Excessive fluid gain in a chronic laxative abuser: "pseudo-idiopathic" oedema

(Section Editor: M. G. Zeier)

Ze'ev Korzets, Galit Hasdan, Eduardo Podjarny and Jacques Bernheim

Department of Nephrology Meir Hospital Sapir Medical Center Kfar-Saba, and the Sackler School of Medicine Tel-Aviv University Tel-Aviv Israel

Case

A 43-year-old Caucasian female, employed as a medical secretary, was initially referred for evaluation of acute renal failure discovered following routine laboratory testing (Table 1Go). She had previously been diagnosed as having an obsessive, compulsive personality disorder and was a known chronic laxative abuser. Purgative consumption was in excess of 20 tablets per day for nearly three decades. Notably, for the past several years, severe osteoporosis had been documented and the patient was on oral alendronate therapy. Her height was 1.60 m and weight was 55 kg. On admission, she was tachypnoeic with a blood pressure of 85/62 mmHg and a reduced skin turgor. Intravenous saline was administered, resulting in an improvement of renal function (serum urea and creatinine decreased to 54 and 1.0 mg/dl respectively). The patient was urged to cease all laxative and/or diuretic medications. A week later, she was re-admitted complaining of a `bloated’ feeling, swelling of the extremities and shortness of breath. She had gained no less than 13 kg in weight. Clinical examination revealed 4+pitting oedema of the legs, extending up to the lower abdomen. There were signs of a right pleural effusion and on auscultation, bilateral rales. A chest X-ray confirmed the presence of pleural fluid and pulmonary congestion. Laboratory data are given in Table 1Go.


View this table:
[in this window]
[in a new window]
 
Table 1. Laboratory data on the two admissions

 
She was treated with intravenous frusemide. However, her fluid overload proved difficult to control because of her non-compliance regarding fluid restriction and a low-salt diet. Currently, a month after discharge, she continues to abuse both purgatives and diuretics.

Questions

What caused the excessive fluid gain in this patient? What laboratory data would help substantiate this diagnosis?

Answer to quiz on preceding page

This woman, a chronic laxative abuser, initially presented with pre-renal acute renal failure due to hypovolaemia. On rapid rehydration and abrupt cessation of purgative use she became markedly oedematous and was on the verge of pulmonary oedema. This condition has been termed `pseudo-idiopathic’ oedema [1]. It has mainly been described after diuretic withdrawal but rare cases occur following removal of purgatives. The postulated mechanism involves protracted stimulation of the renin–angiotensin system, leading to a self-perpetuating hyperreninaemic hyperaldosteronaemic state. Meyers et al. [1] actually performed renal biopsies in two of their nine patients, which revealed marked hyperplasia of the juxtaglomerular apparatus constituent cells as well as the presence of proliferating medullary interstitial cells. A repeat biopsy in one patient after a 12-month period of habit withdrawal still showed the same features, although less prominently than in the first biopsy. Thus, complete involution of these hyperplastic cells, even in the face of stimuli removal, may require a prolonged period of time.

Measurement of plasma renin activity (PRA) and aldosterone (PA) would help support the diagnosis. In our patient, supine PRA was 3.2 ng/ml/h (normal 0.2–2.8) and PA 256 pg/ml (normal 10–160). MacGregor et al. [2] have shown that the magnitude of weight gain was directly related to the level of PRA before drug withdrawal (diuretic in their series). During this oedematous phase it must be emphasized that patience on the part of each subject is essential. The usual scenario, as was seen in our case, is that patients will typically return to diuretic or purgative abuse.

Therefore, rehydration in these patients must be accomplished in a gradual, carefully monitored manner with close attention to electrolyte disturbances. Surprisingly, serum potassium, calcium, magnesium, and phosphate were all within normal limits in our patient. However, she did suffer from severe osteoporosis. Chronic laxative or diuretic abuse may be associated with a variety of bone disorders. Continued magnesium deficiency effectively results in a hypoparathyroid state and consequent impaired renal synthesis of 1,25-dihydroxycholecalciferol. This combination, if sustained long enough, will eventually lead to osteomalacia. Prostaglandin E2, elevated in these patients due to the induction of a pseudo-Bartter's syndrome, is known to promote bone resorption. Four out of the nine patients in the study by Meyers et al. had widespread osteoporosis [1].

Finally, the diagnosis of pseudo-idiopathic oedema is often not suspected. Our patient was subjected to a duplex examination of the inferior vena cava (IVC) and iliac veins with the incorrect diagnosis of IVC occlusion syndrome before the true situation was realized.

Notes

Supported by an education grant from

References

  1. Meyers AM, Feldman C, Sonnekus MI et al. Chronic laxative abusers with pseudo-idiopathic oedema and autonomous pseudo-Bartter's syndrome. S Afr Med J1990; 78: 631–636[ISI][Medline]
  2. MacGregor GA, Markandu ND, Roulston JE, Jones JC, de Wardener HE. Is "idiopathic" oedema idiopathic? Lancet1979; 1(8113): 397–400[Medline]




This Article
Extract
FREE Full Text (PDF)
Alert me when this article is cited
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Disclaimer
Request Permissions
Google Scholar
Articles by Korzets, Z.'e.
Articles by Bernheim, J.
PubMed
PubMed Citation
Articles by Korzets, Z.'e.
Articles by Bernheim, J.