Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infusions of corticosteroids in massive doses (methylprednisolone 1 g/day for 1 to 3 days) are used by nephrologists against acute episodes of rejection of transplanted kidneys and in acute glomeruloneppritis , especially lupic , with threatening renal failure. During the last few years this method has been tried in collagen diseases, notably in acute episodes of systemic lupus erythematosus without renal insufficiency, in rheumatoid arthritis and in ankylosing spondylitis. Published controlled studies concerning these three diseases are too few for firm conclusions to be drawn. The improvement obtained during 3 months on average after 3 g (1 g/day for 3 days) is not observed in all patients and it is not certain that such high doses are innocuous: they do not seem to have been responsible for deaths, as reported in patients with renal transplantation, but undesirable side-effects are observed in one-half of the cases. Close supervision with repeated measurement of blood electrolytes and electrocardiograms is mandatory during and immediately after treatment.
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PMID:[Pulse corticoid therapy in rheumatology]. 623 85

Diabetes affects the microcirculation, the large arteries and occasionally the large and small veins, by inducing vessel wall sclerosis. The degree of stiffening produced is linked to its duration. The ability of the diabetic's circulation to distribute blood is affected, especially during increased blood flow. In most tissues this causes no serious burden, but three tissues are unusually susceptible to disturbance--the retina, renal cortex, and peripheral nerve. They develop serious problems in many longstanding diabetics. Damage to the kidney appears to be linked to its unique combination of high blood flow rate and precise control of intraglomerular filtration pressure. As renal arteriolar intima hyalinizes, the glomerular mesangium increases in volume. Diabetic renal changes appear to become irreversible when a critical stage, manifested be albuminuria and hypertension, is reached. The resulting renal failure is associated with clumpy deposits of type IV collagen in the cortex, suggesting that local microvascular autoregulation has been lost. The retinal circulation forms late in fetal life in a process in which local oxygen tension controls new vessel formation. In adult diabetics, local retinal oxygenation is disrupted by a condition called capillary closure, and intraretinal microaneurysms form. In advanced retinopathy, new microvessel systems grow into the vitreous through defects in the internal limiting membrane, producing hemorrhage and vitreous opacification. Macular degeneration is also seen in older diabetics, suggesting that the choroidal circulation may also be compromised. Evidence for a microcirculatory role in diabetic peripheral nerve damage is not as conclusive as for the kidney and retina. The longest peripheral nerves are typically the most affected. Recent studies suggest that nerve damage can be produced by a disturbance in local pressure-flow relationships combined with epineurial mechanical constraint. Hypotheses about the pathogenesis of diabetic vascular sclerosis are reviewed, including collagen-stiffening, elastin degeneration, hemorheologic burden, metabolic disruption, increased permeability, and auto-immune disturbance.
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PMID:The microcirculation in diabetes. 640 Apr 26

Liver examination performed in seven patients who had renal failure related to light chain deposits demonstrated in all cases the presence of liver light chain deposits. In all of our patients clinical renal involvement antedated the liver disease. The portal areas and the Disse spaces contained a granular material which strongly reacted with antilight chain antiserum (kappa or gamma). In one patient in whom lesions were severe, the sinusoid edge was ruptured and a pelliosis -like lesion was observed. In the five patients who were hemodialyzed for more than several months at the time of discovery of liver deposits, increased amounts of collagen were present in the Disse spaces, and one patient had extensive liver fibrosis by light microscopy. Clinical liver involvement was defined by moderate hepatomegaly in five patients, with ascites in two. A slight increase in phosphatase alkaline activity was frequently observed and bromsulphalein retention was present in two. In one patient liver tests remained entirely normal despite the presence of diffuse kappa light chain deposits.
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PMID:Liver involvement in nonamyloid light chain deposits disease. 642 20

MRL/l mice exhibit many characteristics of human systemic lupus erythematosus including antinuclear antibodies, circulating immune complexes, glomerulonephritis, and death secondary to renal failure. In addition, these mice have elevated levels of rheumatoid factor and spontaneously develop arthritis that has many similarities to human rheumatoid arthritis. Our present studies indicate that, with age, they also develop reactivity to types I and II collagen. The levels of antibodies against native or denatured types I and II collagen in the sera of 4-5-month-old MRL/l mice are significantly higher than those in the sera of age-matched Balb/c or MRL/n mice. The specificity of these antibodies for collagen was demonstrated by a competitive binding assay. The T cells from 1- or 2-month-old MRL/l mice exhibited a significant proliferative response in the presence of type I collagen and a mild or no response to type II collagen. Both antigenic and mitogenic responses decreased with age. The results suggest that the development of autoimmunity to collagen may play an important role in the perpetuation of arthritis, vasculitis, and glomerulonephritis in MRL/l mice.
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PMID:Autoreactivity to collagen in a murine lupus model. 660 54

Five hundred Ga-67 images, requested for detection or follow-up of inflammatory or neoplastic diseases, were reviewed to evaluate the incidence of delayed renal localization and the clinical significance of different degrees of uptake. Renal uptake in 48- or 72-hr images was graded as follows: 0 = background activity; 1+ = greater than background but less than spine; 2+ = close to spine but less than liver; 3+ = same as liver; 4+ = greater than liver. On the 500 images, 996 kidneys were evaluated and among them 600 (60%) had 0 uptake and 340 (34%) had 1+. These 940 kidneys were all considered to be normal. Fifty-six (6%) had 2+ or more uptake, with possible causes for uptake being: infection 27, drug-induced renal damage ten, urinary stasis or slow excretion seven, collagen vascular disease six, renal failure four, acute tubular necrosis one (ATN), and indeterminate one. Cases of renal infection or failure tended to show more or less 4+ uptake, while drug damage, ATN, or urinary stasis tended to have 2+ uptake.
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PMID:Delayed renal localization of Ga-67: concise communication. 661 59

A newly recognized clinical and morphologic pattern of acute alcoholic liver disease is described. Twenty-one patients, having the hepatic morphologic features of alcoholic foamy degeneration, were retrospectively analyzed. All patients had a significant history of chronic alcoholism. Jaundice and hepatomegaly were usually present. Hepatic encephalopathy, ascites, bleeding esophageal varices, or functional renal failure occurred in less than 10%. Usually this was the first episode of decompensation. Laboratory studies revealed a pattern of very transiently marked elevation of serum aminotransferase and more prolonged elevation of alkaline phosphatase activity and bilirubin levels. In the majority of cases, leukocytosis was absent, and serum cholesterol was elevated. The laboratory profile differed significantly from that of acute sclerosing hyaline necrosis. Serologic markers of acute viral hepatitis A and B were absent. Needle biopsy specimens of the liver revealed intact lobular architecture except for 1 case of cirrhosis. The perivenular hepatocytes revealed foamy fatty change characterized by striking cell swelling with massive accumulation of microvesicular fat, bile pigment deposition in the cytoplasm, and no displacement of the nucleus to the periphery of the cell. Megamitochondria were frequently identified. Multiple foci of hepatocyte dropout without significant parenchymal neutrophilic exudation and delicate intrasinusoidal collagen fibers were present in the perivenular area. Macrovesicular fatty change coexisted to a variable degree. The affected hepatocytes had extensive disorganization of the organelles by electron microscopy and decreased or absent functional activity by enzyme histochemical staining. These changes appear to be a purely degenerative process without inflammatory reaction. All patients in the present series showed a rapid recovery upon abstaining from alcohol.
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PMID:Alcoholic foamy degeneration--a pattern of acute alcoholic injury of the liver. 682 80

Serum immunoreactive parathyroid hormone in patients with juvenile-onset diabetes mellitus and end-stage renal failure on chronic haemodialysis treatment is significantly lower than the values obtained from patients with adult-onset diabetes mellitus and non-diabetic patients with end-stage renal disease being similarly dialysed. The major determinants of parathyroid hormone secretion, such as calcium and magnesium, do not seem to be the factors responsible for this difference. The histology of the parathyroid glands in juvenile-onset patients shows fibrosis and collagen infiltration which reduce the functional mass of the glands.
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PMID:Parathyroid hormone in patients with diabetes mellitus and end-stage renal disease on chronic haemodialysis. 687 35

A term newborn suffered disseminated herpes simplex virus (HSV) type II infection five days after cesarean section delivery for fetal distress. The mother had no history or evidence of herpetic lesions; the father had a history of genital herpetic lesions. The infant's terminal course was dominated by disseminated intravascular coagulation (DIC) with hepatic and renal failure. Microscopic examination revealed a necrotizing vasculitis of small and medium-sized lung and peripancreatic arteries. Nuclear inclusions characteristic of HSV were found in these arteries, as well as in the adrenal parenchyma, spleen, and lymph node; electron microscopy confirmed replication of virus within the arterial endothelial cells. The mechanism of arterial damage in severe herpetic infection contrasts with the immune-complex mechanism postulated for other viral vasculitides. Direct, virally induced arterial damage resulting in exposure of collagen may set the stage of DiC, a commonly fatal complication of this disease.
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PMID:Necrotizing vasculitis in a case of disseminated neonatal herpes simplex infection. 689 28

The clinical entity of progressive systemic sclerosis (PSS, or scleroderma) has remained unchanged since Osler's first description in 1892. Several related or overlap syndromes have now been recognized, which may afford some insight into etiologic events in the development of PSS. As yet, the cause of PSS remains elusive. Abnormalities of collagen synthesis, the role of cellular and humoral immunity, and the relationship of these to vascular disease and hyperreactivity represent current areas of research. Few therapeutic advances of proven efficacy have been forthcoming over this period except for the use of vigorous antihypertensive therapy or early nephrectomy, dialysis, and transplantation in the control of malignant hypertension and progressive renal failure.
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PMID:Scleroderma: developments from Osler to the present. 699 40

The clinical course of 40 patients with significant quantities of mixed cryoglobulins, but without lymphoproliferative, collagen-vascular or chronic infectious diseases, is presented. These cases comprise 51.3 percent of all mixed and 31.7 percent of all types of cryoglobulins evaluated by us over the period 1960--1978. A characteristic clinical syndrome, consisting of recurrent palpable purpura (100 percent), polyarthralgias (72.5 percent) and renal disease (55 percent), was seen. Biopsy specimens of skin lesions showed cutaneous vasculitis, and half had immune reactants in vessel walls. Seventy percent of patients had evidence of hepatic dysfunction, often subclinical, and more than 60 percent of those tested had serologic evidence of prior infection with hepatitis B virus. Hepatic lesions ranged from minimal triaditis to chronic active hepatitis and/or cirrhosis. All 22 patients in whom clinical renal disease developed had significant proteinuria; 63.6 percent had diastolic hypertension, 77.3 percent edema, 45.5 percent renal failure and 22.7 percent were nephrotic. Glomerular disease associated with deposition of immunoglobulin G, immunoglobulin M and complement, often with coexistent renal arteritis, was confirmed pathologically in 15 cases. All cryoglobulins had rheumatoid factor activity and consisted of IgM and polyclonal IgG; five also contained IgA. Thirteen had a monoclonal IgM kappa component. Serum protein electrophoresis was unremarkable or showed diffuse hyperglobulinemia. Striking depression of early complement components was noted but did not correlate well with the cryoprotein concentration, renal involvement or clinical course. Follow-up for periods up to 21 years from onset of symptoms revealed that renal involvement has a deleterious effect on prognosis. Postmorten examinations of nine patients demonstrated widespread vasculitis in addition to renal involvement. Preterminal infection was found in eight.
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PMID:Mixed cryoglobulinemia: clinical aspects and long-term follow-up of 40 patients. 699 82


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