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ABSTRACT: BACKGROUND AND OBJECTIVES: Critically ill patients with AKI necessitating renal replacement therapy (RRT) have high in-hospital mortality, and survivors are at risk for kidney dysfunction at hospital discharge. The objective was to evaluate the association between impaired kidney function at hospital discharge with long-term renal and overall survival. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Degree of kidney dysfunction in relation to long-term effects on renal survival and patient mortality was investigated in a retrospective cohort study of 1220 adults admitted to an intensive care unit who received continuous RRT between 1994 and 2010. RESULTS: After hospital discharge, median follow-up of survivors (n=475) was 8.5 years (range, 1-17 years); overall mortality rate was 75%. Only 170 (35%) patients were discharged with an estimated GFR (eGFR) >60 ml/min per 1.73 m(2). Multivariate proportional hazards regression analysis demonstrated that age, nonsurgical type of admission, preexisting kidney disease, malignancy, and eGFR of 29-15 ml/min per 1.73 m(2) (hazard ratio [HR], 1.62; 95% confidence interval [CI], 1.01 to 2.58) and eGFR <15 ml/min per 1.73 m(2) (HR, 1.93; 95% CI, 1.23 to 3.02) at discharge were independent predictors of increased mortality. Renal survival was significantly associated with degree of kidney dysfunction at discharge. An eGFR of 29-15 ml/min per 1.73 m(2) (HR, 26.26; 95% CI, 5.59 to 123.40) and <15 ml/min per 1.73 m(2) (HR, 172.28; 95% CI, 37.72 to 786.75) were independent risk factors for initiation of long-term RRT. CONCLUSIONS: Most critically ill patients surviving AKI necessitating RRT have impaired kidney function at hospital discharge. An eGFR <30 ml/min per 1.73 m(2) is a strong risk factor for decreased long-term survival and poor renal survival.
Clinical Journal of the American Society of Nephrology 04/2013; · 5.23 Impact Factor
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ABSTRACT: BACKGROUND: Electrolyte disorders have been studied mainly in hospitalized patients, whereas data in the general population are limited. The aim of this study was to determine the prevalence and risk factors of common electrolyte disorders in older subjects recruited from the general population. METHODS: A total of 5179 subjects aged 55 years or more were included from the population-based Rotterdam Study. We focused on hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia. Multivariable logistic regression was used to study potential associations with renal function, comorbidity, and medication. The adjusted mortality also was determined for each electrolyte disorder. RESULTS: A total of 776 subjects (15.0%) had at least 1 electrolyte disorder, with hyponatremia (7.7%) and hypernatremia (3.4%) being most common. Diabetes mellitus was identified as an independent risk factor for hyponatremia and hypomagnesemia, whereas hypertension was associated with hypokalemia. Diuretics were independently associated with several electrolyte disorders: thiazide diuretics (hyponatremia, hypokalemia, hypomagnesemia), loop diuretics (hypernatremia, hypokalemia), and potassium-sparing diuretics (hyponatremia). The use of benzodiazepines also was associated with hyponatremia. Hyponatremic subjects who used both thiazides and benzodiazepines had a 3 mmol/L lower serum sodium concentration than subjects using 1 or none of these drugs (P < .001). Hyponatremia and hypomagnesemia were independently associated with an increased mortality risk. CONCLUSIONS: Electrolyte disorders are common among older community subjects and mainly associated with diabetes mellitus and diuretics. Subjects who used both thiazides and benzodiazepines had a more severe degree of hyponatremia. Because even mild electrolyte disorders were associated with mortality, monitoring of electrolytes and discontinuation of offending drugs may improve outcomes.
The American journal of medicine 01/2013; · 4.47 Impact Factor
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ABSTRACT: Recent interest focuses on urinary renin and angiotensinogen as markers of renal renin-angiotensin system activity. Before concluding that these components are independent markers, we need to exclude that their presence in urine, like that of albumin (a protein of comparable size), is due to (disturbed) glomerular filtration. This review critically discusses their filtration, reabsorption and local release. Given the close correlation between urinary angiotensinogen and albumin in human studies, it concludes that, in humans, urinary angiotensinogen is a filtration barrier damage marker with the same predictive power as urinary albumin. In contrast, in animals, tubular angiotensinogen release may occur, although tubulus-specific knockout studies do not support a functional role for such angiotensinogen. Urinary renin levels, relative to albumin, are >200-fold higher and unrelated to albumin. This may reflect release of renin from the urinary tract, but could also be attributed to activation of filtered, plasma-derived prorenin and/or incomplete tubular reabsorption.
Current Hypertension Reports 01/2013; · 2.50 Impact Factor
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ABSTRACT: Acute hyponatremia can cause death if cerebral edema is not treated promptly. Conversely, if chronic hyponatremia is corrected too rapidly, osmotic demyelination may ensue, which also potentially is lethal. However, these severe complications of hyponatremia are relatively uncommon and often preventable. More commonly, hyponatremia predicts mortality in patients with advanced heart failure or liver cirrhosis. In these conditions, it generally is assumed that hyponatremia reflects the severity of the underlying disease rather than contributing directly to mortality. The same assumption holds for the recently reported associations between hyponatremia and mortality in patients with pulmonary embolism, pulmonary hypertension, pneumonia, and myocardial infarction. However, recent data suggest that chronic and mild hyponatremia in the general population also are associated with mortality. In addition, hyponatremia has been associated with mortality in long-term hemodialysis patients without residual function in whom the underlying disease cannot be responsible for hyponatremia. These new data raise the question of whether hyponatremia by itself can contribute to mortality or it remains a surrogate marker for other unknown risk factors. We review hyponatremia and mortality and explore the possibility that hyponatremia perturbs normal physiology in the absence of cerebral edema or osmotic demyelination.
American Journal of Kidney Diseases 01/2013; · 5.43 Impact Factor
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ABSTRACT: PURPOSE: Identification of risk factors for impaired renal function at hospital discharge in critically ill patients with acute kidney injury (AKI) requiring renal replacement therapy (RRT). METHODS: A single-center retrospective cohort study was performed evaluating demographic and clinical parameters as potential risk factors for a modest to severely impaired renal function at hospital discharge in patients with AKI requiring RRT in the intensive care unit. RESULTS: Of the 353 patients in our cohort, 90 (25.5%) patients had pre-existing chronic kidney disease (CKD). An estimated glomerular filtration rate (eGFR) ≤60 mL min(-1) 1.73 m(-2) at hospital discharge occurred in 64.0% of which 63.7% without known renal impairment before hospital admission and 8.2% of all cases left the hospital dialysis-dependent. Multivariable logistic regression showed that age (OR = 1.051, P < .001), serum creatinine concentration at start of RRT (OR = 1.004, P < .001) and administration of iodine-containing contrast fluid (OR = 0.830, P = .045) were associated with an eGFR ≤60 mL min(-1) 1.73 m(-2). Furthermore, a medical history of CKD (OR = 5.865, P < .001) was associated with dialysis dependence. CONCLUSIONS: Elderly and patients with pre-existing CKD are at a high risk for modest to severely impaired renal function at hospital discharge after AKI requiring RRT.
Journal of critical care 12/2012; · 2.13 Impact Factor
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Pieter M Jansen,
Wijnanda J Frenkel,
Bert-Jan H van den Born,
Emile L E de Bruijne,
Jaap Deinum,
Michiel N Kerstens,
Joyce H A Arnoldus,
Arend Jan Woittiez,
Johanna A M Wijbenga, Robert Zietse,
A H Jan Danser,
Anton H van den Meiracker
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ABSTRACT: BACKGROUND:: Add-on therapy with aldosterone receptor antagonists has been reported to lower blood pressure (BP) in patients with uncontrolled hypertension. We assessed potential predictors of this response. METHODS:: In essential hypertensive patients with uncontrolled BP, despite the use of at least two antihypertensives, plasma renin and aldosterone concentrations and the transtubular potassium gradient (TTKG) were measured. Patients were treated with eplerenone 50 mg daily on top of their own medication. The office and ambulatory BP response and biochemical changes were evaluated after 1 week and 3 months of treatment and 6 weeks after discontinuation. Potential predictors for the change in 24-h ambulatory BP were tested in a multivariate regression model. RESULTS:: One hundred and seventeen patients with a mean age of 50.5 ± 6.6 years were included. Office BP decreased from 149/91 to 142/87 mmHg (P < 0.001) and ambulatory BP from 141/87 to 132/83 mmHg after 3 months of treatment (P < 0.001). Six weeks after discontinuation of eplerenone, office and ambulatory BP measurements returned to baseline values. Treatment resulted in a small rise in serum potassium and creatinine, and a small decrease in the TTKG. In a multivariate model, neither renin, aldosterone, or their ratio, nor the TTKG predicted the BP response. Only baseline ambulatory SBP predicted the BP response, whereas the presence of left ventricular hypertrophy was associated with a smaller BP reduction. CONCLUSION:: Add-on therapy with eplerenone effectively lowers BP in patients with difficult-to-treat primary hypertension. This effect is unrelated to circulating renin-angiotensin-aldosterone system activity and renal mineralocorticoid receptor activity as assessed by the TTKG.
Journal of hypertension 12/2012; · 4.02 Impact Factor
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ABSTRACT: PURPOSE OF REVIEW: The aim is to review the recently reported effects of angiotensin II (Ang II) on sodium and potassium transport in the aldosterone-sensitive distal nephron, including the signaling pathways between receptor and transporter, and the (patho)physiological implications of these findings. RECENT FINDINGS: Ang II can activate the sodium chloride cotransporter (NCC) through phosphorylation by Ste20-related, proline-alanine rich kinase (SPAK), an effect that is independent of aldosterone but dependent on with no lysine kinase 4 (WNK4). A low-sodium diet (high Ang II) activates NCC, whereas a high-potassium diet (low Ang II) inhibits NCC. NCC activation also contributes to Ang-II-mediated hypertension. Ang II also activates the epithelial sodium channel (ENaC) additively to aldosterone, and this effect appears to be mediated through protein kinase C and superoxide generation by nicotinamide adenine dinucleotide phosphate oxidase. While aldosterone activates the renal outer medullary potassium channel (ROMK), this channel is inhibited by Ang II. The key kinase responsible for this effect is c-Src, which phosphorylates ROMK and leaves WNK4 unphosphorylated to further inhibit ROMK. SUMMARY: The effects of Ang II on NCC, ENaC, and ROMK help explain the renal response to hypovolemia which is to conserve both sodium and potassium. Pathophysiologically, Ang-II-induced activation of NCC appears to contribute to salt-sensitive hypertension.
Current opinion in nephrology and hypertension 11/2012; · 3.96 Impact Factor
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ABSTRACT: Disorders of calcium and magnesium balance are physiologically interesting and clinically challenging. In this review, we attempt to bridge the gap between physiology and practice by providing a physiology-based approach to understanding hypocalcemia, hypercalcemia and hypomagnesemia. Calcium and, to a lesser extent, magnesium balance is achieved through a complex interplay between the parathyroid gland, bone, the intestine and the kidney. Our understanding of the molecular physiology of calcium and magnesium balance has grown considerably following the discovery of the calcium-sensing receptor (CaSR) and the main intestinal and renal transporters for calcium and magnesium, namely, the transient receptor potential channels TRPV5, TRPV6 and TRPM6. The regulation of parathyroid hormone (PTH) secretion by CaSR and the subsequent effects of PTH and vitamin D on TRPV5 constitute an increasingly characterized regulatory loop. In contrast, no truly magnesiotropic hormones have been identified, although the recently established interactions between the epidermal growth factor and TRPM6 suggest a possible candidate. Overall, the aim of this review is to illustrate the clinical disorders of calcium and magnesium balance from the perspective of their integrated physiology.
Pediatric Nephrology 11/2012; · 2.52 Impact Factor
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ABSTRACT: Urinary exosomes are vesicles derived from renal tubular epithelial cells. Exosomes often contain several disease-associated proteins and are thus useful targets for identifying biomarkers of disease. Here, we hypothesized that the phosphorylated (active) form of the sodium chloride cotransporter (pNCC) or prostasin could serve as biomarkers for aldosteronism. We tested this in 2 animal models of aldosteronism (aldosterone infusion or low-sodium diet) and in patients with primary aldosteronism. Urinary exosomes were isolated from 24-hour urine or spot urine using ultracentrifugation. In rats, a normal or a high dose of aldosterone for 2, 3, or 8 days increased pNCC 3-fold in urinary exosomes (P<0.05 for all). A low-sodium diet also increased pNCC in urinary exosomes approximately 1.5-fold after 4 and after 8 days of treatment. The effects of these maneuvers on prostasin in urinary exosomes were less clear, showing a significant 1.5-fold increase only after 2 and 3 days of high-aldosterone infusion. In urinary exosomes of patients with primary aldosteronism, pNCC was 2.6-fold higher (P<0.05) while prostasin was 1.5-fold higher (P=0.07) than in patients with essential hypertension. Urinary exosomal pNCC and, to a lesser extent, prostasin are promising markers for aldosteronism in experimental animals and patients. These markers may be used to assess the biological activity of aldosterone and, potentially, as clinical biomarkers for primary aldosteronism.
Hypertension 07/2012; 60(3):741-8. · 6.21 Impact Factor
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ABSTRACT: We and others have recently shown that angiotensin II can activate the sodium chloride cotransporter (NCC) through a WNK4-SPAK-dependent pathway. Because WNK4 was previously shown to be a negative regulator of NCC, it has been postulated that angiotensin II converts WNK4 to a positive regulator. Here, we ask whether aldosterone requires angiotensin II to activate NCC and if their effects are additive. To do so, we infused vehicle or aldosterone in adrenalectomized rats that also received the angiotensin receptor blocker losartan. In the presence of losartan, aldosterone was still capable of increasing total and phosphorylated NCC twofold to threefold. The kinases WNK4 and SPAK also increased with aldosterone and losartan. A dose-dependent relationship between aldosterone and NCC, SPAK, and WNK4 was identified, suggesting that these are aldosterone-sensitive proteins. As more functional evidence of increased NCC activity, we showed that rats receiving aldosterone and losartan had a significantly greater natriuretic response to hydrochlorothiazide than rats receiving losartan only. To study whether angiotensin II could have an additive effect, rats receiving aldosterone with losartan were compared with rats receiving aldosterone only. Rats receiving aldosterone only retained more sodium and had twofold to fourfold increase in phosphorylated NCC. Together, our results demonstrate that aldosterone does not require angiotensin II to activate NCC and that WNK4 appears to act as a positive regulator in this pathway. The additive effect of angiotensin II may favor electroneutral sodium reabsorption during hypovolemia and may contribute to hypertension in diseases with an activated renin-angiotensin-aldosterone system.
Pflügers Archiv - European Journal of Physiology 05/2012; 463(6):853-63. · 4.46 Impact Factor
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Kidney International 04/2012; 81(7):711-2. · 6.61 Impact Factor
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ABSTRACT: Hyponatremia is the most common electrolyte disorder and is mainly known for its neurological complications. New studies suggest previously unrecognized complications of hyponatremia, including falls, osteoporosis and fractures. Because these novel associations are mainly derived from epidemiological studies, it remains unclear whether hyponatremia has a direct effect on bone or whether it is a surrogate marker of another etiology. However, one animal and one in vitro study now show that hyponatremia can have direct effects on bone, mainly via activation of osteoclasts. The association between hyponatremia and fractures appears to be independent of osteoporosis (defined as low BMD). Also, data suggest that this association cannot be fully explained by the possibility that hyponatremia predisposes to falls. Hyponatremia, therefore, also has an effect on bone quality that is not captured by BMD. Here, the emerging relationship between hyponatremia and bone is reviewed, with special emphasis on possible mechanisms, unanswered questions and clinical implications.
Nature Reviews Endocrinology 01/2012; 8(1):33-9. · 9.97 Impact Factor
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ABSTRACT: Recent studies suggest that mild hyponatremia is associated with fractures, but prospective studies are lacking. We studied whether hyponatremia is associated with fractures, falls, and/or bone mineral density (BMD). A total of 5208 elderly subjects with serum sodium assessed at baseline were included from the prospective population-based Rotterdam Study. The following data were analyzed: BMD, vertebral fractures (mean follow-up 6.4 years), nonvertebral fractures (7.4 years), recent falls, comorbidity, medication, and mortality. Hyponatremia was detected in 399 subjects (7.7%, 133.4 ± 2.0 mmol/L). Subjects with hyponatremia were older (73.5 ± 10.3 years versus 70.0 ± 9.0 years, p < .001), had more recent falls (23.8% versus16.4%, p < .01), higher type 2 diabetes mellitus prevalence (22.2% versus 10.3%, p < .001), and more often used diuretics (31.1% versus 15.0%, p < .001). Hyponatremia was not associated with lower BMD but was associated with increased risk of incident nonvertebral fractures [hazard ratio (HR) =1.39, 95% confidence interval (CI) 1.11–1.73, p = .004] after adjustment for age, sex, and body mass index. Further adjustments for disability index, use of diuretics, use of psycholeptics, recent falls, and diabetes did not modify results. In the fully adjusted model, subjects with hyponatremia also had increased risk of vertebral fractures at baseline [odds ratio (OR) = 1.78, 95% CI 1.04–3.06, p = .037] but not at follow-up. Finally, all-cause mortality was higher in subjects with hyponatremia (HR = 1.21, 95% CI 1.03–1.43, p = .022). It is concluded that mild hyponatremia in the elderly is associated with an increased risk of vertebral fractures and incident nonvertebral fractures but not with BMD. Increased fracture risk in hyponatremia also was independent of recent falls, pointing toward a possible effect on bone quality. © 2011 American Society for Bone and Mineral Research
Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 07/2011; 26(8):1822 - 1828. · 6.04 Impact Factor
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Kidney International 06/2011; 79(12):1382. · 6.61 Impact Factor
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Clinical Journal of the American Society of Nephrology 05/2011; 6(5):951-3. · 5.23 Impact Factor
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ABSTRACT: Encapsulating peritoneal sclerosis (EPS) is a serious complication of peritoneal dialysis (PD) with a multifactorial pathophysiology and possible increasing incidence. The aim of the present study was to evaluate the independent associations of PD duration, age, dialysis fluids, and kidney transplantation with EPS.
A multicenter case-control study was performed in the Netherlands from 1 January 1996 until 1 July 2007. The population comprised 63 patients with EPS and 126 control patients. Control patients were selected from the national registry and were matched for date of PD start. Associations were analyzed using a log linear regression model. Primary outcome was appearance of EPS.
Compared with control patients, patients with EPS were younger at the start of PD (34.7 ± 15.4 years vs. 51.5 ± 14.7 years, p < 0.0001). The cumulative period on PD was longer in EPS patients than in control patients (78.7 ± 37.8 months vs. 32.8 ± 24 months, p < 0.0001), and the cumulative period on icodextrin was also longer in EPS patients (32.7 ± 23.3 months vs. 18.1 ± 15.7 months, p = 0.006). Compared with control patients, more EPS patients underwent kidney transplantation (47 vs. 59, p < 0.0001). With regard to the period after transplantation, the yearly probability of EPS increased in the year after transplantation to 7.5% from 1.75%. In multivariate regression analysis, cumulative PD duration, age at PD start, transplantation, time from last transplantation to EPS, calendar time, time on icodextrin, and ultrafiltration failure were independently associated with EPS. Transfer from PD to hemodialysis for reasons other than suspected EPS could not be identified as a risk factor for EPS.
Duration of PD, age at PD start, kidney transplantation, time since last transplantation, ultrafiltration failure, and time on icodextrin were associated with a higher risk of EPS.
Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. 03/2011; 31(3):269-78.
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ABSTRACT: Hyponatremia is the most common electrolyte disorder, but a lack of well-characterized cohorts is hindering a full appreciation of this complex and heterogeneous disorder.
During 4 months, clinical, biochemical, treatment and outcome data were collected for patients presenting with hyponatremia (serum sodium =130 mmol/L) to an urban university hospital.
Forty-three patients were included (serum sodium 126.6 ± 3.7 mmol/L). The most common causes of hyponatremia were diuretics (n=12), syndrome of inappropriate antidiuretic hormone secretion (n=11) and heart or liver disease (n=5). Renal insufficiency was frequent (n=18, 42%), and usually represented acute kidney injury (AKI; n=14, 78%). In patients with AKI, admission serum creatinine was 271 ± 252 µmol/L (3.4 ± 3.1-fold increase from baseline) and the origin was usually prerenal (12/14, 86%, fractional sodium excretion 0.54% ± 0.38%). Of these, patients with potentially reversible causes (salt loss or sepsis, n=7) had more favorable outcomes than patients with severe underlying disease (heart or liver disease, n=5), despite similar predictions using the RIFLE criteria. Survivors recovered with fluid resuscitation only. No overly rapid correction of hyponatremia was observed.
AKI is common in patients presenting with hyponatremia and is usually of prerenal origin. The concurrence of AKI and hyponatremia has previously not been emphasized, but is important pathophysiologically and to plan rational management for both disorders. In this cohort, isotonic fluid replacement corrected both disorders and did not lead to overly rapid correction of hyponatremia.
Journal of nephrology 03/2011; 24(6):749-55. · 1.65 Impact Factor
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ABSTRACT: Recent studies suggest that mild hyponatremia is associated with fractures, but prospective studies are lacking. We studied whether hyponatremia is associated with fractures, falls, and/or bone mineral density (BMD). A total of 5208 elderly subjects with serum sodium assessed at baseline were included from the prospective population-based Rotterdam Study. The following data were analyzed: BMD, vertebral fractures (mean follow-up 6.4 years), nonvertebral fractures (7.4 years), recent falls, comorbidity, medication, and mortality. Hyponatremia was detected in 399 subjects (7.7%, 133.4 ± 2.0 mmol/L). Subjects with hyponatremia were older (73.5 ± 10.3 years versus 70.0 ± 9.0 years, p < .001), had more recent falls (23.8% versus 16.4%, p < .01), higher type 2 diabetes mellitus prevalence (22.2% versus 10.3%, p < .001), and more often used diuretics (31.1% versus 15.0%, p < .001). Hyponatremia was not associated with lower BMD but was associated with increased risk of incident nonvertebral fractures [hazard ratio (HR) =1.39, 95% confidence interval (CI) 1.11-1.73, p = .004] after adjustment for age, sex, and body mass index. Further adjustments for disability index, use of diuretics, use of psycholeptics, recent falls, and diabetes did not modify results. In the fully adjusted model, subjects with hyponatremia also had increased risk of vertebral fractures at baseline [odds ratio (OR) = 1.78, 95% CI 1.04-3.06, p = .037] but not at follow-up. Finally, all-cause mortality was higher in subjects with hyponatremia (HR = 1.21, 95% CI 1.03-1.43, p = .022). It is concluded that mild hyponatremia in the elderly is associated with an increased risk of vertebral fractures and incident nonvertebral fractures but not with BMD. Increased fracture risk in hyponatremia also was independent of recent falls, pointing toward a possible effect on bone quality.
Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 03/2011; 26(8):1822-8. · 6.04 Impact Factor
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ABSTRACT: A 57-year-old woman was referred to a nephrology clinic because of chronic hypokalemia. She had a history of polycystic kidney disease, resistant hypertension, atrial fibrillation, type 2 diabetes, stroke, and end-stage renal disease, and had received a kidney transplant from a deceased donor at the age of 48 years. At presentation, the patient described symptoms of chronic fatigue and muscle aches, but she did not report pareses. Her medications included four antihypertensive agents, glucose-lowering drugs, immunosuppressants, digoxin, a coumarin derivative, and potassium chloride.
Full history, physical examination, laboratory testing of blood and urine, including aldosterone-torenin ratio, and a saline infusion test.
Primary aldosteronism.
Treatment with spironolactone resulted in prompt control of hypertension and hypokalemia, allowing discontinuation of potassium chloride and reduction in antihypertensive medication.
Nature Reviews Nephrology 01/2011; 7(1):55-60. · 7.09 Impact Factor
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ABSTRACT: Hyponatremia is a common diagnostic challenge.
An index case is presented to discuss the diagnostic approach to chronic and unexplained hyponatremia.
The index case concerns a 60-year-old man with chronic hepatitis C and previous alcohol use who was referred because of weight loss, poor dietary intake, dizzy spells, and unexplained hyponatremia (serum sodium 124-129 mmol/l). A low urine sodium concentration (20 mmol/l) and a low fractional sodium excretion (0.07%) were observed repeatedly, while urine osmolality was high (>400 mosm/kg). The central questions in this case are: what is the differential diagnosis, which tests are needed to confirm or exclude a diagnosis, and how would you proceed if no obvious cause is found?
The diagnosis of this case of unexplained hyponatremia was unexpected, but important because it was treatable. The challenges and caveats of the diagnostic approach to hyponatremia are discussed. A diagnostic algorithm to guide clinicians who are confronted with similar cases is presented.
Nephron Physiology 01/2011; 118(3):p66-71. · 2.55 Impact Factor
