[Medical complications of hemodialysis].
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Biomedical subjects
Publications and source records attributed to M Rainfray.
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Lupus anticoagulant was present in this case of paraneoplastic scleroderma revealed by hemolytic-uremic syndrome, suggesting that the autoantibody played a significant role in the sequence of events leading to anuria. Reviewing the literature we found several observations of paraneoplastic scleroderma, and in other series cases of scleroderma-linked (and in rare instances cancer-linked) antiphospholipid autoantibodies. Search for antiphospholipid antibodies should be considered in patients with systemic scleroderma as well as in patients with metastatic cancer. Presence of such procoagulant autoantibodies might predict future complications and should influence treatment strategy.
RATIONALE: atheromatous stenosis of both renal arteries, or of the artery of a functionally solitary kidney is a frequent cause of renal failure in the elderly. Atheromatous Ischemic Renal Insufficiency (AIRI) can be ameliorated by surgery or angioplasty. However, such procedures can be hazardous in a patient with extensive aortic atheromatous plaques. This justified a study of the validity of Pulsed Doppler (PD), a diagnostic procedure less invasive than renal angiography in AIRI. OBJECTIVES: to evaluate the diagnostic interest of PD in AIRI, using renal angiography as a criterion of adequacy. METHODS: renal arteries PD (Ultramak-4, 3.5 and 5 Mhz probes) followed by renal angiography (Seldinger). "Significant" stenosis = 50% on angiography. "Positive" PD = turbulences and/or acceleration. PATIENTS: 32 patients were investigated for suspected AIRI on the grounds of 1) age greater than 50; 2) atheromatous background and 3) renal insufficiency with no other evident etiology, or rapidly declining GFR in such a patient treated with ACE inhibitors. RESULTS: 16/32 angiographies disclosed significant stenosis of at least 1 renal artery. 56 renal arteries were investigated with both angio. and PD. Prevalence of stenoses was 16/56. PD had 93.7% sensitivity and 55% specificity. Positive predictive value was 45.5% and negative predictive value was 95.7%. Specificity was 80% when PD disclosed acceleration. CONCLUSIONS: negative PD is sufficient argument to reconsider the indication of renal angiography in a high risk pt with suspected AIRI.
We present here a glomerulonephritis in a patient with dermatomyositis, Sjögren's syndrome and Hashimoto's thyroiditis. Glomerulonephritides are rarely described in dermatomyositis and Sjögren's syndrome. Glomerular histology is variable. Nephrotic syndrome and renal failure are not frequent. Moderate doses of corticosteroids produce a rapid improvement.
Fifty-five cases of primary (that is, without urinary tract abnormalities), acute pyelonephritis (PN) were studied by computed tomodensitometry (CT). There were 48 women and 7 men. All were febrile and 16 had positive blood cultures. In 7 cases, (4 diabetics and 3 malnourished alcoholics) PN was painless, diagnosis was delayed and lesions were severe. Two diabetics underwent emergency nephrectomy for sepsis. Conventional radiological techniques (IVP and ultrasonography) were poorly informative. In contrast, initial CT abnormalities were visible in 44 patients. They consisted of triangular or round hypodense images, diffuse hypodensity in a grossly swollen kidney, and/or abscesses. Hypodense images were presumably due to acute focal ischemia. Renal histology was available in five patients. It showed acute interstitial nephritis with leukocyte infiltrates, edema and hemorrhagic streaks. Pyelonephritis was due to E. coli in 48 cases (87.5%). In 27 cases E. coli isolates were studied by genotypic assays which detect the three most frequent (pap, afa and sfa) of the four operons known to encode adhesin. In all cases, at least one of these genotypic markers of uropathogenicity was found. In 27 cases, repeat CT was done shortly after treatment. It showed healing in only 12. Early cortical scar formation was visible in 2. Final evaluation in 27 cases with adequate follow-up showed that (in addition to the 2 patients who had been nephrectomized), in only 17 of 27 (63%) had the kidneys recovered a normal appearance. In two cases one kidney had undergone atrophy; renal biopsy showed subacute-chronic interstitial nephritis.(ABSTRACT TRUNCATED AT 250 WORDS)
Pharmacokinetics of tertatolol were investigated in 22 hypertensive patients (12 men and 10 women; mean age +/- SD: 52.6 +/- 12.3 years) with chronic renal failure defined by a mean creatinine clearance (Clcr) of 24.6 +/- 15.9 mL/min/1.73 m2 (range: 6.2 to 68.7). A daily single dose of 5 mg tertatolol was administered orally for 4 weeks, except in the 72 h following the first administration. Plasma samples and urine collections were carried out over 72 h after the first (D0) and the last dose (D27). After the first administration, tertatolol was rapidly absorbed (time to peak concentration: 1.2 +/- 0.7 h) and peak concentration was 160 +/- 80 ng/mL. Plasma concentrations decreased following a biphasic curve, with two half-lives of 2.5 +/- 1.1 and 17.0 +/- 8.5 h, respectively. These parameters were not modified by repeated administration of tertatolol and did not significantly correlate with Clcr either at D0 or at D27. Plasma levels were stable along the study with similar areas under plasma curves following the first and the last dose (P = NS). In addition, plasma levels extrapolated from first dose data did not significantly differ from those observed during repeated dosage. Plasma levels of the 4-OH metabolite which possesses a beta-blocking activity were low, inconstantly detectable, not related to the degree of renal impairment, and no accumulation occurred after chronic dosage. Renal excretion of tertatolol and 4-OH tertatolol was significantly increased by repeated administration (P less than .01) and correlated well with Clcr either at D0 or at D27. Four week treatment was well tolerated and significantly improved Clcr (+6.5%, P less than .02). In conclusion, tertatolol was well tolerated and did not accumulate in patients with renal failure of various degrees. The usual daily single dose of 5 mg may be kept unchanged whatever the degree of renal impairment.
Intravenous injection of iodinated contrast media usually induces modifications of renal function. Adverse effects of contrast media on renal function may affect diuresis, blood flow or glomerular filtration rate. These modifications are mainly related to osmolality but also chemotoxicity. This open study showed that after i.v. injection of a bolus of iopromide 370, a new nonionic contrast medium, there was no untoward effect on renal function in patients with renal insufficiency. This justifies comparative studies in patients with renal impairment including elderly subjects, to confirm the tolerance of this product in high risk groups.
A case of diffuse primary interstitial lung fibrosis associated with familial benign hypercalcaemia is reported. This, and the 3 cases previously published, suggests that both diseases share a common genetic mode of transmission.
PURPOSE: Atheroma as a cause of renal failure has been largely overlooked. We wanted to report our experience with atheromatous renal disease over a 12-year period. PATIENTS AND METHODS: Observations on 32 cases of various forms of renal failure in patients with atheromatous renal disease are presented. These patients had been hypertensive for an average of 10.2 +/- 9.2 years. The length of deterioration was an average of 17 months, and at presentation renal insufficiency was severe, with serum creatinine levels of (mean +/- SD) 616 +/- 358 mumol/liter (6.8 +/- 4.0 mg/dl). At this stage, the clinical picture was indistinguishable from other common causes of chronic renal failure in the elderly. Thus, the precise diagnosis would have been overlooked without an aggressive diagnostic workup. All patients underwent angiography and six patients underwent renal biopsy. RESULTS: In 22 cases, renal insufficiency was mainly due to atheromatous stenosis of renal arteries. In six of six patients, the results of renal biopsy showed cholesterol crystal embolism. In four additional cases, there was clinical or histologic evidence of extrarenal cholesterol embolism. In eight, renal artery plaques coexisted with cholesterol embolism. In two patients, renal failure was due only to cholesterol embolism. Renal atheromatous stenoses were developing, as shown on serial angiographies performed in five cases. In seven cases, stenoses involved both the main trunks of renal arteries and several intrarenal branches of too small a diameter to allow reconstructive surgery or percutaneous transluminal angioplasty. In addition, the general condition of most patients was so poor as to preclude surgery. Dialysis was begun in 11 patients, four other patients died, and renal failure was managed conservatively in 11. When undertaken, reconstructive surgery was successful in five of six patients. CONCLUSIONS: Atheromatous renal disease is a frequent and easily overlooked cause of chronic renal insufficiency. It is not only due to renal artery stenosis but also to complex intrarenal lesions, with multiple stenoses of intrarenal vasculature and cholesterol embolism. It should be diagnosed by early angiography and renal biopsy, before the stage of multivisceral complications and at a time when surgery can still be undertaken.
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Severe hypertension developed in 4 patients who had sustained blunt renal trauma 2-32 years previously. A protracted period of normal blood pressure separated the renal injury from the onset of hypertension. Angiography disclosed lesions which had been underestimated by intravenous pyelography. These lesions consisted of traumatic dissection of branches of the renal artery, leading to renal infarct. In 3 cases, unilateral high renin secretion was demonstrated, and in 1 case this was confirmed by immunofluorescence with an anti-renin antiserum which showed abundant renin granules within the infarcted zone. In all patients, total or polar nephrectomy was followed by return of blood pressure to normal or near-normal levels. Blunt renal trauma is an underestimated cause of renovascular hypertension.
The "syndrome of inappropriate calcitriol secretion" may be observed in diseases with disseminated granulomas. The main examples are sarcoidosis and tuberculosis, but it can also be observed in fungal infections, in granulomas due to foreign bodies and in lymphomas. The syndrome is due to autonomous production of 1 alpha hydroxylase by granulomas. The insuing synthesis of calcitriol escapes normal regulation by serum calcium and phosphate levels. The syndrome includes hypercalcemia, hypercalciuria, high 1,25(OH)2D3 serum levels and reduced PTH secretion. It can supervene in anephric or hypoparathyroid patients. The notion that calcitriol may be secreted extrarenally is new. It could have important bearings on several issues in nephrology, immunology and oncology.
1. Nineteen patients with a spectrum of immunologically related disorders were studied before and immediately after plasmapheresis for changes in plasma aldosterone, insulin and arginine vasopressin (AVP). Renin was also measured in 11 of these patients by direct radioimmunoassay. 125% of the initial plasma volume was replaced, which corresponded to a predicted removal of 72% for any plasma constituent. 2. The initial, final (experimental) and final (predicted) concentrations (means +/- SEM) were 337 +/- 50, 185 +/- 23 and 100 +/- 16 pg/ml respectively for renin, 465 +/- 86, 146 +/- 38 and 124 +/- 22 pmol/l respectively for aldosterone, 218 +/- 35, 69 +/- 11 and 63 +/- 11 pmol/l respectively for insulin, 7.2 +/- 1.9, 6.1 +/- 0.5 and 1.8 +/- 0.2 pmol/l respectively for AVP. The predicted final concentration was calculated from the initial concentration and the fraction of plasma volume exchanged. The experimental final concentration was lower than the initial concentration for renin, aldosterone and insulin (P less than 0.001) but not for AVP. The predicted final concentration was lower than the experimental final concentration for AVP and renin (P less than 0.001) but not for aldosterone and insulin. Plasma volume, osmolality, glucose, sodium and potassium concentrations did not change significantly. 3. The concentrations of renin, aldosterone, insulin and AVP in the removed plasma were 84 +/- 17 pg/ml, 179 +/- 36, 98 +/- 15 and 4.8 +/- 0.7 pmol/l respectively. The amount subtracted expressed as percentage of the total amount present in plasma was markedly greater for AVP than for the three other plasma constituents.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma arginine vasopressin (AVP), renin activity (PRA) and aldosterone (ALD) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing in 10 untreated healthy subjects (group 1), eight asthmatic patients treated with prednisone (group 2) and 13 heart-transplant recipients treated with prednisone and cyclosporin (group 3). Three different tests for cardiac vagal innervation were performed in the study population. They confirmed that the patients of group 3 were denervated whereas those of groups 1 and 2 had an intact cardiac innervation. Plasma volume depletion after frusemide administration estimated from the rise in plasma proteins was 10-12%. Mean blood pressure was higher in the transplant recipients but did not change in the three groups. Heart rate was also greater in the transplant recipients as a result of vagal denervation. PRA and ALD increased in all the subjects: 2.8, 3.3 and 2.2 times basal value for PRA, 2.7, 4.6 and 2.1 times basal value for ALD in groups 1, 2 and 3 respectively. In contrast, plasma AVP increased only in the two control groups (x1.45 and x1.65 in groups 1 and 2 respectively) whereas it was unchanged in the group of heart-transplant recipients (x1.05). In order to better understand the etiology of the high basal AVP plasma levels observed in group 3, AVP response to a standard water load was studied in eight supplementary heart-transplant recipients: 81.5% of the water load was excreted over 3 h and plasma AVP fell significantly (x0.76).(ABSTRACT TRUNCATED AT 250 WORDS)