Kevin J. Lavelle

Iodine absorption in burn patients treated topically with povidone‐iodine

Povidone‐iodine is used as a topical antimicrobial in burn patients. Although absorption of iodine has been thought to be negligible, several patients have recently.been noted with substantial elevations of serum free iodide. Unexplained abnormalities occurred in several of these patients, renal failure, metabolic acidosis, and elevation of serum glutamic oxaloacetic transaminase. It is conceivable that the large iodide loads noted were at least in part responsible for these abnormalities.

Case Report Increased serum iodide concentration from iodine absorption through wounds treated topically with povidone-iodine

Increased serum iodide concentrations secondary to iodine absorption through wounds treated with povidone-iodine dressings is described. Hyperchloremic acidosis and a disparity between serum chloride concentrations determined by two different methods suggested the presence of an unidentified halide. Cardiovascular instability and renal failure occurred concurrent with systemic iodide accumulation. Measurement of serum iodide concentration should be performed when povidone-iodine is used topically in patients with impaired renal function.

Ureteral Obstruction Owing to Endometriosis: Reversal with Synthetic Progestin

A case of unilateral ureteral obstruction owing to extensive pelvic endometriosis is presented. There was complete resolution of ureteral obstruction following treatment with synthetic progestin. Sequential assessment of renal function was provided by renal imaging and renograms. It would appear that selected patients with obstructive uropathy may respond favorably to medical management, which would allow for preservation of reproductive capabilities and restoration of renal excretory function.

Identification of a new platelet aggregating factor released by sensitized leukocytes

Abstract Sensitized mononuclear cells from the spleen of nephritic New Zealand white rabbits will, on re-exposure to the sensitizing antigen, produce a substance capable of inducing platelet aggregation. The reaction producing the platelet aggregating factor (PAF) is antigen specific. This factor has several characteristics of the lymphokines, including molecular weight, rate of synthesis, and thermal stability. The mechanism by which PAF produces aggregation appears to be by induction of the platelet release reaction. The effect of PAF on platelets is inhibited by acetylsalicylic acid and heparin. PAF had no effect by tests used on purified fibrinogen. This factor may be responsible for the platelet aggregates seen in the glomeruli of both animals and patients with various types of glomerulonephritis.

Nephrotoxicity of Radiocontrast Media in Ischemic Renal Failure in Rabbits

Ischemic renal failure was produced in rabbits by occluding the renal arteries for 90 min. Group 1 (n = 8) received radiocontrast media at the time of occlusion, group 2 (n = 8) 24 h after occlusion, and group 3 (n = 8) 3 days after occlusion. Group 4 (n = 12) was subjected to ischemic injury alone, group 5 (n = 4) served as sham-operated controls and group 6 (n = 4) did not undergo surgery but received radiocontrast media. Serum creatinine concentration in group 1 increased to a greater degree (p less than 0.001) than all other groups and did not return to normal during the 8-day observation period. Creatinine concentration in groups 2, 3, 4, and 6 were comparable and significantly increased compared to sham-operated group (p less than 0.05). Urinary excretion of alanine aminopeptidase and N-acetyl-beta-glucosaminidase in group 1 was significantly greater than all other groups (p less than 0.05). Microscopic analysis indicated tubular necrosis was more prominent in group 1. Radiocontrast media is nephrotoxic and in the setting of ischemic injury may prevent recovery of renal function. Toxicity was dependent on the time of administration since functional impairment was not increased if dye was given 1 or 3 days after ischemic injury.

Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion.

A 69-year-old man with glucose-6-phosphate dehydrogenase deficiency was treated with nitrofurantoin for pyuria. Four days later he presented with metabolic acidosis due to excess lactic acid, a decline in curculating hemoglobin, reticulocytosis, elevated serum transaminase levels, and hyperbilirubinemia. The drug was withdrawn and the hyperlactatemia subsided in three days without specific treatment. In vitro, nitrofurantoin is capable of stimulating erythrocyte glucose utilization aand lactate production, and inhibiting the generation of reduced glutathione. In vivo, this drug is capable of producing hemolysis in susceptible subjects and hepatocellular injury. The temporal proximity of drug ingestion and hemolysis, increased glucose utilization, lactate excess, and hepatic insufficiency suggests that nitrofurantoin may have been responisble for precipitating the clinical and chemical abnormalities observed.

Ferritin- and Apoferritin-Induced Immune Complex Glomerulonephritis in Mice

In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.

Effect of antigen charge on immune complex interaction with glomerular cells in culture

The effect of antigen charge on immune complex (IC) interaction with glomerular cells was evaluated using cultured rabbit glomerular cells. Rat albumin (Alb) was modified to produce a cationic charge; isoelectric point (pI) 7.4-8.0; anionic charge, pI 4.0-4.2; or left unmodified, pI 6.2-6.4. I125-IC (100 micrograms Alb in complex) was incubated with cells for 44 hr. Cationic Alb IC (CAT IC) interaction was 7 and 10 times greater than unmodified (UM) and anionic (AN) IC, 7596 +/- 613 vs 1016 +/- 176 and 746 +/- 106 pg I125-Alb/micrograms cell protein, mean +/- SE (P less than 0.01). A 10-fold excess of unlabeled CAT Alb decreased CAT IC interaction (6342 +/- 432 vs 1246 +/- 296 pg I125-Alb/micrograms cell protein, P less than 0.01) increased UM IC (981 +/- 186 vs 3994 +/- 394 pg I125-Alb/micrograms cell protein, P less than 0.01), and had no effect on AN IC. A 10-fold excess unlabeled CAT IC increased interaction of both CAT IC (7067 +/- 514 vs 37,416 +/- 3026 pg I125-Alb/micrograms cell protein) and UM IC (994 +/- 123 vs 12,922 +/- 566 pg I125-Alb/micrograms cell protein) but not of AN IC. Incubation of cells with CAT, UM, or AN Alb followed by specific antibody demonstrated increased antibody interaction with cells exposed to CAT Alb (15,212 +/- 676 vs 3866 +/- 406 and 1785 +/- 206 pg I125-IgG/microgram cell protein for UM and AN Alb, respectively).

Effect of indomethacin and benoxaprofen on immune complex interaction with cultured glomerular cells

Prostaglandins of the E series (PGE) increased immune complex (IC) interaction with cultured glomerular cells in a previous study. The present study examines the effect of indomethacin (IND) and benoxaprofen (BEN) on interaction of IC with cultured cells and their effect on PGE enhanced cell-IC interaction. IC were formed with antigen modified to produce a cationic (CAT) charge or left unmodified (UM). IND increased cell interaction with IC formed with CAT antigen (CAT IC). BEN had no effect on the interaction of IC formed with either antigen. The combined use of IND and PGE increased CAT IC interaction to the same degree as when each was used alone. BEN prevented the increased CAT IC interaction produced by IND or PGE when used in combination. Protamine sulfate prevented the enhanced CAT IC interaction produced by IND or PGE while sodium heparin had no effect. The results indicate IND and PGE increase cell IC interaction, the increase is not additive when they are combined, the effects of both are blocked by BEN, and protamine sulfate inhibits the effects of both compounds.

Effect of Prostaglandins on Immune Complex Interaction With Glomerular Cells in Vitro

Previous studies demonstrated that prostaglandins of the E1 (PGE1) series reduced immune complex (IC) accumulation and inflammation in murine glomeruli in IC glomerulonephritis (GN). This study examines the effect of PGE1 on IC interaction with cultured rabbit glomerular cells and heparan sulfate synthesis by the cells. IC were formed with antigen chemically modified to produce a cationic (CAT) charge or left unmodified (UM). CAT IC binding to cells was greater than UM IC in the absence of PGE1. CAT IC binding to cells was increased by PGE1 while UM IC interaction was not affected. Prolonged exposure of cells to PGE1 enhanced CAT IC binding. Heparan sulfate synthesis by the cells was not affected by the concentrations of PGE1 employed. The findings suggest the benefit provided by PGE1 in murine IC GN may not be due to a direct effect on glomerular cells which reduces glomerular IC accumulation.