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Biomedical subjects

L Raij

Publications and source records attributed to L Raij.

At least 109 records · Page 6Linked to original sources

Severe hypokalemia induced by hemodialysis.

During dialysis, it is assumed that the serum electrolyte levels asymptotically approach the concentration in the dialysate. In five patients, we observed an average 20% fall in serum potassium level, although the dialysate contained 42% more potassium than the predialysis serum. One patient had quadriplegia and near respiratory arrest as a complication of hypokalemia. The cause of the hypokalemia was a rapid shift of potassium from the extracellular to the intracellular space secondary to correction of acidosis. All patients entered dialysis with a history suggesting prolonged potassium loss, marked acidosis, and moderate hypokalemia; thus, the dialysate potassium concentration should be higher than normal, and frequent determinations of the serum potassium level should be performed. Therapy resulting in rapid correction of acidosis in uremic patients undergoing hemodialysis may cause large transcompartmental shifts of potassium. Potassium transfer across the dialysis membrane may be inadequate to compensate for such shifts, and life-threatening hypokalemia may occur.

Acidosis↗

Comparison of 4 and 10 days of doxycycline treatment for urinary tract infection.

A total of 105 ambulatory patients presenting with symptoms suggestive of cystitis was allocated randomly to a 4 or a 10-day course of doxycycline therapy. Of these patients 62 (59 per cent) had documented infections and 41 (66 per cent) were infected with doxycycline-sensitive organisms: 24 were randomized to a 4-day course and 17 to a 10-day course of antibiotic. The groups were similar with respect to age, history of urinary tract infection, bacteriology and site of infection. Of the 4-day treatment group 90 per cent were free of infection 42 days after completion of therapy, compared to 92 per cent in the 10-day treatment group. Thus, patients with symptoms of cystitis may be treated with a short course of an appropriate antibiotic, provided careful followup is made 4 to 6 weeks after cessation of therapy. The site of urinary infection of doxycycline-resistant and sensitive organisms was determined by the antibody-coated bacteria techniques in 56 episodes: 13 (23 per cent) originated in kidneys, 34 (61 per cent) originated in bladder foci and the results in 9 (16 per cent) were indeterminate. Results of the antibody-coated bacteria technique did not predict therapeutic outcome.

Adolescent↗

Impaired mesangial clearance of macromolecules in rats with chronic mesangial ferritin-antiferritin immune complex deposition.

The mesangial egress, but not the uptake of radiolabeled aggregated human immunoglobulin G (AHIgG125I) (macromolecular proteins biologically akin to immune complexes), deviated markedly from normal in rats with preexisting ferritin-antiferritin immune complexes in the mesangium. Sprague-Dawley rats, given daily intraperitoneal ferritin, 8 mg. per 100 gm. of body weight, for 6 weeks (Ferritin rats), uniformly developed intense mesangial staining for IgG and C3 by immunofluorescence microscopy but minimal glomerular proliferation by light microscopy. With electron microscopy, ferritin was seen in mesangial channels and also in mesangial cells. These rats had normal serum creatinine, no hematuria or proteinuria. AHIgG125I, 50 mg. per 100 gm of body weight, was given intravenously to control and to Ferritin rats; groups of five control and five Ferritin rats were sacrificed at 2, 4, 8, 16, and 24 hours after injection. AHIgG125I was measured in preparations of isolated glomeruli and compared with simultaneous spleen, liver, and blood levels. At all time intervals, blood levels of > 7 S AHIgG125I were similar in control and Ferritin rats. Initial, 2-hour mesangial uptake of AHIgG125I was similar in control and Ferritin rats. During the 2- to 16-hour interval, the disappearance of AHIgG125I from glomeruli of Ferritin rats was delayed; glomerular AHIgG125I concentration decreased 85 per cent in control but only 38 per cent in Ferritin rats. After the administration of AHIgG125I, hematuria (2 to 3+) developed in 60 per cent of Ferritin rats but not in control rats. These studies suggest that immune complexes of different antigen-antibody systems may influence the kinetics of each other locally, at the glomerular level. This impaired mesangial clearance of immune complexes may favor the development of glomerular injury. The experimental model described may be relevant to some forms of human glomerulonephritis in which mesangial pathology and immunopathology are characteristic, and may explain some of the pathogenetic mechanisms operative in these diseases in man.

Animals↗

Mesangial function in ureteral obstruction in the rat. Blockade of the efferent limb.

The kinetics for mesangial uptake and transport of radiolabeled aggregated human immunoglobulin (Ig)G (AHIgG(125)I) deviated markedly from normal in male Sprague-Dawley rats with ureteral obstruction. Four experimental groups, each containing 25 rats, were used: (a) bilateral ureteral ligation (BUL) with release of one ureter 24 h later; (b) unilateral ureteral ligation with release 24 h later [UUL(R)]; (c) unilateral ureteral ligation without release (unreleased) [UUL(U)]; (d) uremia-control, which consisted of rats with ligated left ureter and a severed right ureter. A similar number of sham-operated rats served as control for each group. AHIgG(125)I (45 mg/100 g body wt) was given intravenously 1 h after release of the ureteral obstruction (25 h after ureteral obstruction or sham surgery). Groups of five control and five experimental animals were sacrificed at 2, 4, 8, 16, and 24 h after injection. At all time intervals, concentrations of AHIgG(125)I in isolated glomeruli from control animals were similar to values obtained from nonobstructed kidneys of UUL(U) and UUL(R) rats: a linear decrease in concentration over a period of 24 h was observed when the logarithm of glomerular AHIgG(125)I concentration was plotted against time. Aberrations in the kinetics were apparent in obstructed kidneys but not in liver, spleen, or blood concentrations of AHIgG(125)I: (a) At 2 h in all obstructed kidneys, glomerular concentration of AHIgG(125)I was markedly reduced. (b) In BUL (released or unreleased), glomerular concentrations of AHIgG(125)I from 4 to 16 h were congruent with 10-fold those in UUL(U) or UUL(R) kidneys. (c) The significant decline in glomerular concentration between 4 and 16 h in control and nonobstructed kidneys was not observed in UUL(R), UUL(U), or BUL (released or unreleased) kidneys; in all obstructed kidneys, a plateau in glomerular concentrations of AHIgG(125)I was observed between 4 and 16 h. (d) After 16 h at a time when the blood level of AHIgG(125)I had decreased to 3% of initial values, there was progressive fall in glomerular AHIgG(125)I. Similar results were obtained in the uremia-control group in rats, which indicated that uremia per se had no measurable effect on mesangial kinetics. These studies demonstrate that ureteral occlusion induces alterations in mesangial uptake (afferent limb) and egress (efferent limb) of macromolecules. Particularly evident is the "blockade" of the efferent limb which is demonstrable at high blood levels of AHIgG(125)I. These alterations in the transit of macromolecules through the mesangium may be mediated in part by the hemodynamic changes that accompany ureteral obstruction.

Animals↗

Unilateral Shwartzman reaction: cortical necrosis in one kidney following in vivo perfusion with endotoxin.

Unilateral renal cortical necrosis was selectively induced by in situ perfusion of the rabbit kidney with a perfusate containing 50 microgram of endotoxin followed by the i.v. administration of 250 microgram of endotoxin 24 hr later. The results strongly support the idea that the initial event in the genesis of renal cortical necrosis during the Shwartzman reaction is a specific local effect of endotoxin on the vascular endothelium.

Animals↗

Irreversible acute renal failure in idiopathic nephrotic syndrome.

In five adult patients (aged 44 to 74 years) with idiopathic nephrotic syndrome, irreversible acute renal failure developed. Prior renal disease, associated systemic illness or occlusion of major renal vasculature was not present. All patients continued to excrete large amounts of proteins (8.6 to 15 g/24 hours) despite a minimal glomerular filtration rate and severe oliguria. One patient died after five months without recovering renal function. Four patients have required hemodialysis for a period of 12 to 58 months. The failure to recover renal function could not be explained by the light microscopic findings. It is suggested that the irreversibility of the renal failure may be related to either permanent alterations in renal blood flow or ultrastructural changes, or to both. Clinically, adult patients in whom acute renal failure develops during the course of idiopathic nephrotic syndrome seem to have a grave prognosis. Protracted oliguria or irreversible renal failure can be expected to occur.

Acute Kidney Injury↗

Successful renal transplantation in progressive systemic sclerosis.

Hemodialysis and renal transplantation were done in a patient with progressive systemic sclerosis and renal failure. The patient's clinical course following transplantation was uncomplicated, and a biopsy of the renal allograft done 14 months after transplantation did not show recurrence of the original disease. These observations favor the consideration of early renal transplantation in patients with scleroderma and renal failure.

Adult↗

An air sampling technique for hepatitis B surface antigen.

A filter-rinse technique capable of detecting low levels of airborne hepatitis B surface antigen (HBsAg) was devised and evaluated. Laboratory tests showed the procedure to have an efficiency of 22% with a coefficient of variation of 11% and a capability of detecting as little as 5 x 10(-5) ml of aerosolized antigen positive serum in a single air sample. The technique was field-tested in a hemodialysis center serving a patient population with a high prevalence of HBsAg seropositivity. The antigen was not detected in any of 60 air samples collected under conditions favoring the occurrence of aerosols.

Aerosols↗

Recurrence of idiopathic membranous nephropathy in a renal allograft.

A middle-aged man with idiopathic membranous nephropathy, who developed chronic renal failure, received a cadaver renal allograft. Two months later, massive, persistent proteinuria developed. A biopsy specimen of the allograft showed changes characteristic of membranous nephropathy and identical to those present in the patient's own kidney. The criteria for recurrence of glomerulonephritis in renal allografts are met in this case.

Animals↗