Use of hemodialysis after ingestion of a mixture of acids containing hydrofluoric acid.

Hydrofluoric acid (HF) is a highly toxic poison that can be rapidly fatal. Death usually results from the many systemic effects of dissociated fluoride ions, including hypocalcemia, hypomagnesemia, hyperkalemia, and direct cardiotoxicity. A patient is described who accidentally ingested a hydrofluoric acid-containing substance and who likely benefited from hemodialysis. His fluoride level post-dialysis was reduced by approximately 70% from a level drawn three hours prior to the initiation of hemodialysis. However, the single treatment did not reduce the fluoride level to normal. A review of the pathophysiology of hydrofluoric acid intoxication and the outcomes of prior exposures suggests that hemodialysis could play a vital role in the management of poisonings with fluoride-containing substances. However, the initial hemodialysis treatment should be prolonged beyond the standard four-hour session.

Collapsing glomerulopathy in a patient with mixed connective tissue disease.

Collapsing glomerulopathy (CG) is a distinct clinicopathological entity characterized by glomerular capillary collapse, podocyte proliferation, diffuse mesangial sclerosis, and podocyte maturation arrest. Initially noted primarily in HIV infected patients, a number of other diseases have now been associated with CG. Mixed connective tissue disease (MCTD) is a disease with overlapping features of systemic lupus erythematosus, progressive systemic sclerosis, and polymyositis. It was originally thought that renal involvement was a rare complication of MCTD. However, over the years, it has become clearer that renal involvement, although not always clinically apparent, is frequent. In this report we present a patient with MCTD who developed CG.

Immune complex-mediated renal involvement in relapsing polychondritis.

A patient with relapsing polychondritis who presented with rapidly progressive glomerulonephritis is described. This is the fourth case in which this association is reported. Crescentic glomerulonephritis was found on renal biopsy. Evidence for immunologic participation in the pathogenesis of this condition is suggested by the demonstration of circulating immune complexes, immunoglobulin and complement deposition by immunofluorescence, and electron dense deposits by electron microscopy of the kidney. Favorable response followed therapy with prednisone and dapsone.

Rapidly progressive glomerulonephritis. Combined antiglomerular basement membrane antibody and immune complex pathogenesis.

We present the clinical and pathologic data from two patients with rapidly progressive glomerulonephritis in whom the unusual combination of antiglomerular basement membrane antibody and immune complex disease was observed. In both patients the diagnosis of antiglomerular basement membrane disease was confirmed by renal tissue immunofluorescence and by positive assays for circulating antiglomerular basement membrane antibody. Ultrastructural studies revealed membranous nephropathy in one patient. Our data from this patient suggested evolution of pre-existing membranous nephropathy into antiglomerular basement membrane disease. In the second patient electron microscopy of renal tissue demonstrated numerous subendothelial, mesangial, and subepithelial deposits. It was impossible to ascertain in this patient whether antiglomerular basement membrane antibody or immune complex mediated injury was the primary pathogenetic event. Our data provide additional evidence for the rare clinical appearance of concurrent antiglomerular basement membrane and immune complex disease. Although the coexistence in both patients of antiglomerular basement membrane disease with immune complexes may have been coincidental, we think that this is unlikely. Rather our data suggest that the two mechanisms are causally related and that either one could have been the primary disease process.

Glomerulonephritis and virus-like particles associated with prostatic cancer.

A patient with carcinoma of the prostate and metastases developed the nephrotic syndrome following hormonal therapy. A decrease in the dose of estrogens was associated with decreased proteinuria, but when therapy was increased the nephrotic syndrome became more severe. Renal biopsy performed when proteinuria was present showed subendothelial electron dense deposits, complement by immunofluorescence, and a morphologic pattern of membranoproliferative glomerulonephritis. There was evidence of resorption of the deposits by endothelial cells. Microspherical particles resembling those described in prostatic cancer were found in the glomeruli. On the basis of previous reports it is concluded that circulating tumor antigen-antibody complexes produced glomerulonephritis, the severity of which was related to the amount of soluble antigen released by tumor cell destruction. Apparent phagocytosis of immune complexes by glomerular endothelial cells was believed to account for the reversibility of the nephrotic syndrome. The role of the virus-like particles in the process is as yet unclear.

Deafness associated with oral furosemide.

A patient with Hodgkin's disease and renal insufficiency became deaf while being treated with high dose oral furosemide. Cessation of furosemide was associated with improvement in his hearing. However, at the time of his death, 11 days after stopping the furosemide, significant hearing impairment was still present. It is suggested that oral furosemide be considered potentially ototoxic, particularly in patients with compromised renal function.

Amphetamine-induced angiitis leading to renal failure.

A patient is presented who developed angiitis associated with intravenous usage of amphetamine. Her disease exacerbated after further amphetamine usage and progressed, over a two-year period, to terminal renal failure. Various etiologic possibilities are discussed, and it is suggested that amphetamine-induced angiitis is a distinct clinical entity that is potentially lethal.

Pharmacokinetics and hemodialyzability of cefazolin in uremic patients.

Cefazolin may be used in azotemic patients at reduced dosage as suggested by others. Although hemodialysis removes some of the drug, therapeutic levels are maintained throughout dialysis after a single intravenous dose of 500 mg. Imperfect transport from blood to dialysate is related to protein binding but varies with the degree of azotemia. Small amounts of cefazolin may be administered to patients during dialysis by addition to dialysate.