[Parathyroid cystic adenoma as the cause of primary hyperparathyroidism].
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Biomedical subjects
Publications and source records attributed to J Montoliu.
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Two patients with diabetic nephropathy on maintenance hemodialysis developed extreme hyperkalemia (7.9 and 9.3 mmol/L, respectively) in association with severe episodes of hyperglycemia (1,152 and 1,185 mg/dL, respectively). The increase in serum potassium was out of proportion to the degree of metabolic acidosis that both patients had, and no exogenous source of hyperkalemia could be identified. Despite treatment efforts both patients died shortly after arrival as a consequence of cardiac arrest. It is proposed that the hyperosmolality of extracellular fluid produced by severe hyperglycemia drives potassium passively out of the cells, therefore favoring the rapid development of hyperkalemia. Insulin deficiency could also play a role. This situation is particularly dangerous in individuals with impaired renal function. Adequate blood glucose control in diabetic patients on dialysis is important to avoid life-threatening hyperkalemia.
A 28-year-old patient with chronic renal failure on maintenance hemodialysis developed fever, granulomatous hepatitis, pulmonary infiltrates, sacroiliitis, and spondylitis which were unresponsive to conventional antituberculous treatment. Cultures of the sputum gave repeated growth of Mycobacterium fortuitum. This organism was resistant 'in vitro' to most antituberculous drugs and sensitive to some aminoglycosides and doxycycline. No mycobacteria were found in the water used for dialysis. The patient was successfully treated with amikacin and doxycycline. Nontuberculous mycobacterial infection should be considered in the differential diagnosis of febrile illnesses resembling tuberculosis in hemodialysis patients. Defective immune mechanisms could contribute to this complication. Since M. fortuitum is usually resistant to antituberculous drugs, precise identification and sensitivity testing are essential for optimal management.
Four patients (2 were HBsAg positive) with acute icteric viral hepatitis (VH) developed acute renal failure (ARF) in the course of their illness and in the absence of other complications. Their peak serum creatinine values (4.7-10, mean 7 mg/dl) were reached either before or simultaneously with their maximum serum aminotransferase values (1,390-2730, mean 2,032 mU/ml). Apart from VH no other factors responsible for precipitating ARF could be identified. In the HBsAg-negative patients, serological investigations for infectious mononucleosis, cytomegalovirus infection, and leptospirosis were negative. In 2 patients liver biopsy showed changes consistent with VH. Proteinuria was absent in all cases, making glomerulonephritis unlikely. The urinary sodium excretion was uniformly high (57-104, mean 78 mmol/l in random samples). Two patients required short courses of dialysis. All cases recovered completely with return of serum creatinine to normal values after a mean duration of 25 days. After a normal serum creatinine level had been achieved, 1 case was lost to follow-up, and the other 3 cases maintain normal renal and liver function tests 9 months (mean) after the initial episode. Otherwise uncomplicated VH is a potential cause of ARF, even in the absence of severe hepatic insufficiency. The mechanism of ARF in VH is unknown, but vasoconstriction phenomena induced by endotoxemia might contribute.
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The immunologic alterations in patients on hemodialysis are only partially understood. We studied the Concanavalin A (Con A) induced suppressor cell activity of irradiated and nonirradiated cells in a mixed lymphocyte culture. Peripheral blood lymphocytes from 18 normal individuals and 14 patients on regular hemodialysis were incubated with two different concentrations of Con A (10 micrograms and 40 micrograms of Con A/million cells). Irradiated and nonirradiated cells were then tested for their capacity to suppress a standard MLC. The proliferative response to phytohemagglutinin, pokeweed mitogen and Con A was also determined. Suppressor cell activity of nonirradiated cells in hemodialysis patients was similar to that of controls, at both concentrations of Con A, while irradiated cells of hemodialysis patients showed a suppressor cell activity significantly lower than that of the controls, at a Con A concentration of 40 micrograms/10(6) cells (25.78 +/- 18.86% vs. 46.05 +/- 9.79%, p less than 0.001). The proliferative response of lymphocytes from hemodialysis patients to the three mitogens, did not show any difference when compared with normal controls. The normal proliferative response of lymphocytes from hemodialysis patients to mitogens and the normal suppressor cell activity of nonirradiated cells, suggest a normal T cell function. The abnormal suppressor cell activity in irradiated cells indicate that the radioresistant population has a functional defect. The cell responsible for this suppressor defect probably belongs to the monocyte/macrophage population because of its relative radioresistance.
Changes in plasma volume (PV), extracellular volume (ECV) and intracellular volume (ICV) were studied in seven patients on conventional haemodialysis (HD) and in six patients on stable hypertonic HD. Weight loss and ultrafiltration were similar in both groups. Before HD the spaces of 125RISA (PV), 35SO4Na2 (ECV) and 3H2) (total body water, TBW) were simultaneously determined ICV = TBW - ECV. At the end of HD the space of 35SO4Na2 was again tested. PV and ECV diminished more on conventional HD than on hypertonic HD, whereas ICV increased on conventional HD and decreased on hypertonic HD. The handling of plasma osmolality during HD is an effective method for modifying transcompartmental body fluid shifts in HD by distributing weight loss between intracellular and extracellular spaces allowing for a better maintenance of plasma volume.
This study evaluates if the use of high flux membranes and the type of dialysate influences aluminium removal in haemodialysis. Aluminium kinetics and dialysance were determined in baseline conditions and after infusion of desferrioxamine. The free diffusible fraction of plasma aluminium correlated significantly with the plasma aluminium post desferrioxamine, independently of the type of membrane or dialysate used. Aluminium removal therefore depends on the plasma concentration reached and the dialysate concentration. High flux membranes do not improve aluminium removal in vivo.
Six HBsAg negative patients with cirrhosis of the liver (CL) presented with recurrent bouts of palpable purpura in the legs due to small vessel leucocytoclastic vasculitis. In addition, all patients had renal failure, proteinuria and microhaematuria. Renal biopsy disclosed either diffuse proliferative (3 cases) or focal necrotising glomerulonephritis with crescents (2 cases). One patient had IgM-IgG mixed cryoglobulinaemia (type II). Four patients died of complications of their CL. Hepatocellular carcinoma was found in 1 case. In the patient without renal biopsy renal function improved following steroids and cyclophosphamide. The pathogenesis of this syndrome of cutaneous vasculitis with severe glomerular involvement in CL is unknown but could be immune-complex mediated.
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Immune complex deposition in the vessel wall is presumed to be the major pathogenetic mechanism leading to hypersensitivity vasculitis. Despite this, histologic evidence of vascular immune complex deposition such as that provided by electron-dense deposits has been reported only rarely in dermal vessels and never in visceral organs. The cases of two patients with hypersensitivity vasculitis affecting primarily the skin and the kidney are reported. Clinical renal involvement was manifested by proteinuria, hematuria, and a moderate increase in serum creatinine in one case. Renal biopsy showed minimal glomerular changes in one patient and focal necrotizing glomerulitis in the other. The arterioles appeared normal on light microscopic examination. However, obvious electron-dense deposits in the arteriolar wall could be demonstrated electron microscopically in both cases. This observation lends strong support to the theory of immune-complex-mediated vascular damage as the main pathophysiologic mechanism in vasculitis with visceral involvement.
Glomerulonephritis is a very unusual feature of relapsing polychondritis. A 16-year-old woman presented with microscopic hematuria and severe renal insufficiency during the course of relapsing polychondritis. A renal biopsy specimen disclosed focal segmental proliferative glomerulonephritis with necrotizing lesions and crescent formation. Immunofluorescent studies suggested immune complex mediated glomerular injury. The renal involvement appeared during high-dose steroid therapy. Subsequently, she was treated by adding plasmapheresis and cyclophosphamide during 6 weeks, with sustained improvement. A regimen of plasmapheresis and immunosuppression warrants consideration for use in cases of relapsing polychondritis with glomerulonephritis.
A 56 year old man presented with hypertension, hypokalemia and depressed plasma renin activity. Plasma aldosterone was normal, but was considered inappropriate in the presence of hypokalemia. An adrenal scan showed unilateral uptake of 131I-cholesterol and a presumptive diagnosis of adrenal adenoma was made. At surgery, no adenoma was found. Instead, the adrenal was atrophic, and in this case also contained caseating granulomas. Postoperative plasma aldosterone values were consistently normal and adrenocortical insufficiency was ruled out. On requestioning, the patient admitted long-term topical use of a skin cream containing 9-alpha-fluorprednisolone. Withdrawal of the fluorprednisolone cream led to normalization of blood pressure and serum potassium, and on renewed contact with the drug, hypertension and hypokalemia reappeared. The patient is now normotensive and normokalemic after permanent discontinuation of the cream. Topical cutaneous application of 9-alpha-fluorprednisolone can induce a syndrome closely mimicking primary aldosteronism. A high degree of suspicion and adequate history taking are critical for the appropriate management of such patients and the avoidance of unnecessary or dangerous procedures.
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