Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with primary amyloidosis and the nephrotic syndrome had diarrhea and gastrointestinal bleeding probably due to intestinal ischemia. He died with extensive intestinal infarction. The infarction was most likely caused by decreased splanchnic perfusion secondary to the chronic hypotension of the nephrotic syndrome and to amyloid deposition within the walls of the small blood vessels supplying the gut. Although amyloidosis was suspected prior to death, a fixation artifact probably prevented the correct antemortem biopsy diagnosis.
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PMID:Persistent hypotension and intestinal infarction in a patient with primary amyloidosis. 113 38

Acute aortic thrombosis associated with spinal cord infarction in a 47-year-old man with nephrotic syndrome is described. He was admitted to our hospital presenting with the nephrotic syndrome. Renal biopsy revealed mild mesangial proliferative glomerulonephritis. The urinary protein excretion rate transiently decreased after the start of treatment with prednisolone, but it increased again and was followed by the development of the signs and symptoms of spinal cord infarction, which was diagnosed by magnetic resonance signal abnormalities, and then symptoms of ischemia in the lower limbs. Digital subtraction angiography revealed an obstruction at the bifurcation of the abdominal aorta. Emergency thrombectomy was performed, and the arterial blood flow was reestablished. Laboratory data on the fibrinocoagulation system showed a hypercoagulable state. In this case, fibrinocoagulation abnormalities due to the nephrotic syndrome led to the hypercoagulable state, and dehydration might have triggered the thrombotic complication.
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PMID:Acute aortic thrombosis associated with spinal cord infarction in nephrotic syndrome. 139 31

Many renal structural and functional abnormalities have been associated with sickle cell disease. The patients have an impaired urinary concentrating ability but an intact diluting capacity. There are defects in both urinary acidification and potassium excretion, although overt metabolic acidosis and hyperkalemia occur infrequently. Proximal tubular function is supranormal, as manifested by increased reabsorption of phosphate and increased secretion of creatinine. The former results in mild hyperphosphatemia, while the latter causes substantial overestimation of the glomerular filtration rate (GFR) by creatinine clearance. Both GFR and renal plasma flow are increased in young patients with sickle cell disease, but prostaglandin inhibitors decrease the GFR. The GFR progressively decreases with increasing age. Proteinuria, and even nephrotic syndrome, are relatively frequent; the most common renal lesion in children is focal glomerular sclerosis, which may be associated with progressive deterioration in renal function. Glomerular hyperfiltration has been implicated in the pathogenesis of the glomerular lesions, as well as in the development of renal failure. In patients with end-stage renal disease, both hemodialysis and kidney transplantation have been successful. Recurrent hematuria is a relatively common problem in patients with sickle cell disease. The bleeding usually remits spontaneously, but occasionally requires therapy with aminocaproic acid. Papillary necrosis may occur, and is thought to result from medullary ischemia.
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PMID:Renal abnormalities in sickle cell disease. 217 77

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis in particular organ veins. 268 Aug 53

A thirty-year-old woman, who had onset of nephrotic syndrome during the last part of her pregnancy, experienced recurrent acute ischemia of both lower limbs, leading to three conservative surgical procedures one month after delivery. Investigations disclosed no cause of embolism and were suggestive of thrombosis. The arteriography showed a diffuse reduction in diameter of the aorta and iliac vessels without localised stenosis or other vascular lesions. This complication is presumably related to several factors associated with the reduction in arterial diameter: hypovolemia, hyperfibrinemia, hyperlipidemia and abnormalities of hemostasis.
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PMID:[Acute ischemia of the lower limbs in nephrotic syndrome in a young woman]. 631 45

This is a study of the incidence and clinicopathological significance of focal segmental glomerulosclerosis (FSG) in 154 renal allografts (22 biopsies, 128 nephrectomies and four necropsies) from 137 cadaveric and 17 living-related donors. FSG was identified in 18 grafts (11.7%) from 16 patients: six as recurrent FSG in four patients (two developed FSG in two consecutive transplants) and 12 as de novo FSG. The incidence of recurrent FSG in patients who had FSG as their original kidney disease was 30.8% whereas that of de novo FSG in patients who had renal diseases other than FSG was 8.7%. Histologically, recurrent FSG was characterized by mild degrees of obliterative arteriopathy of rejection and preferential involvement of the juxtamedullary glomeruli. Whereas, in de novo FSG, the occlusive vascular changes of rejection were severe and the glomeruli in the outer cortical region were mostly involved. Clinically, however, the differences between them were less clear, although nephrotic syndrome tends to occur more often and earlier in patients with recurrent FSG. Obliterative arteriopathy of chronic rejection and consequent glomerular ischemia appeared to be of major importance in the pathogenesis of de novo FSG in renal allografts.
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PMID:Focal segmental glomerulosclerosis in renal transplants. 633 79

To determine whether preexistent glomerular injury and the nephrotic syndrome increase renal susceptibility to ischemic renal injury, normal rats and rats with either experimental minimal-change disease (Adriamycin nephropathy) (AN) or membranous nephropathy (passive Heymann nephritis) (PHN) underwent renal functional and histologic studies under either basal conditions or 18 h after bilateral renal artery occlusion (over 30 min). Prior to renal ischemia AN and PHN rats had minimally depressed glomerular filtration rate (GFR), normal (AN) or increased (PHN) renal blood flow (RBF), heavy proteinuria, hypoalbuminemia, decreased urine sodium excretion, extensive glomerular foot process fusion, and intratubular hyalin cast formation. Losses of GFR in response to ischemia were comparable among the three groups of rats (controls, 0.29; AN, 0.28; PHN, 0.25 ml X min-1 X 100 g body wt-1) despite prevailing differences in postischemic hemodynamics. Neither light nor transmission electron microscopy showed any differences in the degree of ischemic renal injury. These results suggest that 1) glomerulopathy and the nephrotic syndrome do not significantly increase renal susceptibility to ischemic renal injury; 2) the syndrome of acute renal failure that occurs in patients with minimal-change glomerulopathy is not due to a marked susceptibility of these kidneys to clinically occult ischemic events; and 3) foot process fusion is probably not a pathophysiologically significant lesion in ischemic acute renal failure, as previously suggested.
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PMID:Glomerulopathy does not increase renal susceptibility to acute ischemic injury. 670 61

We describe the clinical features of four pediatric patients (20 months to 10 years of age) in whom reversible idiopathic acute renal failure (RIARF) developed during the course of primary nephrotic syndrome (PNS). All patients had severe PNS and were in relapse at the onset of RIARF. This complication of PNS was preceded by primary peritonitis in three of four patients. Renal biopsy done in the early phases of RIARF showed tubular epithelial changes similar to those observed in acute tubular ischemia. All patients required dialysis. Recovery of renal function followed fluid removal in three of four patients. The RIARF lasted from 12 days to 1 year and was followed by complete recovery of renal function in all patients. We conclude that (1) RIARF is a potential complication in children with severe PNS, (2) RIARF is associated with primary ischemic renal tubular injury, and (3) recognition of the reversibility of this complication of PNS could alter long-term plans for management of renal failure in these patients.
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PMID:Reversible idiopathic acute renal failure in children with primary nephrotic syndrome. 796 23

The radiographic appearance of intestinal edema, including colonic edema, has been well described in the literature. Severe wall circumferential thickening can occur within the colon in a number of conditions. This includes edema secondary to colitis, allergy, ischemia, and infiltrative neoplastic processes. Edema may be secondary to low protein levels, as from protein losing enteropathy, nephrotic syndrome, and hepatic cirrhosis. The following case, in which there was severe ascending colonic wall thickening due to edema, is unusual in two respects: it had well-developed demonstrated "protective" right colonic varices and a normal protein level.
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PMID:CT demonstration of ascending colon varices. 818 Aug 60


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