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Biomedical subjects

L Revert

Publications and source records attributed to L Revert.

At least 145 records · Page 8Linked to original sources

Malignant or accelerated hypertension in IgA nephropathy.

A retrospective analysis of 66 adult patients diagnosed as having IgA nephropathy by renal biopsy revealed that 24 (36%) were hypertensive when first seen. Of these hypertensive patients, 10 (15%) had malignant or accelerated hypertension. All patients but one were male and had no knowledge of their renal disease and sought medical advice for symptoms due to hypertension. Five patients had no history of gross hematuria. Histological vascular findings showed, in three proliferative endarteritis and fibrinoid necrosis, in five arteriolosclerosis and in two vascular hypertrophy. In spite of good blood pressure control, six patients reached terminal uremia within a maximum of 14 months. In summary, the incidence of malignant hypertension in adults with IgA nephropathy is higher than previously reported, and its true incidence can only be known if more histopathologic studies of patients with malignant hypertension are performed. Patients with this association reach end stage renal failure in a short period of time.

Adult↗

Potassium-lowering effect of albuterol for hyperkalemia in renal failure.

To study the effect of specific beta 2-adrenergic stimulation on potassium metabolism in renal failure, we intravenously administered albuterol (Salbutamol) sulfate, 0.5 mg, to 20 patients with chronic renal failure (glomerular filtration rate, less than 5 mL/min) receiving maintenance hemodialysis. Within 30 minutes after albuterol administration, serum potassium level dropped from 5.6 +/- 0.2 (+/- SEM) to 4.5 +/- 0.2 mEq/L (5.6 +/- 0.2 to 4.5 +/- 0.2 mmol/L). There were no changes in plasma aldosterone levels or arterial pH, but blood glucose and serum insulin levels increased. Albuterol, however, induced similar decreases in serum potassium levels in three diabetic patients while free C peptide levels remained undetectable or subnormal after administration of the drug. Albuterol sulfate alone (0.5 mg intravenously) was also used to treat 24 patients with acute or chronic renal failure and hyperkalemia. Their serum potassium levels dropped from 7 +/- 0.2 mEq/L (7 +/- 0.2 mmol/L) to 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 6 +/- 0.2 mEq/L (6 +/- 0.2 mmol/L), and 6.2 +/- 0.2 mEq/L (6.2 +/- 0.2 mmol/L) at 30, 60, 180, and 360 minutes after receiving albuterol, respectively, and this was accompanied by reversal of the electrocardiographic manifestations of hyperkalemia. Despite inducing transient tachycardia, albuterol was remarkably well tolerated and no serious side effects were observed. beta 2-adrenergic stimulation of intracellular potassium uptake by albuterol is a safe and effective alternative for the treatment of hyperkalemia in renal failure.

Adult↗

Glomerular disease in cirrhosis of the liver: low frequency of IgA deposits.

Twelve HBsAg-negative patients with histologically documented cirrhosis of the liver of either alcoholic (8 of 12) or cryptogenic (4 of 12) origin underwent renal biopsy to investigate proteinuria, hematuria and/or renal failure. Immunofluorescence was positive for IgA in 2 patients with mesangiocapillary glomerulonephritis (MCGN) and could not be performed in 2 additional patients with the same diagnosis. However, in the remaining 8 patients, immunofluorescence was negative for IgA and frequently positive for C3, IgG, IgM and/or fibrinogen. These 8 patients without IgA were classified as follows: MCGN with subendothelial electron-dense deposits (2 cases), IgM-IgG cryoglobulinemia with diffuse endocapillary glomerulonephritis (1 case), membranous nephropathy (1 case), diffuse endocapillary proliferative glomerulonephritis (1 case), vasculitis with focal segmental necrotizing glomerulitis and crescentic glomerulonephritis (2 cases). These results show that cirrhosis of the liver can be associated with a wide variety of glomerular disorders. Contrary to previous belief, IgA is absent in two thirds of patients with cirrhosis and glomerulopathy. Therefore, the pathogenetic importance of IgA in the development of glomerular disease in such patients is doubtful.

Adult↗

Cellular infiltrate in renal graft rejection: T lymphocyte subsets detected by monoclonal antibodies.

We have examined the interstitial cellular infiltrate using monoclonal antibodies against T cells (Cris 1), helper/inducer T cells (OKT4) and suppressor/cytotoxic T cells (OKT8) by indirect immunofluorescence in renal biopsies taken from 14 transplanted patients during clinical episodes suggestive of acute (n = 9), chronic (n = 2) and no rejection (n = 3). Infiltrating T cells and T cell subsets were found to be significantly increased during all types of rejection (n = 11) as compared to no rejection (n = 3). Two types of biopsies could be distinguished according to the predominance of T cell subsets. In some biopsies (n = 6), OKT8+ cells were significantly more numerous that OKT4+ cells. In the remaining biopsies (n = 5), OKT4+ cells were more common that OKT8+ cells, the OKT4/OKT8 ratio being significantly higher. No association was observed between HLA mismatch and predominating T cell subset, neither for type nor outcome of graft rejection. Our results suggest that the OKT4+ cells may play a more important role than previously reported in renal graft rejection.

Adolescent↗

Defective platelet adhesion on vessel subendothelium in uremic patients.

Bleeding time, platelet retention on glass beads, and ristocetin-induced platelet agglutination (RIPA) in platelet-rich plasma were simultaneously determined for 20 patients with chronic renal failure and previous hemorrhagic history. In seven patients chosen at random out of a group of 16 in whom the three tests were abnormal, RIPA of uremic-isolated platelets in presence of normal platelet-poor plasma (PPP) and of normal platelets in presence of patient PPP were performed. In all cases, the first assay showed diminished agglutination, suggesting a platelet defect; however, uremic PPP did not inhibit the agglutination of normal platelets. In the same patients, the interaction of platelets with subendothelium was evaluated using Baumgartner's perfusion method. The subendothelial surface covered by platelets was significantly decreased in experiments with uremic whole blood when compared to normal controls. The interaction of platelets with subendothelium was also decreased when perfusions were carried out with platelet-plasma mixtures containing either normal washed platelets and uremic PPP or uremic washed platelets and normal PPP. These results show an impaired platelet adhesion caused both by a platelet and a plasmatic abnormality. Since uremic PPP decreased the adhesion of normal platelets to subendothelium but did not inhibit RIPA, it seems probable that the plasmatic defect could result in a defective binding between vWF and subendothelium. The influence of the red cell count on the platelet adhesion to subendothelium was reconfirmed by comparing perfusions of reconstituted blood with hematocrit values of 20% to 23% and 40% to 45%. In summary, a defective platelet adhesion to subendothelium has been postulated in uremic patients, caused by platelet and plasmatic alterations that are influenced by a low hematocrit.

Adult↗

Lethal hyperkalemia associated with severe hyperglycemia in diabetic patients with renal failure.

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.

Aged↗

Disseminated visceral infection with Mycobacterium fortuitum in a hemodialysis patient.

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.

Adult↗

Acute renal failure complicating viral hepatitis in the absence of severe hepatic insufficiency.

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.

Acute Kidney Injury↗

Defective radioresistant suppressor cell activity in hemodialysis patients.

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.

Adult↗

Changes in body compartments on different types of haemodialysis.

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.

Adult↗