[Primary glomerulopathies].
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Biomedical subjects
Publications and source records attributed to L Juncos.
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In the present study, we evaluated the renal response to a 4-hour infusion of amino acids in essential hypertensive patients, as well as the effects that dietary sodium restriction and enalapril (a converting enzyme inhibitor) had on this renal response. During normal sodium intake, amino acid infusion significantly increased renal plasma flow from 383 +/- 58 to 478 +/- 51 mL/min and glomerular filtration rate from 82 +/- 8 to 100 +/- 13 mL/min. All these effects were abolished when the patients received a low sodium diet (40 mmol/d) for 3 days before the amino acid infusion. The administration of enalapril to the patients during sodium restriction restored the amino acid-induced increment in renal plasma flow (from 388 +/- 35 to 573 +/- 48 mL/min) and glomerular filtration rate (from 88 +/- 9 to 103 +/- 10 mL/min). Mean arterial pressure remained unaltered under all experimental conditions. The results show that in patients with essential hypertension dietary sodium restriction prevents amino acid-induced increments in glomerular filtration rate and renal plasma flow and that this effect is restored during the simultaneous administration of enalapril.
This study was undertaken to investigate the role played by renal functional and structural changes in the development of radiation-induced hypertension. Four groups of rats were studied: 1) left kidney radiated, 2) sham procedure, 3) uninephrectomy followed 3 weeks later by radiation of the contralateral kidney, and 4) uninephrectomy followed by sham procedure 3 weeks later. All radiated rats became hypertensive at 12 weeks (p less than 0.05) and had higher protein excretion (p less than 0.05). In the presence of an intact contralateral kidney, radiation causes mild-to-moderate histological abnormalities, and therefore, creatinine clearance and water and sodium handling do not change. Plasma renin activity increased in this group (p less than 0.05). Radiated uninephrectomized rats showed decreased creatinine clearance (p less than 0.05), but renin activity remained unchanged. These rats developed severe histological abnormalities in glomeruli, interstitia, tubuli, and vessels resulting in increased sodium and water output. The average of individual tubular and interstitial scores correlated significantly with both water intake and output but not with sodium excretion. These studies suggest that in the presence of an intact kidney, renin is an important determinant in the development or maintenance of radiation hypertension, whereas in the absence of the contralateral kidney, severe histological changes and renal failure are prominent despite increased water intake and output. The more severe glomerular sclerosis and proteinuria in the latter model could be related to diminished renal mass.
Glycoside toxicity, a common and potentially fatal complication among patients taking digoxin, is treated basically by managing cardiac arrythmias until the patient can excrete enough drug to decrease the intoxication. Patients with renal failure, however, are particularly difficult to manage. We describe a case of advanced digoxin toxicity in an elderly man with severe renal failure, treated with a charcoal hemoperfusion device.
Twenty-eight patients with demonstrated chronic renal vein thrombosis were studied. In seven, only small venous channels were involved; in 21, both small and large veins were thrombosed. A constellation of findings occurred with such frequency in these patients that we believe it virtually diagnostic of renal venous obstruction. These findings include the nephrotic syndrome, great variability in proteinuria and glomerular filtration rate, pulmonary embolization, sterile pyuria, hematuria, hyperchloremic acidosis, decreased renal tubular threshold for glucose and increased fibrin degradation products. These findings are an indication for definitive angiographic and biopsy procedures. Prolonged anticoagulant therapy was generally very effective.
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Renal biopsies from 10 patients staining predominantly for immunoglobulin A are reviewed. Historically, nine of 10 patients were less than 32 years of age; they all presented with either microscopic or gross hematuria. The initial creatinine clearances demonstrated good function in all patients; only one patient experienced a progressive decline in the creatinine clearance. Similarly, proteinuria was mild. The light and electron microscopic findings presented a variable pattern, including a group with changes confined to the mesangium, another group also having glomerular basement membrane changes, and one patient with severe, progressive glomerular sclerosis. Immunogluorescence demonstrated large amounts of IgA predominantly within the mesangium but occasionally involving the peripheral capillary loops. Serum IgA levels were elevated in six of eight patients tested, and two of five patients had elevated nasal IgA concentrations. These data suggest that there is an immunologic entity, IgA glomerulonephritis, characterized by the above clincial findings in association with elevated serum and occasionally nasal IgA levels, but that the pathologic findings are highly variable. Neither the mechanism nor the particular pathogenetic significance of the raised IgA levels is presently known. The similarities of this entity to the reported findings in anaphylactoid purpura are mentioned.
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