Publications by authors named "Juan Carlos Ayus"

56 Publications

Risks of Hip and Nonvertebral Fractures in Patients With CKD.

Am J Kidney Dis 2021 04 12;77(4):546. Epub 2021 Feb 12.

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

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http://dx.doi.org/10.1053/j.ajkd.2020.10.018DOI Listing
April 2021

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

Chronic prolonged hyponatremia and risk of hip fracture in elderly patients with chronic kidney disease.

Bone 2019 10 27;127:556-562. Epub 2019 Jul 27.

Renal Consultants of Houston, Houston, TX, United States; University of California, Irving, CA, United States. Electronic address:

Background: Chronic prolonged hyponatremia (CPH) is a risk factor for hip fracture in the general population. Whether CPH increases hip fracture risk in chronic kidney disease (CKD) patients is unknown.

Methods: Case-control study in patients over 60 years of age with stage 3 or greater CKD. Patients who had a hip fracture were referred to as cases (n = 1236) and controls had no hip fracture (n = 4515). Patients were classified as having CPH if serum sodium was <135 mEq/L on at least two occasions separated by a minimum of 90 days prior to the diagnosis of hip fracture (cases) or at any time during the study period (controls). Conditional logistic regression models were used to test the association between CPH and hip fracture. Analyses were conducted for patients with and without osteoporosis and falls and for patients with age >70 years versus ≤70 years.

Results: CPH was present in 21% of cases and 10% of controls (p < 0.001; sodium level: 131-134 mEq/L). In univariate logistic regression analysis, CPH was associated with higher odds of hip fracture (odds ratio [OR] 2.44, (95% [CI] 2.07-2.89). In a multivariate model adjusted for comorbidities, medications and laboratory parameters CPH association with higher odds of Hip fracture was attenuated but remained significant (OR 1.36, 95% CI 1.04-1.78). The association between CPH and risk of hip fracture was consistent in patients with or without osteoporosis and falls and across the age strata.

Conclusion: Chronic prolonged hyponatremia is a risk factor for hip fracture in CKD patients older than 60 years of age.
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http://dx.doi.org/10.1016/j.bone.2019.07.029DOI Listing
October 2019

Fragility fractures and reversible osteopaenia due to chronic hyponatraemia in an adolescent male.

BMJ Case Rep 2019 Jul 27;12(7). Epub 2019 Jul 27.

Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Fragility fractures are common in older adults and rare in children. Recent studies have demonstrated that hyponatraemia is a novel risk factor for the development of osteoporosis and hip fractures in older people. Animal studies suggest that hyponatraemia can lead to decreased bone mineral density by stimulating osteoclastic activity in order to mobilise sodium from the bone. Reported is a 16-year-old man with intractable epilepsy and an 11-year history of chronic hyponatraemia (126-135 mEq/L) due to valproic acid induced syndrome of inappropriate antidiuresis who sustained low-impact fragility fractures and had evidence of osteopaenia on both X-ray and dual energy X-ray absorptiometry (DEXA). Hyponatraemia resolved following the discontinuation of valproic acid and bone mineral density normalised on a repeat DEXA 19 months later. This case provides evidence supporting the contention that chronic hyponatraemia contributes to osteopaenia and fragility fractures and that the bone abnormalities are potentially reversible following the correction of hyponatraemia.
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http://dx.doi.org/10.1136/bcr-2019-229875DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6663176PMC
July 2019

Hyponatremia in the Dialysis Population.

Kidney Int Rep 2019 Jun 1;4(6):769-780. Epub 2019 Mar 1.

Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine, Orange, California, USA.

Sodium derangements are among the most frequently encountered electrolyte disorders in patients with end-stage renal disease. As dialysis patients are predisposed to hyponatremia via multiple pathways, assessment of extracellular volume status is an essential first step in disentangling potential etiologic factors. In addition, multiple large population-based studies indicate that proxies of malnutrition (e.g., low body mass index, serum albumin, and serum creatinine levels) and loss of residual kidney function are important determinants of hyponatremia in dialysis patients. Among hemodialysis and peritoneal dialysis patients, evidence suggests that incrementally lower sodium levels are associated with increasingly higher death risk, highlighting the long-term risk of hyponatremia. Whereas in conventional survival models incrementally lower serum sodium concentrations are associated with worse mortality in hemodialysis patients, studies that have examined repeated measures of predialysis sodium have demonstrated mixed associations of time-varying sodium with higher mortality risk (i.e., U-shaped vs. inverse linear relationships). Although the causality of the hyponatremia-mortality association in dialysis patients remains uncertain, there are several plausible pathways by which lower sodium levels may lead to higher death risk, including central nervous system toxicity, falls and fractures, infection-related complications, and impaired cardiac function. Areas of uncertainty ripe for future studies include the following: (i) mechanistic pathways by which lower serum sodium levels are linked with higher mortality in dialysis patients, (ii) whether correction of sodium derangements improves outcomes, (iii) the optimal sodium target, and (iv) the impact of age and other sociodemographic factors on hyponatremia-outcome associations.
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http://dx.doi.org/10.1016/j.ekir.2019.02.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6551474PMC
June 2019

Misconceptions and Barriers to the Use of Hypertonic Saline to Treat Hyponatremic Encephalopathy.

Front Med (Lausanne) 2019 15;6:47. Epub 2019 Mar 15.

Division of Nephrology, UPMC Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

Hyponatremic encephalopathy is a potentially life-threatening condition with a high associated morbidity and mortality. It can be difficult to diagnose as the presenting symptoms can be non-specific and do not always correlate with the degree of hyponatremia. It can rapidly progress leading to death from transtentorial herniation. Hypertonic saline is the recommended treatment for hyponatremic encephalopathy, whether acute or chronic, yet it is infrequently used. We believe that the main barriers to its use is the perception that hypertonic saline is associated with a significant risk for cerebral demyelination, that it can't be administered through a peripheral IV and that it requires monitoring in the ICU. Two illustrative cases are presented followed by a discussion of how intermittent bolus's of 100-150 ml of 3% NaCl in rapid succession to acutely increase the plasma sodium by 4-6 mEq/L is a safe and effective way to treat hyponatremic encephalopathy, that can be administered through a peripheral IV in a non-ICU setting.
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http://dx.doi.org/10.3389/fmed.2019.00047DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428704PMC
March 2019

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

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

Hyponatremia and bone disease.

Rev Endocr Metab Disord 2017 03;18(1):67-78

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

Hip fractures represent a serious health risk in the elderly, causing substantial morbidity and mortality. There is now a considerable volume of literature suggesting that chronic hyponatremia increases the adjusted odds ratio (OR) for both falls and fractures in the elderly. Hyponatremia appears to contribute to falls and fractures by two mechanisms. First, it produces mild cognitive impairment, resulting in unsteady gait and falls; this is probably due to the loss of glutamate (a neurotransmitter involved in gait function) as an osmolyte during brain adaptation to chronic hyponatremia. Second, hyponatremia directly contributes to osteoporosis and increased bone fragility by inducing increased bone resorption to mobilize sodium stores in bone. Low extracellular sodium directly stimulates osteoclastogenesis and bone resorptive activity through decreased cellular uptake of ascorbic acid and the induction of oxidative stress; these effects occur in a sodium level-dependent manner. Hyponatremic patients have elevated circulating arginine-vasopressin (AVP) levels, and AVP acting on two receptors expressed in osteoblasts and osteoclasts, Avpr1α and Avpr2, can increase bone resorption and decrease osteoblastogenesis. Should we be screening for low serum sodium in patients with osteoporosis or assessing bone mineral density (BMD) in patients with hyponatremia? The answers to these questions have not been established. Definitive answers will require randomized controlled studies that allocate elderly individuals with mild hyponatremia to receive either active treatment or no treatment for hyponatremia, to determine whether correction of hyponatremia prevents gait disturbances and changes in BMD, thereby reducing the risk of fractures. Until such studies are conducted, physicians caring for elderly patients must be aware of the association between hyponatremia and bone disorders. As serum sodium is a readily available, simple, and affordable biochemical measurement, clinicians should look for hyponatremia in elderly patients, especially in those receiving medications that can cause hyponatremia. Furthermore, elderly patients with an unsteady gait and/or confusion should be evaluated for the presence of mild hyponatremia, and if present, treatment should be initiated. Finally, elderly patients presenting with an orthopedic injury should have serum sodium checked and hyponatremia corrected, if present.
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http://dx.doi.org/10.1007/s11154-016-9387-7DOI Listing
March 2017

Serum sodium and mortality in a national peritoneal dialysis cohort.

Nephrol Dial Transplant 2017 Jul;32(7):1224-1233

Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine Medical Center, Orange, CA, USA.

Background: Sodium disarrays are common in peritoneal dialysis (PD) patients, and may be associated with adverse outcomes in this population. However, few studies of limited sample size have examined the association of serum sodium with mortality in PD patients, with inconsistent results. We hypothesized that both hypo- and hypernatremia are associated with higher death risk in a nationally representative cohort of US PD patients.

Methods: We sought to examine the association of serum sodium over time and mortality among 4687 adult incident PD patients from a large US dialysis organization who underwent one or more serum sodium measurements within the first 3 months of dialysis over January 2007 to December 2011. We examined the association of time-dependent and baseline sodium with all-cause mortality as a proxy of short- and long-term sodium-mortality associations, respectively. Hazard ratios were estimated using Cox models with three adjustment levels: minimally adjusted, case-mix adjusted, and case-mix + laboratory adjusted.

Results: In time-dependent analyses, sodium levels <140 mEq/L were associated with incrementally higher death risk in case-mix models (ref: 140 to <142 mEq/L); following laboratory covariate adjustment, associations between lower sodium and higher mortality remained significant for levels <136 mEq/L. In analyses using baseline values, sodium levels <140 mEq/L were associated with higher mortality risk across all models (ref: 140 to <142 mEq/L).

Conclusions: In PD patients, lower time-dependent and baseline sodium levels were independently associated with higher death risk. Further studies are needed to determine whether correction of dysnatremia improves longevity in this population.
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http://dx.doi.org/10.1093/ndt/gfw254DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837718PMC
July 2017

Mild prolonged chronic hyponatremia and risk of hip fracture in the elderly.

Nephrol Dial Transplant 2016 10 23;31(10):1662-9. Epub 2016 Mar 23.

Internal Medicine Research Unit, Internal Medicine Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.

Background: Hip fractures are among the most serious bone fractures in the elderly, producing significant morbidity and mortality. Several observational studies have found that mild hyponatremia can adversely affect bone, with fractures occurring as a potential complication. We examined if there is an independent association between prolonged chronic hyponatremia (>90 days duration) and risk of hip fracture in the elderly.

Methods: We performed a retrospective cohort study in adults >60 years of age from a prepaid health maintenance organization who had two or more measurements of plasma sodium between 2005 and 2012. The incidence of hip fractures was assessed in a very restrictive population: subjects with prolonged chronic hyponatremia, defined as plasma sodium values <135 mmol/L, lasting >90 days. Multivariable Cox regression was performed to determine the hazard ratio (HR) for hip fracture risk associated with prolonged chronic hyponatremia after adjustment for the propensity to have hyponatremia, fracture risk factors and relevant baseline characteristics.

Results: Among 31 527 eligible patients, only 228 (0.9%) had prolonged chronic hyponatremia. Mean plasma sodium was 132 ± 5 mmol/L in hyponatremic patients and 139 ± 3 mmol/L in normonatremic patients (P < 0.001). The absolute risk for hip fracture was 7/282 in patients with prolonged chronic hyponatremia and 411/313 299 in normonatremic patients. Hyponatremic patients had a substantially elevated rate of hip fracture [adjusted HR 4.52 (95% CI 2.14-9.6)], which was even higher in those with moderate hyponatremia (<130 mmol/L) [adjusted HR 7.61 (95% CI 2.8-20.5)].

Conclusion: Mild prolonged chronic hyponatremia is independently associated with hip fracture risk in the elderly population, although the absolute risk is low. However, proof that correcting hyponatremia will result in a reduction of hip fractures is lacking.
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http://dx.doi.org/10.1093/ndt/gfw029DOI Listing
October 2016

Pre-dialysis serum sodium and mortality in a national incident hemodialysis cohort.

Nephrol Dial Transplant 2016 06 25;31(6):992-1001. Epub 2015 Sep 25.

Harold Simmons Center for Chronic Disease Research and Epidemiology, University of California Irvine, Orange, CA, USA Renal Consultants of Houston, Houston, TX, USA.

Background: A consistent association between low serum sodium measured at a single-point-in-time (baseline sodium) and higher mortality has been observed in hemodialysis patients. We hypothesized that both low and high time-varying sodium levels (sodium levels updated at quarterly intervals as a proxy of short-term exposure) are independently associated with higher death risk in hemodialysis patients.

Methods: We examined the association of baseline and time-varying pre-dialysis serum sodium levels with all-cause mortality among adult incident hemodialysis patients receiving care from a large national dialysis organization during January 2007-December 2011. Hazard ratios were estimated using multivariable Cox models accounting for case-mix+laboratory covariates and incrementally adjusted for inter-dialytic weight gain, blood urea nitrogen and glucose.

Results: Among 27 180 patients, a total of 7562 deaths were observed during 46 194 patient-years of follow-up. Median (IQR) at-risk time was 1.4 (0.6, 2.5) years. In baseline analyses adjusted for case-mix+laboratory results, sodium levels <138 mEq/L were associated with incrementally higher mortality risk, while the association of sodium levels ≥140 mEq/L with lower mortality reached statistical significance only for the highest level of pre-dialysis sodium (reference: 138-<140 mEq/L). In time-varying analyses, we observed a U-shaped association between sodium and mortality such that sodium levels <138 and ≥144 mEq/L were associated with higher mortality risk. Similar patterns were observed in models incrementally adjusted for inter-dialytic weight gain, blood urea nitrogen and glucose.

Conclusions: We observed a U-shaped association of time-varying pre-dialysis serum sodium and all-cause mortality in hemodialysis patients, suggesting that both hypo- and hypernatremia carry short-term risk in this population.
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http://dx.doi.org/10.1093/ndt/gfv341DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4876967PMC
June 2016

In Reply to 'Treatment of Hyponatremic Encephalopathy'.

Am J Kidney Dis 2015 Sep;66(3):540

University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.

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http://dx.doi.org/10.1053/j.ajkd.2015.05.026DOI Listing
September 2015

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

Acute symptomatic hyponatremia in a flight attendant.

Clin Nephrol 2015 Aug;84(2):108-10

Acute symptomatic hyponatremia after thiazide diuretic initiation is a medical emergency. Here we describe the case of a flight attendant who developed acute hyponatremia during a flight and the potential risk factors for developing this condition. A 57-year-old flight attendant with history of essential hypertension was recently started on a thiazide diuretic. As she did routinely when working, she increased her water intake during a flight from London to Mexico City. She complained of nausea and headache during the flight. Upon arrival, she developed severe disorientation and presented to the hospital emergency room (ER) with a Glasgow scale of 12, hypoxia, and a generalized tonic clonic seizure. Her laboratory results on arrival were consistent with severe hyponatremia (serum Na 116 mEql/L) and severe cerebral edema by CT scan. She was treated with hypertonic saline, with complete resolution of the neurologic symptoms. We describe high water intake and hypoxia related to decreased partial pressure of oxygen in the cabin as the two main risk factors for thiazide-induced acute hyponatremia in this case.
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http://dx.doi.org/10.5414/CN108472DOI Listing
August 2015

Treatment of hyponatremic encephalopathy with a 3% sodium chloride protocol: a case series.

Am J Kidney Dis 2015 Mar 25;65(3):435-42. Epub 2014 Nov 25.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh School of Medicine, Pittsburgh, PA.

Background: 3% sodium chloride solution is the accepted treatment for hyponatremic encephalopathy, but evidence-based guidelines for its use are lacking.

Study Design: A case series.

Setting & Participants: Adult patients presenting to the emergency department of a university hospital with hyponatremic encephalopathy, defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause, and treated with a continuous infusion of 500mL of 3% sodium chloride solution over 6 hours through a peripheral vein.

Predictors: Hyponatremic encephalopathy defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause.

Outcomes: Change in serum sodium level within 48 hours, improvement in neurologic symptoms, and clinical evidence of cerebral demyelination, permanent neurologic injury, or death within 6 months' posttreatment follow-up.

Results: There were 71 episodes of hyponatremic encephalopathy in 64 individuals. Comorbid conditions were present in 86% of individuals. Baseline mean serum sodium level was 114.1±0.8 (SEM) mEq/L and increased to 117.9±1.3, 121.2±1.2, 123.9±1.0, and 128.3±0.8 mEq/L at 3, 12, 24, and 48 hours following the initiation of 3% sodium chloride solution treatment, respectively. There was a marked improvement in central nervous system symptoms within hours of therapy in 69 of 71 (97%) episodes. There were 12 deaths, all of which occurred following the resolution of hyponatremic encephalopathy and were related to comorbid conditions, with 75% of deaths related to sepsis. No patient developed neurologic symptoms consistent with cerebral demyelination at any point during the 6-month follow-up period.

Limitations: Lack of a comparison group and follow-up neuroimaging studies. Number of cases is too small to provide definitive assessment of the safety of this protocol.

Conclusions: 3% sodium chloride solution was effective in reversing the symptoms of hyponatremic encephalopathy in the emergency department without producing neurologic injury related to cerebral demyelination on long-term follow-up in this case series.
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http://dx.doi.org/10.1053/j.ajkd.2014.09.021DOI 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

Ecstacy-associated hyponatremia: why are women at risk?

Nephrol Dial Transplant 2013 Sep 26;28(9):2206-9. Epub 2013 Jun 26.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, The University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

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http://dx.doi.org/10.1093/ndt/gft192DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769979PMC
September 2013

Is chronic hyponatremia a novel risk factor for hip fracture in the elderly?

Nephrol Dial Transplant 2012 Oct;27(10):3725-31

Renal Consultants of Houston, Houston, TX, USA.

Hip fractures represent a serious health risk in the elderly, with significant associated morbidity and mortality. There is now an emerging literature that suggests that chronic hyponatremia increases the adjusted odds ratio (OR) for both falls and fractures in the elderly. Hyponatremia appears to contribute to falls and fractures by two mechanisms: (i) it produces mild cognitive impairment resulting in unsteady gait and falls and (ii) it directly contributes to osteoporosis and increased bone fragility by inducing increased bone resorption to mobilize sodium. There is debate over the effect of hyponatremia on the production of osteoporosis, as one study found decreased bone mineral density (BMD) and another did not. Should we be screening for low serum sodium in patients with osteoporosis or assessing BMD in patients with hyponatremia? The final answer is yet to come from prospective studies that allocate elderly individuals with mild hyponatremia to receive active treatment or not for hyponatremia and see if this intervention prevents gait disturbances and changes in BMD reducing fracture risk. In the meantime, physicians caring for elderly patients must be aware of the association between hyponatremia and bone problems. As serum sodium is a readily available, simple and affordable biochemical measurement, clinicians should look for hyponatremia in elderly patients who take medications that can cause hyponatremia. Also, elderly patients with unsteady gait and/or confusion should be checked for the presence of mild hyponatremia and if present it should not be ignored. Finally, elderly patients presenting with an orthopedic injury should have serum sodium checked and corrected if hyponatremia is present.
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http://dx.doi.org/10.1093/ndt/gfs412DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484731PMC
October 2012

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

Effects of frequent hemodialysis on measures of CKD mineral and bone disorder.

J Am Soc Nephrol 2012 Apr 23;23(4):727-38. Epub 2012 Feb 23.

University of Illinois at Chicago, Chicago, IL 60612, USA.

More frequent hemodialysis sessions and longer session lengths may offer improved phosphorus control. We analyzed data from the Frequent Hemodialysis Network Daily and Nocturnal Trials to examine the effects of treatment assignment on predialysis serum phosphorus and on prescribed dose of phosphorus binder, expressed relative to calcium carbonate on a weight basis. In the Daily Trial, with prescribed session lengths of 1.5-2.75 hours six times per week, assignment to frequent hemodialysis associated with both a 0.46 mg/dl decrease (95% confidence interval [95% CI], 0.13-0.78 mg/dl) in mean serum phosphorus and a 1.35 g/d reduction (95% CI, 0.20-2.50 g/d) in equivalent phosphorus binder dose at month 12 compared with assignment to conventional hemodialysis. In the Nocturnal Trial, with prescribed session lengths of 6-8 hours six times per week, assignment to frequent hemodialysis associated with a 1.24 mg/dl decrease (95% CI, 0.68-1.79 mg/dl) in mean serum phosphorus compared with assignment to conventional hemodialysis. Among patients assigned to the group receiving six sessions per week, 73% did not require phosphorus binders at month 12 compared with only 8% of patients assigned to sessions three times per week (P<0.001). At month 12, 42% of patients on nocturnal hemodialysis required the addition of phosphorus into the dialysate to prevent hypophosphatemia. Frequent hemodialysis did not have major effects on calcium or parathyroid hormone concentrations in either trial. In conclusion, frequent hemodialysis facilitates control of hyperphosphatemia and extended session lengths could allow more liberal diets and freedom from phosphorus binders.
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http://dx.doi.org/10.1681/ASN.2011070688DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312501PMC
April 2012

Maintenance intravenous fluids with 0.9% sodium chloride do not produce hypernatraemia in children.

Acta Paediatr 2012 Mar 15;101(3):222-3. Epub 2011 Dec 15.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, The University of Pittsburgh School of Medicine, PA, USA.

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http://dx.doi.org/10.1111/j.1651-2227.2011.02535.xDOI Listing
March 2012

Prevention of hospital-acquired hyponatremia: do we have the answers?

Pediatrics 2011 Nov 17;128(5):980-3. Epub 2011 Oct 17.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA.

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http://dx.doi.org/10.1542/peds.2011-2015DOI Listing
November 2011

Improving intravenous fluid therapy in children with gastroenteritis.

Pediatr Nephrol 2010 Aug 23;25(8):1383-4. Epub 2010 Mar 23.

Gastroenteritis is one of the most common medical conditions seen by pediatricians. The standard approach to intravenous fluid therapy for these children has been to administer a 0.9% sodium chloride (NaCl) bolus followed by a hypotonic solution ranging from 0.2-0.45% NaCl to replace the remaining deficit plus maintenance. We have questioned the safety of this approach as there have been reports of death or permanent neurologic impairment from hyponatremic encephalopathy. Hanna and Saberi (Pediatr Nephrol. doi: 10.1007/s00467-009-1428-y ) found the incidence of hospital-acquired hyponatremia (sodium < 135 mEq/L) to be 18.5% for patients presenting with isonatremic dehydration from gastroenteritis. This confirms that the current approach of using hypotonic fluids results in a high incidence of hyponatremia. Hypotonic fluids are not appropriate for rehydration in patients with gastroenteritis as it is a state of arginine vasopressin (AVP) excess due to both hemodynamic stimuli from volume depletion and non-hemodynamic stimuli such as nausea and vomiting. Free water will be retained until the volume deficit is corrected and the hemodynamic stimulus for AVP production abates. A safer and more effective approach is the administration of 0.9% NaCl in a continuous infusion following bolus therapy. 0.9% NaCl not only serves as prophylaxis against hyponatremia, but it is superior to hypotonic fluids as an extracellular volume expander and corrects the volume deficit more rapidly.
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http://dx.doi.org/10.1007/s00467-010-1505-2DOI Listing
August 2010

100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy.

Metab Brain Dis 2010 Mar 11;25(1):91-6. Epub 2010 Mar 11.

Division of Nephrology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, The University of Pittsburgh School of Medicine, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA 15224, USA.

Hyponatremic encephalopathy is a potentially lethal condition with numerous reports of death or permanent neurological injury. The optimal treatment for hyponatremic encephalopathy remains controversial. We have introduced a unified approach to the treatment of hyponatremic encephalopathy which uses 3% NaCl (513 mEq/L) bolus therapy. Any patient with suspected hyponatremic encephalopathy should receive a 2 cc/kg bolus of 3% NaCl with a maximum of 100 cc, which could be repeated 1-2 times if symptoms persist. The approach results in a controlled and immediate rise in serum sodium with little risk of inadvertent overcorrection.
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http://dx.doi.org/10.1007/s11011-010-9173-2DOI Listing
March 2010

Bone disease as a new complication of hyponatremia: moving beyond brain injury.

Clin J Am Soc Nephrol 2010 Feb 14;5(2):167-8. Epub 2010 Jan 14.

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http://dx.doi.org/10.2215/CJN.09281209DOI Listing
February 2010