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http://dx.doi.org/10.1681/ASN.2005040392DOI Listing
September 2005

Effects of erythropoietin on left ventricular hypertrophy in adults with severe chronic renal failure and hemoglobin <10 g/dL.

Kidney Int 2005 Aug;68(2):788-95

The University of Texas Health Science Center at San Antonio, San Antonio, Texas 782293, USA.

Background: Left ventricular hypertrophy (LVH) frequently complicates chronic renal insufficiency. Anemia is also common in these patients and may contribute to LVH.

Methods: We conducted an open-label interventional trial to evaluate the effect of recombinant erythropoietin (rhEPO) on left ventricular mass index (LVMI) in anemic patients with renal insufficiency. Adults with creatinine clearance 10 to 30 mL/min (nondiabetics) or 20 to 40 mL/min (diabetics) were recruited, and rhEPO was given to those with anemia (hemoglobin level <10 g/dL). Baseline and 6-month LVMI and LVH (LVMI >130 g/m(2) in men and >100 g/m(2) in women), hemoglobin levels, creatinine clearance, blood pressure, medications, and medical history were obtained. Forty anemic and 61 nonanemic control subjects were enrolled.

Results: Overall, the prevalence of LVH was 68.3% (95% CI 58.3-77.2), and entry hemoglobin level was the only significant predictor of baseline LVH (adjusted OR 0.69 per g/dL increase in hemoglobin, 95% CI 0.50-0.94). After 6 months, LVMI decreased in anemic patients receiving rhEPO (142 +/- 56 vs. 157 +/- 56 g/m(2)) (P= 0.007), with an increase in hemoglobin (11.3 +/- 1.9 vs. 9.1 +/- 0.7 g/dL) (P= 0.001). There were no changes in LVMI or hemoglobin level among controls. After adjusting for confounders and change in hemoglobin, receipt of rhEPO was associated with a significant reduction in LVMI (P= 0.01).

Conclusion: Treatment with rhEPO was not independently associated with significant changes in blood pressure or renal function. LVH is a common finding in chronic renal insufficiency and is associated with lower hemoglobin levels. Treatment with rhEPO may decrease LVH in patients with severe renal insufficiency and anemia.
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http://dx.doi.org/10.1111/j.1523-1755.2005.00458.xDOI Listing
August 2005

At the peril of dialysis patients: ignoring the failed transplant.

Semin Dial 2005 May-Jun;18(3):180-4

Recently it has been shown that patients returning to hemodialysis (HD) following kidney transplant loss have poor survival, though the factors responsible for these poor outcomes remain largely unknown. In the past, we have shown that occult infection of clotted arteriovenous grafts (AVGs) leads to a chronic inflammatory state characterized by erythropoietin resistance, hypoalbuminemia, elevated C-reactive protein (CRP), and poor outcomes. It is well known that failed renal allografts induce graft intolerance syndrome, a clinical syndrome of pain, fever, and anemia, in the majority of patients. Similarly we have shown that failed renal allografts, by their nature as a nidus of chronic immunoreactivity, also induce a chronic inflammatory state. We speculate that this chronic inflammatory state, characterized by biochemical markers of poor HD outcomes, may be responsible for the excess mortality in this group. It is currently standard practice to leave failed kidney transplants in place upon return to HD and to treat symptomatic graft intolerance syndrome with immunosuppression. While this approach may reduce clinical symptoms in the short term, treatment failure and ultimately transplant nephrectomy occur in the majority of cases. There is also evidence that continued immunosuppression can even be dangerous. It should be noted that medical treatment of graft intolerance syndrome has not been shown to reduce chronic inflammation or decrease mortality. Similarly embolization of failed kidney transplants, another option for handling failed kidney transplants, has a high rate of treatment failure, has not been shown to reduce chronic inflammation, and nothing is known about the long-term safety of this approach. Therefore failed kidney transplants in patients with biochemical markers of chronic inflammation (as is the case for infected, clotted AVGs) should be removed prior to the development of clinical symptoms in order to eliminate the chronic inflammatory state.
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http://dx.doi.org/10.1111/j.1525-139X.2005.18304.xDOI Listing
October 2005

The role of vitamin D in left ventricular hypertrophy and cardiac function.

Kidney Int Suppl 2005 Jun(95):S37-42

Division of Nephrology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.

The role of vitamin D in left ventricular hypertrophy and cardiac function. Cardiovascular disease is the leading cause of death among patients with end-stage renal disease (ESRD). Traditional cardiac risk factors, as well as other factors specific to the ESRD population such as hyperphosphatemia, elevated calcium and phosphate product, abnormal lipid metabolism, hyperhomocysteinemia, and chronic inflammation play a role in the excessive risk of cardiovascular death in this population. Left ventricular disorders are proven risk factors for cardiac mortality in hemodialysis patients. These disorders are present in incident ESRD patients at rates far above the general population. There is an accumulating body of evidence that suggests that vitamin D plays a role in cardiovascular disease. Abnormal vitamin metabolism, through deficiency of the active form of 1,25-dihydroxyvitamin D(3), and acquired vitamin D resistance through the uremic state, have been shown to be important in ESRD. Vitamin D deficiency has long been known to affect cardiac contractility, vascular tone, cardiac collagen content, and cardiac tissue maturation. Recent studies using vitamin D receptor deficient mice as a model demonstrate a crucial role of vitamin D in regulation of the renin-angiotensin system. Additionally, there is emerging evidence linking treatment with vitamin D to improved survival on hemodialysis and improvement in cardiac function. The emergence of this data is focusing attention on the previously underappreciated nonmineral homeostatic effects of vitamin D that very likely play an important role in the pathogenesis of cardiac disease in ESRD.
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http://dx.doi.org/10.1111/j.1523-1755.2005.09506.xDOI Listing
June 2005

The role of daily dialysis in the control of hyperphosphatemia.

Kidney Int Suppl 2005 Jun(95):S28-32

Division of Nephrology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.

The role of daily dialysis in the control of hyperphosphatemia. In patients with end-stage renal disease (ESRD), hyperphosphatemia occurs in the vast majority of patients. The numerous clinical sequelae of hyperphosphatemia include secondary hyperparathyroidism and increased risk of cardiovascular death. Chronic hemodialysis as it is currently practiced in the United States does not remove sufficient phosphate to control serum levels within accepted guidelines. The inadequacy of conventional hemodialysis in removing phosphate mandates the use of phosphate binders in virtually all hemodialysis patients. Despite their proven efficacy, these medications fail to control phosphorous in 70% of hemodialysis patients. Additionally, these medications may have untoward side effects that must be considered since they are typically intended for lifetime use. Quotidian hemodialysis has in previous uncontrolled studies shown promise in reducing serum phosphorus while at the same time reducing or eliminating the need for phosphate binders. Recent results from our group demonstrate for the first time in a controlled fashion the efficacy of short daily dialysis in controlling serum phosphorus.
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http://dx.doi.org/10.1111/j.1523-1755.2005.09504.xDOI Listing
June 2005