“End-stage kidney” in longstanding bulimia nervosa

Yasuhara, Daisuke; Naruo, Tetsuro; Taguchi, Shuhei; Umekita, Yoshihisa; Yoshida, Hiroki; Nozoe, Shigeo

doi:10.1002/eat.20198

Cited by 20 publications

(16 citation statements)

References 9 publications

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“…However, few studies have examined the extent of renal damage, especially morphologic changes, over long-term bulimic symptoms [16,17]. Yasuhara et al [17] described a case of a woman with longstanding BN and end-stage renal disease (ESRD). After the patient died of pneumonia and sepsis at age 52 years, autopsy of her kidney showed chronic interstitial nephritis and proximal tubular swelling.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, autopsy examination of the kidneys revealed diffuse glomerular sclerosis, which may be also induced by obesity during the period of increased body weight. Indeed, a positive association between high body mass index (BMI) and risk for chronic kidney disease has been reported [17,18]. In a large study performed in 320,252 adult volunteers, the adjusted relative risk for ESRD was 3.6 (95% CI, 3.05–4.18) for those with class I obesity (BMI, 30.0–34.9), 6.1 (95% CI, 5.0–7.5) for those with class II obesity (BMI, 35.0–39.9) and 7.1 (95% CI, 5.4–9.30) for those with morbid obesity (BMI ≥40) compared with persons who had normal weight (BMI, 18.5–24.9) [16].…”

Section: Discussionmentioning

confidence: 99%

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Renal Involvement in Psychological Eating Disorders

2011

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Psychological eating disorders – anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder – are an increasing public health problem with severe clinical manifestations: hypothermia, hypotension, electrolyte imbalance, endocrine disorders and kidney failure; they are of interest to nephrologists, but pathophysiological mechanisms in determining the renal involvement are still unclear. We describe pathophysiology, histological features and clinical manifestations of the most frequent psychological eating disorders: AN and BN. Regarding AN, we analyze the recent literature, and identify 3 principal pathways towards renal involvement: chronic dehydration-hypokalemia, nephrocalcinosis and chronic rhabdomyolysis. Regarding BN, we describe the correlation between obesity and many proinflammatory cytokines, chemokines, growth factors and adipokines, having potential metabolic and hemodynamic effects on the kidney and an important role in the pathogenesis of obesity-related renal injury, independently of hypertension and diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Renal Involvement in Psychological Eating Disorders

2011

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“…Autopsy revealed chronic interstitial nephritis, proximal tubular swelling, and diffuse glomerular sclerosis, suggesting chronic glomerular injury associated with longterm binging/purging 80. With respect to renal function, acute renal failure induced by the presence of rhabdomyolysis has been reported to have been caused by refeeding-induced hypophosphatemia 81…”

Section: Resultsmentioning

confidence: 99%

Sudden death in eating disorders

Jáuregui¹,

Jáuregui‐Lobera²

2012

VHRM

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Eating disorders are usually associated with an increased risk of premature death with a wide range of rates and causes of mortality. “Sudden death” has been defined as the abrupt and unexpected occurrence of fatality for which no satisfactory explanation of the cause can be ascertained. In many cases of sudden death, autopsies do not clarify the main cause. Cardiovascular complications are usually involved in these deaths. The purpose of this review was to report an update of the existing literature data on the main findings with respect to sudden death in eating disorders by means of a search conducted in PubMed. The most relevant conclusion of this review seems to be that the main causes of sudden death in eating disorders are those related to cardiovascular complications. The predictive value of the increased QT interval dispersion as a marker of sudden acute ventricular arrhythmia and death has been demonstrated. Eating disorder patients with severe cardiovascular symptoms should be hospitalized. In general, with respect to sudden death in eating disorders, some findings (eg, long-term eating disorders, chronic hypokalemia, chronically low plasma albumin, and QT intervals >600 milliseconds) must be taken into account, and it must be highlighted that during refeeding, the adverse effects of hypophosphatemia include cardiac failure. Monitoring vital signs and performing electrocardiograms and serial measurements of plasma potassium are relevant during the treatment of eating disorder patients.

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“…Most incidents of AKI in these patients have been reported as pre-renal dysfunction caused by volume depletion and circulating insufficiency, or parenchymal injury caused by rhabdomyolysis, in turn induced by hypokalemia or circulating insufficiency [1][2][3]. CKD has also been reported in these patients, which are assumed to have been induced by chronic hypokalemia following tubulointerstitial damage or potential metabolic and hemodynamic effects [3,10]. Duration of illness and abuse of diuretics or laxatives have been reported as risk factors of CKD and the decline of the glomerular filtration rate (GFR) [11].…”

Section: Discussionmentioning

confidence: 99%

Two cases of eating disorder revealed by the breakout of acute kidney injury after angiotensin II receptor blocker administration

Kaneko

Tsukamoto

2013

CEN Case Rep

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Case 1: A 39-year-old woman with schizophrenia, obesity, hypertension and dyslipidemia was admitted to our hospital for deteriorating serum Cr level, from 97.2 to 645.3 lmol/l. She had been started on losartan 5 months earlier. After suspension of losartan and infusion of saline, her serum Cr level gradually recovered and she was discharged. Unfortunately, her physician restarted her on losartan, and 5 months after this discharge, her serum Cr level rose again to 194.5 lmol/l; again, serum Cr promptly recovered when losartan was discontinued. Selfinduced vomiting after overeating, suggesting bulimia nervosa, was revealed via the detection of a remarkable reduction of chloride compared to sodium in her spot-urine sample. Case 2: A 39-year-old woman who had been diagnosed with bipolar disorder and diabetes mellitus was admitted to our hospital with suspected diabetic ketoacidosis. After improvement in her blood sugar level, olmesartan administration for hypertension was begun. Four days later, her serum Cr level had risen from 60.1 to 256.4 lmol/l. After suspension of olmesartan and infusion of saline, her serum Cr level gradually fell to normal levels. Urinalysis revealed the dissociation of sodium and chloride. During her hospitalization, habitual self-induced vomiting was discovered. The measurement of urinary electrolytes may be useful for the detection of eating disorders with self-induced vomiting; in these patients, the administration of angiotensin II receptor blockers may induce acute kidney injury.

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“End-stage kidney” in longstanding bulimia nervosa

Cited by 20 publications

References 9 publications

Renal Involvement in Psychological Eating Disorders

Renal Involvement in Psychological Eating Disorders

Sudden death in eating disorders

Two cases of eating disorder revealed by the breakout of acute kidney injury after angiotensin II receptor blocker administration

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