Intermittent hepatitis B surface antigenuria in a renal transplant recipient

It has been demonstrated that hepatitis B surface antigen (HB₈Ag) can be detected in the urine of a majority of persistent serum carriers of HB₈Ag undergoing hemodialysis with urinary output. Therefore we have proposed that, in this population, urine may represent a potential vehicle for nonparental transmission of hepatitis B. Described here is a renal transplant recipient with intermittent HB₈Ag in the urine who has never been subjected to hemodialysis and who underwent bilateral nephrectomy before renal transplantation. Determinations of HB₈Ag or antibody to HB₈Ag (anti-HB₈) in serum obtained from this patient and three household contacts, as well as in serial urine samples from the patient, were performed by radioimmunoassay. The patient has consistently had HB₈Ag in her serum (HB₈Ag positive) (subtype ad) for at least three years. Four of five urines obtained over a four-month period also contained HB₈Ag. Two serum samples, one year apart, obtained from the son of this index patient both contained HB₈Ag. Serum samples from her former husband and a current cohabitant were void of HB₈Ag, but did contain anti-HB₈, indicating previous exposure to hepatitis B. We believe this information implicates the index patient as a potential source of hepatitis B to a number of persons. The epidemiologic consequences of HB₈Ag positive persons receiving a renal transplant have not been adequately emphasized. Furthermore, the presence of HB₈Ag in the urine eight years after a bilateral nephrectomy and successful renal transplantation suggests that the transplanted kidney allows passage of HB₈Ag into the urine and that the presence of an end-stage kidney is not required for antigenuria. Finally, because successful renal transplantation results in normal urine volume and increased interaction of the recipient with the general population, the urine of HB₈Ag carriers could have an important role in the spread of hepatitis B.     

Angiomyolipoma presenting as fever of unknown origin

A case of renal angiomyolipoma presenting as fever of unknown origin unassociated with tuberous sclerosis is described. Important features include (1) infrequent occurrence in absence of tuberous sclerosis, (2) angiographic appearance suggesting neoplasm, (3) absence of documented malignant tissue transformation, and (4) presenting symptoms most frequently included abdominal pains, palpable flank mass and hematuria. Surgical removal of the lesion in this instance was associated with cessation of fever.     

Rotor's syndrome: A distinct inheritable pathophysiologic entity

Urinary total, isomer I and isomer III coproporphyrin excretion was determined in 11 patients with Rotor's syndrome, 23 phenotypically normal family members, 16 patients with the DubinJohnson syndrome and 20 normal control subjects. Control subjects excreted 24.8 ± 1.3 per cent (mean SEM) of urinary coproporphyrin as isomer I. Patients with the Dubin-Johnson syndrome excreted 88.9 ± 1.3 per cent as urinary coproporphyrin I, and patients with Rotor's syndrome excreted 64.8 ± 2.5 per cent as urinary coproporphyrin I, significantly different from the control subjects and the patients with the Dubin-Johnson syndrome (p < 0.001). Eight phenotypically normal parents and children of patients with Rotor's syndrome excreted 42.9 ± 5.4 per cent as urinary coproporphyrin I, intermediate between results in patients with Rotor's syndrome and control subjects (p < 0.001). Total urinary coproporphyrin excretion was markedly increased in patients with Rotor's syndrome (332 ± 86 μg/g creatinine) as compared to that in control subjects (p < 0.001) or obligate heterozygotes (p < 0.025).With respect to urinary coproporphyrin excretion, Rotor's syndrome and Dubin-Johnson syndrome are both inherited as autosomal recessive traits and are separate pathophysiologic entities. Study of rare but distinct inheritable disorders, such as these, provide insight into the functional dissociation of hepatic transport mechanisms.     

Ultrastructure of the lung in Loeffler's pneumonia

A case is presented fulfilling the diagnostic criteria of “Loeffler's eosinophilic pneumonia.” No etiologic factors could be determined, and the chest roentgenogram returned to normal. Lung biopsy at the peak of the disease demonstrated an interstitial eosinophilic pneumonia without tissue necrosis or vasculitis. By electron microscopy, the alveolar capillary basement membranes were intact and exhibited no immune deposits. Normal appearing eosinophils were abundant in the alveolar capillaries, interstitium and alveolar spaces. Occasional eosinophils released their granules within the alveolar wall. Macrophages were increased in number in both the alveolar wall and alveolar spaces.     

Immunologically diagnosed malignancy in Sjögren's pseudolymphoma

Studies of lymphocyte markers in a patient with Sjögren's syndrome who exhibited histologically benign lymphoproliferation in the lung revealed a malignant cell clone. T and B cells were quantitated according to their ability to form spontaneous rosettes with sheep erythrocytes and to fluoresce with fluorescein-conjugated antiserums, respectively. Circulating lymphocytes were 66 per cent T cells (N = 58 ± 2 per cent) and 14 per cent B cells (N = 22 ± 1 per cent), the latter exhibiting normal polyclonal distribution of membrane immunoglobulins. However, lymphocyte suspensions obtained from fresh lymph node and from biopsy specimens from a lymphoid lung nodule revealed 95 per cent and 88 per cent B cells, with 1 per cent and 2 per cent T cells, respectively. Moreover, when cryostat-frozen sections from both tissues were reacted with each of the heavy and light chain-specific antiserums, most cells demonstrated the presence of intracytoplasmic μ kappa immunoglobulin exclusively. Twenty-two months later, a clinically and histologically classic lymphoma developed. Repeat marker studies performed on cells freshly isolated and on frozen sections from the histologically malignant lymph node revealed persistence of the monoclonal marker on most cells.     

Cardiac failure in Addison's disease

In an average 30 years of follow-up study, seven of 22 patients with primary adrenal insufficiency have had cardiac failure. Comparison of these seven with the 15 who remain free of this complication revealed that the former group were somewhat older and had higher incidences of unrelated cardiac disease and of nonsteroid-dependent hypertension, but that their replacement regimens, with respect to sodium supplementation and sodium-retaining steroids, were identical with the latter. Coincident with the appearance of cardiac failure, all seven patients had a decrease in sodium requirements. Adequate control of the adrenal disease was subsequently possible with elimination of mineralocorticoid support in one of the six who had initially required this therapy and a reduction in dosage in the other five. In all seven, dietary sodium supplements were no longer required. In three patients with severe failure, sodium restriction was imposed and diuretics were added, although the latter therapy has required close monitoring to avoid sodium depletion.