[Acute renal insufficiency in pregnancy and puerperium].
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Biomedical subjects
Publications and source records attributed to A Kanfer.
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Renal transplantation was performed in five adult patients with thrombotic microangiopathy, three of whom had had a bilateral nephrectomy prior to transplantation. The graft remained functional in three patients 72, 18, and 12 months after transplantation. One patient developed a thrombosis of the renal artery and one patient died from infection. There was no clinical or histological evidence of recurrence of thrombotic microangiopathy in the five patients after transplantation. Immunological investigations were performed in four of five patients before transplantation: C3 and C1q levels were low in two patients; serum C3-splitting activity and circulating immune complexes were present in all four patients and remained unchanged on haemodialysis and/or after bilateral nephrectomy. Complement abnormalities and immune complexes were not detected in the three patients with successful renal transplantation.
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In 9 patients aged 16 to 71 years with acute renal failure, histological examination disclosed polyarteritis nodosa. Symptoms of rapidly progressive glomerulonephritis (GN) were present in 7 cases. Hypertension was a constant feature. Fever and muscular articular and cutaneous signs occured at times simulating Henoch-Schönlein purpura. Necrotizing angiitis was a constant finding, with perivascular granuloma in 7 cases. Lesions affecting smaller arteries were associated with diffuse or segmental extracapillary GN, and lesions of larger arteries with ischaemic appearance of the glomeruli. Diagnosis was obtained during life by percutaneous renal biopsy in 5 patients and muscular or cutaneous biopsy in 2 other patients, whereas the evidence was only obtained on post mortem examination in the 2 remaining patients. In the 6 renal biopsies examined by immunofluorescence, fibrinogen was always present in glomeruli and/or arteries. In one patient there was a linear deposit of IgG along glomerular basement membrane (GBM) and there were circulating antibodies directed against GBM. Arteries of different sizes may be damaged in various organs, as showed by arteriography and autopsy. Steroid therapy and immunosuppressive drugs had no effect on renal symptoms. 8 out of 9 patients died rapidly, in 6 the death was due to extrarenal localization of the disease, even though uraemia was controlled by haemodialysis. The last patient died 2 years after onset of the disease, while being on maintenance haemodialysis treatment.
We studied 11 patients who had visceral abscesses and in whom acute renal failure developed. All renal biopsies showed a diffuse proliferative and crescentig glomerulonephritis. In seven patients blood cultures were repeatedly negative. Endocarditis could be ruled out in six patients. Seven patients had circulating cryoglobulins; serum complement levels were normal in seven and decreased in four; circulating immune complexes were found in the three patients studied. The evolution of the glomerulonephritis, documented by serial biopsies, closely paralleled the course of the infection. A complete recovery of renal function occurred in four cases in which a rapid and complete cure of the infection was obtained. Of five patients in whom the infection was not cured, four died, and chronic renal failure developed in one. In two patients in whom therapy was delayed, chronic renal failure also developed. Deep suppuration, even in the absence of bacteremia, may be responsible for a severe but possibly reversible glomerulonephritis with circulating immune complexes.
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A report of the treatment by repeated dialysis of irreversible renal failure complicating 4 cases of multiple myeloma. The latter condition continued to progress, with death occurring after three, six, eight and twenty seven months. The last case was the only one with an indiscutable haematological and clinical remission. The effectiveness of chemotherapy is the reason for the use of the artifical kidney. Treatment may be hoped to be active if the renal failure is acute, a presenting feature of the myeloma. Such a hope is practically vain if the renal failure develops progressively, in a patient already on treatment. The indication for haemodialysis is thus more than open to discussion.
Described are six patients with acute renal insufficiency due to histologically proven massive lymphomatous infiltration of the kidneys. All patients were admitted to a renal intensive care unit over a period of six years. Oliguria was the presenting symptom in two of the patients. This complication of lymphoma is suggested by enlargement of the kidneys and mild proteinuria in the absence of other causes of uremia and can be demonstrated by renal biopsy. Local radiation therapy performed in two patients produced improvement of renal function.
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Four patients with thrombotic microangiopathy had evidence of intravascular C3 activation on presentation which persisted after bilateral nephrectomy. In several serum samples, C3-splitting activity was not associated with the presence of circulating immune complexes, which were detected in all four patients before nephrectomy and in three after nephrectomy.
Plasmatic slow plasmin-inhibitor activity was assessed in 20 patients with acute renal failure and 12 controls with the fibrin plate method. The area of fibrinolysis was 250-5 +/- 5 mm2 in the patients and 289 +/- 6mm2 in the controls (P less than 0.001) and was negatively correlated with antiplasmin activity. Thirteen patients had areas of lysis equal to or inferior to the minimal lysis observed in the controls. No correlation was found between antiplasmin activity and serum fibrin-fibrinogen related antigen titres, the presence or absence of disseminated intravascular coagulation, or the causative disease.
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The effects of thrombin perfusion on glomerular fibrinolytic activity (GFA) have been assessed quantitatively in isolated rat glomeruli. Gfa was augmented by increasing total thrombin perfused to a maximal dose of 120 units per 100 gm. Fifty per cent maximal GFA occurred at a dose of 38 to 42 units of thrombin per 100 gm. independent of duration or rate of perfusion. After termination of infusion, GFA diminished and thrombi were no longer observed. Simultaneous administration of thrombin and epsilon-aminocaproic acid was associated with sustained high GFA and persistence of thrombi, presumably due to inhibition of the action of plasmin on fibrin, but it had no effect on tissue activators of plasminogen.
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