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1.
Bone ; 127: 556-562, 2019 10.
Article in English | MEDLINE | ID: mdl-31362067

ABSTRACT

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.


Subject(s)
Hip Fractures/epidemiology , Hip Fractures/etiology , Hyponatremia/complications , Renal Insufficiency, Chronic/complications , Aged , Aged, 80 and over , Case-Control Studies , Chronic Disease , Female , Humans , Male , Risk Factors
2.
Endocr Pract ; 25(4): 366-378, 2019 Apr.
Article in English | MEDLINE | ID: mdl-30720342

ABSTRACT

Objective: Hyponatremia decreases bone mineral density and is a major risk factor for fragility fractures. Objectives of our systematic review and meta-analysis were to analyze the overall effects of hyponatremia on bone fractures, osteoporosis, and mortality. Methods: We extracted data from Medline, Cochrane Central, and EMBASE 1960-2017 and conference abstracts from 2007-2017. We included studies with data on serum sodium, fractures, bone density, or diagnoses of osteoporosis. Studies were independently reviewed by two authors and assessed for bias using the Newcastle-Ottawa scale. Random effect models meta-analysis was used when at least three studies reported the same outcome measures. We reported summary odds ratios (ORs) and 95% confidence intervals (CIs). Results: We included 26 studies for qualitative analysis. Fifteen studies were included in the meta-analysis to evaluate the effects of hyponatremia on fractures, four studies for bone mineral density changes, and six for mortality. Hyponatremia increased the odds of fractures at all sites (summary OR, 2.34 [95% CI, 1.86, 2.96]. There was an increase in the odds of osteoporosis (summary OR, 2.67 [95% CI, 2.07, 3.43]). Mortality risk among the included studies remained high (summary OR, 1.31 [95% CI, 1.16, 1.47]). Conclusion: Our meta-analysis confirms a statistically significant association of hyponatremia with bone fractures and osteoporosis along with higher mortality. Long-term prospective studies evaluating the impact of correcting hyponatremia on bone health, fractures, and mortality are required. Abbreviations: AVP = arginine vasopressin; CI = confidence interval; CKD = chronic kidney disease; OR = odds ratio; SIADH = syndrome of inappropriate antidiuretic hormone.


Subject(s)
Fractures, Bone , Hyponatremia , Osteoporosis , Bone Density , Humans , Prospective Studies
4.
Int J Technol Assess Health Care ; 33(1): 63-68, 2017 Jan.
Article in English | MEDLINE | ID: mdl-28434422

ABSTRACT

OBJECTIVES: Patient Web portals (PWPs) have been gaining traction as a means to collect patient-reported outcomes and maintain quality patient care between office visits. PWPs have the potential to impact patient-provider relationships by rendering additional channels for communication outside of clinic visits and could help in the management of common chronic medical conditions. Studies documenting their effect in primary care settings are limited. This perspective aims to summarize the benefits and drawbacks of using PWPs in the management of chronic conditions, such as diabetes mellitus, hypertension, and asthma, focusing on communication, disease management, compliance, potential barriers, and the impact on patient-provider dynamic. After a review of these topics, we present potential future directions. METHODS: We conducted an exploratory PubMed search of the literature published from inception through December 2015, and focused our subsequent searches specifically to assess benefits and drawbacks of using PWPs in the management of diabetes mellitus, hypertension, and asthma. RESULTS: Our search revealed several potential benefits of PWP implementation in the management of chronic conditions with regards to patient-provider relationships, such as improved communication, disease management, and compliance. We also noted drawbacks such as potentially unreliable reporting, barriers to use, and increased workload. CONCLUSIONS: PWPs offer opportunities for patients to report symptoms and outcomes in a timely manner and allow for secure online communication with providers. Despite the drawbacks noted, the overall benefits from successful PWP implementation could improve patient-provider relationships and help in the management of chronic conditions, such as diabetes mellitus, hypertension, and asthma.


Subject(s)
Chronic Disease/therapy , Patient Portals , Physician-Patient Relations , Communication , Humans , Patient Compliance
6.
Endocr Pract ; 11(5): 331-4, 2005.
Article in English | MEDLINE | ID: mdl-16191494

ABSTRACT

OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. METHODS: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.


Subject(s)
Diabetes Mellitus, Type 1/complications , Diabetic Ketoacidosis/drug therapy , Hypokalemia/drug therapy , Potassium/therapeutic use , Adult , Blood Glucose/analysis , Blood Pressure/drug effects , Diabetes Mellitus, Type 1/blood , Diabetes Mellitus, Type 1/physiopathology , Diabetic Coma/complications , Diabetic Coma/drug therapy , Diabetic Coma/physiopathology , Diabetic Ketoacidosis/complications , Diabetic Ketoacidosis/diagnosis , Dose-Response Relationship, Drug , Female , Humans , Hyperglycemia/complications , Hyperglycemia/drug therapy , Hyperglycemia/physiopathology , Hypokalemia/complications , Hypokalemia/diagnosis , Infusions, Intravenous , Insulin/administration & dosage , Insulin/therapeutic use , Osmolar Concentration , Potassium/administration & dosage , Potassium/blood , Vasoconstrictor Agents/administration & dosage , Vasoconstrictor Agents/pharmacology , Vasoconstrictor Agents/therapeutic use
7.
Kidney Int ; 68(4): 1884-7, 2005 Oct.
Article in English | MEDLINE | ID: mdl-16164667

ABSTRACT

BACKGROUND: Variation among clinical laboratories in calibration of serum creatinine assays is a source of error in glomerular filtration rate (GFR) estimation equations. We evaluated impact of this variation on GFR estimates. METHODS: Errors in GFR estimates were computed based on the range of calibration differences from the 1994 College of American Pathologists (CAP) survey using the Modification of Diet in Renal Disease (MDRD) Study GFR equation. RESULTS: Mean (95% CI) calibration difference observed in the CAP survey was +0.14 mg/dL (+12.4 micromol/L) [-0.09, +0.37 mg/dL (-7.96, +32.71 micromol/L)]. Errors in GFR estimates using uncalibrated serum creatinine values were lower in individuals with lower estimated GFR. For GFR of 60 mL/min/1.73 m(2), the mean calibration difference in the CAP survey was associated with errors in GFR estimation between -5.5 to -8.1 mL/min/1.73 m(2) (-9.1 to -13.5%) depending on race and sex. The 95% confidence interval for the calibration difference was associated with a maximal range of error in GFR estimates from +4.6 to -18.1 mL/min/1.73 m(2) (+7.6 to -30.2%). Errors of this magnitude at an estimated GFR of 60 mL/min/1.73 m(2) are not likely to be of clinical significance. However, errors at higher levels of estimated GFR would be greater, making GFR estimates in this range unreliable. CONCLUSION: Recalibration of serum creatinine assays to the MDRD Study clinical laboratory would improve accuracy of GFR estimation using the MDRD Study equation, but is not practical for all clinical laboratories. As an interim solution, clinical laboratories could report GFR estimates <60 mL/min/1.73 m(2) without recalibration with an acceptable accuracy.


Subject(s)
Chemistry, Clinical/methods , Creatinine/blood , Glomerular Filtration Rate , Kidney Diseases/diagnosis , Calibration , Chemistry, Clinical/standards , Creatinine/analysis , Female , Humans , Kidney Diseases/blood , Male , Middle Aged , Reproducibility of Results
8.
J Am Soc Nephrol ; 16(8): 2439-48, 2005 Aug.
Article in English | MEDLINE | ID: mdl-15930090

ABSTRACT

Improving outcomes for chronic kidney disease (CKD) requires early identification and recognition by physicians. There are few data on rates of testing or use of diagnostic codes for CKD. A cross-sectional analysis was performed of patients who were older than 40 yr and had one or more laboratory tests between April 1, 2002, and March 31, 2003, at a Laboratory Corporation of America regional laboratory. Objectives were to determine the frequency of testing for serum creatinine; prevalence of CKD, defined as estimated GFR <60 ml/min per 1.73 m2; and sensitivity of diagnostic codes for CKD for patients with and without risk factors for CKD and with or without cardiovascular disease (CVD). Of the 277,111 patients, 19% had serum creatinine measured, compared with 33 and 71% who had measurements of serum glucose and lipids, respectively. Patients with hypertension, diabetes, and age >60 yr were more likely to be tested for serum creatinine with odds ratio (OR; 95% confidence interval) of 2.09 (2.05 to 2.14), 1.22 (1.19 to 1.25), and 1.24 (1.22 to 1.27) respectively. Among patients tested, 30% had CKD. Sensitivity and specificity of kidney disease diagnostic codes compared with CKD defined by estimated GFR <60 ml/min per 1.73 m2 were 11 and 96%, respectively. In patients with hypertension, diabetes, age >60 years, and CVD, rates of testing and sensitivity of diagnostic codes were 53 and 14%, respectively. Low rates of testing for serum creatinine and insensitivity of diagnostic codes for CKD, even in high-risk patients, suggests inadequate physician awareness of CKD and limited utility of administrative databases for identification of patients with CKD.


Subject(s)
Chemistry, Clinical/methods , International Classification of Diseases , Kidney Failure, Chronic/classification , Kidney Failure, Chronic/diagnosis , Laboratories, Hospital , Mass Screening/methods , Nephrology/methods , Adult , Aged , Blood Chemical Analysis , Cardiovascular Diseases/complications , Cardiovascular Diseases/diagnosis , Creatinine/blood , Cross-Sectional Studies , Databases as Topic , Female , Glomerular Filtration Rate , Health Personnel , Humans , Male , Mass Screening/statistics & numerical data , Middle Aged , Odds Ratio , Physicians , Prevalence , Risk Factors , Sensitivity and Specificity , Treatment Outcome
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