John T. Harrington

An immunopathologic study of rapidly progressive glomerulonephritis in the adult

Abstract Clinical, pathologic, and detailed immunopathologic studies in seven adult patients with rapidly evolving renal failure and glomerular lesions characterized by intense epithelial proliferation (crescents) were reviewed. In six patients deposition of immunoglobulins occurred in a linear pattern in the glomeruli, and/or antiglomerular basement membrane antibodies were detected in the sera or acid eluates of renal tissue. One of these six patients had an elevated ASO titer and two had evidence of vasculitis. The seventh patient had granular deposition of IgG and complement but no antiglomerular basement membrane antibody in the serum or renal eluate. In all patients fibrin was seen in the glomeruli. Transplants were performed in three patients, who showed no clinical or histologic evidence of recurrent glomerulonephritis in the allograft three, six, and 20 months later. The immunopathologic findings in these cases and in the literature are reviewed in relation to the possible pathogenetic mechanisms in rapidly progressive glomerulonephritis, the exceptional demonstration of linear fluorescence and antiglomerular membrane antibodies in a patient with apparent poststreptococcal disease, the similarities between rapidly progressive glomerulonephritis and the microscopic form of polyarteritis, and the significance of data on immunofluorescence to the outcome of transplantation in patients with rapidly progressive glomerulonephritis.

Current concepts. The diagnosis of acute glomerulonephritis.

WE define acute glomerulonephritis as the sudden appearance of hematuria, proteinuria, and red-cell casts. The last finding, which rarely occurs in other types of renal disease,1 is virtually diagn...

Assessment of the cardiac effects of hemodialysis with systolic time intervals and echocardiography

The acute effects of hemodialysis on left ventricular (LV) function were studied with the use of externally recorded LV systolic time intervals and echocardiography; 10 patients with normal or near-normal predialysis LV function and no circulatory congestion were studied. Hemodialysis significantly decreased the LV ejection time (LVET) from 270 +/- 9 ms to 237 +/- 10 ms (p less than 0.001); no significant change was noted in the preejection period (PEP). The PEP/LVET ratio increased from 0.41 +/- 0.05 to 0.45 +/- 0.06 (p less than 0.05). The LV end-diastolic dimension decreased from 5.3 +/- 0.3 cm to 4.8 +/- 0.3 cm (p less than 0.001). Fractional shortening and ejection fraction did not change significantly, but hemodialysis slightly increased mean VCF from 1.2 +/- 0.1 s-1 to 1.4 +/- 0.1s-1 (p less than 0.005). Hemodialysis was associated with a 17% decrease (87 +/- 8 ml to 72 +/- 7 ml; p less than 0.001) in LV stroke volume as calculated from echocardiographic data. Small changes in heart rate and blood pressure were insignificant. We conclude that the postdialysis reduction in stroke volume was due primarily to an acute decrease in LV preload; dialysis also appears to be associated with a small increase in the LV contractile state.

Clinical Use of Rabbit Antihuman Lymphocyte Globulin in Cadaver-Kidney Transplantation

Abstract Twenty-six consecutive recipients of cadaver-kidney transplants were treated with rabbit antihuman lymphocyte globulin (ALG) in addition to conventional immunosuppressive therapy. Each of the first 10 of these recipients has been followed for more than 12 months. The one-year transplant survival in this group was 90 per cent. Rabbit ALG administration was well tolerated. Most patients had no symptoms related to ALG injections. There were four acute transplant rejection episodes in the first 10 patients and four episodes in 16 subsequent patients followed for more than four months. All acute rejection episodes occurred six weeks or more after transplantation, and all were easily and promptly reversed by a temporary increase in the dose of steroid therapy. Immediate, hyperacute rejection by preformed antibodies was the only cause of kidney transplant loss in the entire series.

Immune Complex Glomerulonephritis in Hydralazine-Induced SLE

Renal disease, a major feature of systemic lupus erythematosus (SLE), rarely occurs in drug-induced SLE. Immune complex glomerulonephritis has been demonstrated in a few cases of SLE following procainamide or anticonvulsant therapy but has not been documented in association with hydralazine-induced SLE despite the recognition of this syndrome 30 years ago. We report the clinical and renal pathologic findings in a patient with hydralazine-induced lupus nephritis and review the renal pathologic material in earlier reports of hydralazine-induced SLE.

Nephrostomy in renal transplantation.

Abstract Complications leading to urinary extravasation developed in four of thirty-three renal transplant recipients. The management of these patients was facilitated by the use of temporary nephrostomy drainage, resulting in a functioning kidney and survival in all cases. The advantages of nephrostomy in transplantation, as described, are as follows: fistulas and extravasations, dangerous in the immunosuppressed patient, can be converted to situations of controlled urinary drainage; the success of reoperative surgery of the urinary tract can be secured by total urinary diversion accomplished by nephrostomy; and excellent postoperative radiologic studies of urinary tract disease can easily be performed by nephrostogram. We believe that these cases demonstrate the value of the much maligned nephrostomy in the transplanted patient, converting the potentially fatal complications of urinary leakage and obstruction to more easily manageable problems.

Mixed Acid-Base Disorders

Virtually all recent discussions of the diagnosis and management of mixed acid-base disturbances have focused exclusively on the acid-base disorders per se and have relegated the patient and the clinical setting to a subordinate position. In the 1980s several excellent reviews utilizing primarily a laboratory approach have appeared (1–3). In this laboratory-dominated approach, the acid-base data first are examined to determine whether they are consistent with any of the simple acid-base disorders; if the acid-base data do not fit, and assuming that they reflect a steady state, one can confidently conclude that a mixed acid-base disturbance is present (4). For instance, in a patient with a plasma bicarbonate concentration of 8mEq/l, the finding of a PaCO2 level substantially greater than the value anticipated for simple metabolic acidosis establishes the presence of a concomitant element of respiratory acidosis and thus the presence of a mixed acid-base disorder.