Sean O'Regan

Thyroid antigen-antibody nephritis.

Abstract A patient with autoimmune thyroiditis developed nephrosis. Light, immunofluorescence, and electron microscopic examination of renal biopsy tissue demonstrated epimembranous nephropathy. Thyroglobulin and thyroid microsomal antigen were demonstrable in her glomeruli by indirect immunofluorescence microscopy.

Treponemal Antigens in Congenital and Acquired Syphilitic Nephritis: Demonstration by Immunofluorescence Studies

Two patients, a 4-month-old infant girl with congenital syphilis and a 45-year-old man with secondary syphilis, had the nephrotic syndrome with glomerulonephritis. Immunoglobulins and treponemal antigenic material were seen in the glomeruli of both patients by immunofluorescence microscopic studies of renal tissue. Electron micrographs showed subepithelial electron dense deposits along the glomerular basement membrane. This confirms earlier suggestions that the renal injury is of an immune-complex type.

Renal injury after muscle extract infusion in rats: Absence of toxicity with myoglobin

A crude muscle extract infused into rats produced oliguria, a precipitous drop in total hemolytic complement, and in circulating white cell and platelets counts. A mild vaso-depressor effects was noted. These changes were not produced by myoglobin or saline infusion. Muscle constituents other than myoglobin are responsible for the systemic and renal nephrotoxic effects observed.

Asymmetric Renal Enlargement in Acute Glomerulonephritis

Three children presented with unilateral and asymmetric renal enlargement and clinical and laboratory evidence of acute poststreptococcal glomerulonephritis. This asymmetry resolved at the same time as the nephritis. Angiographic evidence of absence of renal artery stenosis was available in one case. Angiography was not performed in the other 2 cases. The authors suggest that the differential diagnosis of unilateral acute renal inflammation (swelling of the kidney, prolonged nephrogram, calyceal distortion, poor concentration of contrast medium) should include acute glomerulonephritis. Extensive radiological evaluation is probably not necessary unless asymmetry persists.

ACUTE RENAL FAILURE (ARF) FOLLOWING EXPERIMENTAL RHABDOMYOLYSIS

While ARF following rhabdomyolysis or crush syndrome is well documented, its pathophysiology has not been defined. Myoglobin, thought to be responsible for the pathogenesis of ARF, is not toxic unless dehydration or acidosis is already present. To elucidate the pathophysiology of ARF, a new experimental model was established using a crude muscle extract(ME) prepared by homo-genization of saline perfused rat thigh muscle followed by centrifugation and filtration. Experimental rats were injected i.v. with ME and control groups with saline, boiled ME, and myoglobin in normal rat serum. ME caused death at doses >10 mg ME protein/100 g and ARF at 5-10 mg. Oliguria, proteinuria, hemepigmenturia with an active urine sediment, hypocomplementemia, leucopenia and thrombocytopenia developed shortly after ME injection. These findings were not present in the control groups;transient harmless myoglobinuria was present in the control rats given myoglobin. Involvement of the coagulation system suggested by experimental data led to studies using heparin as an anticoagulant. Ten of 10 rats pretreated with heparin before ME injection lived whereas 9 of 10 controls died. This experimental model closely resembles clinical ARF secondary to rhabdomyolysis.Our data also suggest that other biological systems are activated and that muscle constituents other than myoglobin are involved in the pathogenesis of ARF following muscle injury.