Arteriovenous fistula of the native kidney: diagnosis by duplex Doppler ultrasound.
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Biomedical subjects
Publications and source records attributed to G Garibotto.
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Acute bilateral renal artery thrombosis is a rare but surgically correctable cause of acute renal failure. A middle-aged woman with acute renal failure and anuria due to atherosclerotic occlusion of the abdominal aorta and both renal arteries was surgically treated 42 days after the onset of anuria. Revascularization resulted in the reversal of renal failure and complete recovery of renal function in spite of prolonged anuria. An aggressive diagnostic and therapeutic approach is important whenever this condition is suspected.
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Malignant pheochromocytoma is a rare cause of hypertension and still has a high mortality rate. The most accurate way to localize a malignant pheochromocytoma is by a combination of scans, both CT and scintigraphy. Selective sampling of venous blood from multiple sites for plasma catecholamine levels is a safe and reliable technique and may be used successfully in some patients. A case is presented where venous sampling proved to be useful in preoperatively localizing a malignant pheochromocytoma and its metastatic lesions which both CT and ultrasound had failed to demonstrate.
Therapeutic attempts have generally failed to reverse the rapid progression of renal failure after mitomycin C (MMC)-induced hemolytic uremic syndrome (HUS). A patient who developed HUS after MMC and who showed pathologic changes in the kidney consistent with thrombotic microangiopathy is reported. Treatment with plasmapheresis was followed by a favorable outcome and significant recovery of renal function. Accordingly, this therapeutic modality should be considered for patients with MMC-induced HUS.
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Splanchnic exchange (net uptake or release) of amino acids (AAs) was evaluated by measuring arterial-hepatic venous differences for AAs and hepatic blood flow in patients with chronic renal insufficiency (CRI) and control subjects before and for 70 min after the ingestion of an AA mixture simulating an animal protein meal. In CRI after AA ingestion, splanchnic exchange area for total nonessential AAs (NEAAs) is increased 135% over control subjects because of an augmented escape of proline, glutamate, serine, glycine, alanine, and cyst(e)ine; contrarily, glutamine shows an increased splanchnic uptake. Splanchnic exchange area for total essential AAs (EAAs) is increased only by 67% over controls because of a higher escape of threonine, isoleucine, phenylalanine, and histidine. Abnormalities in arterial areas for AAs parallel those in splanchnic areas except for glutamine and isoleucine. Data indicate that in CRI, at least for 70 min after an AA meal, splanchnic organs metabolize abnormally ingested AAs and export an increased and unbalanced bulk of AAs, severely affecting postprandial arterial profile of AAs.
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Arterial whole blood levels of amino acids (AA) were determined in patients with chronic renal failure (CRF) and in healthy volunteers before and for 75 min after the ingestion of an AA mixture simulating the AA content of an animal-protein meal. In CRF patients, total AA increased more than in control subjects as a consequence of an exaggerated rise in nonessential AA (+86%), mainly glutamine, proline, glutamate, serine, glycine, and alanine. Total essential AA in patients increased as much as in control subjects; however, threonine and phenylalanine showed greater increases while leucine had a smaller increase. As a consequence of the observed alterations, a striking unbalance in the postprandial pattern of arterial AA ensued in CRF patients. The flow of AA to all the organs is altered during the absorptive phase, which is crucial for body nitrogen-pool replenishment.
The circadian monitoring of intragastric pH and of the mutagenicity of 440 gastric juice samples collected hourly from 22 subjects provided evidence that, irrespective of diagnosis and treatment, a weak yet consistent increase in revertants can be detected in his- Salmonella typhimurium strains during the 3-4-h periods following each meal. The recorded mutagenic activity was not related to the histidine content of gastric juice, was due to thermostable components and was not significantly inhibited by administration of vitamin C. Various genetic mechanisms were involved, which were different from those consequent to the artificial supplementation of gastric juice with sodium nitrite. Treatment with a histamine H2-receptor antagonist (famotidine), either at dinner or at bedtime, was followed by a nocturnal plateau of mutagenicity. However, such effect was not due to mutagenicity of the drug or of its derivatives, but to the therapeutic rise in pH associated with its antisecretory activity.
Renal metabolism of C-peptide was studied in nine nondiabetic nonobese patients with normal renal function by the arterial-venous difference technique before and after the oral administration of an amino acid mixture simulating an animal protein meal. In the basal state, the kidney removed 25.7 +/- 7.5% (+/- SD) of the arterial plasma C-peptide. Renal uptake was approximately 7-fold greater than urinary excretion, and thus, more than 85% of the amount extracted was metabolized by the kidney. Renal C-peptide clearance was very high and approximated the glomerular filtration rate, whereas urinary C-peptide clearance was only 14% of its renal clearance. Shortly after amino acid ingestion, arterial C-peptide levels increased by 107%, and C-peptide renal fractional extraction, uptake, and net metabolism also increased markedly (67%, 278%, and 328%, respectively); urinary clearance and excretion did not change. Renal clearance became 2-fold greater than the glomerular filtration rate, indicating that in this phase the kidney removed substantial amounts of C-peptide from peritubular blood as well as by filtration. Both renal uptake and urinary excretion of C-peptide were related to its arterial levels (P less than 0.001 and P less than 0.05, respectively), but renal uptake increased much more than urinary excretion for each increment in arterial C-peptide levels. These results indicate that renal C-peptide metabolism is considerable in the postabsorptive state and is even more marked during the postprandial period. The kidney, therefore, plays a key role in both the regulation of circulating plasma levels and the metabolic clearance of C-peptide.
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