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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the prevalence and features of painless myocardial ischemia among diabetic patients, 44 consecutive patients with angiographically-documented coronary artery disease and positive treadmill tests were examined. They were 26 with diabetes and 18 without it. Painless myocardial ischemia was defined as the absence of chest pain with 1 mm or more ST segment depression during the exercise stress tests. The severity of ischemia was determined by the magnitude of the ST segment depression. Painless myocardial ischemia was observed in 18 of the 26 (69%) diabetics, and in three of the 18 (17%) non-diabetics (p less than 0.005). The frequency of painless ischemia in the diabetics was relatively high regardless of the severity of ischemia, while painless ischemia was less frequent in the non-diabetics with severe ischemia. With a level of 2.5 mm ST depression, 11 of 12 (92%) diabetics were free of pain compared to four of 11 (36%) non-diabetics (p less than 0.01). Absence of chest pain during the exercise tests was not concordant with prior angina in diabetics, as opposed to non-diabetics in whom both clinical and exercise-induced angina developed concordantly. The diabetic patients without chest pain had a higher prevalence of three major diabetic complications such as neuropathy, nephropathy and retinopathy compared to those developing chest pain (p less than 0.025). It was concluded that in diabetics, painless myocardial ischemia is frequently observed during exercise stress tests and its prevalence is relatively high regardless of the severity of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia in diabetic patients with coronary artery disease: evaluations by treadmill exercise tests]. 210 4

The authors carried out a prospective study to determine the frequency of silent ischemia (SI) in 50 consecutive patients with end stage renal failure during dialysis by Holter monitoring. Twenty patients had SI (40%). This event was related to the number of cardiovascular risk factors (p = 0.0025), principally diabetes, smoking and the underlying renal disease (p = 0.018), and to a history of coronary artery disease (p = 0.0015). Two patients died during the nine months follow-up period and both had SI on Holter monitoring. Dialysis therapy in anaemic patients may predispose to and facilitate the detection of myocardial ischemia by the simultaneous interplay of hypotension, hypovolemia, hypoxia and tachycardia. The detection of these ischemic events may allow identification of a subgroup of dialysis patients with a high cardiovascular risk. The prognosis of these patients and best therapeutic approach require further study.
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PMID:[Frequency of painless myocardial ischemia during hemodialysis in 50 patients with chronic kidney failure]. 212 44

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

Prolonged treatment with cyclosporine (CS) results in an irreversible renal lesion consisting of interstitial fibrosis and tubular atrophy, as well as prominent hyperplasia of the juxtaglomerular apparatus (JGA). Ischemia to the tubulointerstitial compartment caused by intense CS-mediated renal vasoconstriction may contribute significantly to the development of this lesion. To explore the potential role of volume contraction and activation of the renin-angiotensin system (RAS) in the genesis of this lesion, we have employed a recently described rodent model of chronic cyclosporine nephropathy (CCN). Over 28 days of CS therapy, animals received plain drinking water, 1% saline, or enalapril (ENAL), 50 mg/l in drinking water. At the end of 28 days, Na+ balance in saline-treated animals was markedly positive, and plasma volume was increased; however, glomerular filtration rate (GFR) did not change, and the tubulointerstitial lesion and JGA hyperplasia as evaluated by morphometric techniques were unaffected. Enalapril-treated animals were relatively hypotensive with lower GFR than CS controls. Enalapril conferred no protection against the development of tubulointerstitial disease and exacerbated the development of JGA hyperplasia and hyperkalemia. We conclude that volume contraction is not an important contributor to the reduced GFR, tubulointerstitial lesion, or JGA hyperplasia associated with long-term CS treatment. Blockade of the RAS also conferred no protection against the development of tubulointerstitial disease but resulted in worsening of JGA hyperplasia and hyperkalemia.
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PMID:Effects of chronic volume expansion and enalapril on chronic cyclosporine nephropathy. 218 76

Acute renal failure after contrast media injection has been recognized for at least 35 years but the exact mechanism responsible for the renal injury remains an enigma. The clinical characteristics of contrast-induced nephropathy (CAN) are well-known although more recently the nonoliguric presentation has occurred at an increased frequency--in 70 to 90% of cases. For nonoliguric presentation of CAN, one can expect an asymptomatic increase in serum creatinine, the mean peak occurring at 4.2 days. If oliguric, the fractional excretion of sodium will be less than 1% and resistant to either fluid challenge or loop diuretics. Preexisting renal insufficiency, with or without diabetes mellitus, increases the risk of CAN 6- to 10-fold but recovery is expected, with less than 10% of all patients requiring dialytic support. Despite the growing body of published reports, the lack of a suitable animal model to evaluate various proposed mechanisms of renal injury has compromised our ability to devise a technique for preventing CAN. A popular scheme has been proposed to describe the possible sequence by which ischemia or nephrotoxins, or both, induce acute renal failure. In particular, a vascular mechanism (i.e., ischemia), is an appealing explanation for CAN since acute changes in renal hemodynamics after contrast media injection have been confirmed by several animal experiments. Unlike other vascular beds in which contrast media induce acute vasoconstriction followed by vasodilatation, the initial effect on the renal circulation is acute vasodilatation, followed by progressive vasoconstriction, increasing renal vascular resistance and a concomitant decrease in both renal blood flow and glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental contrast-associated nephropathy and its clinical implications. 223 94

Most urinary tract infections occur without either obstruction or vesicoureteral reflux. Children become colonized by their mother's bacterial flora, that within the nursery or by siblings. Bacterial adherence may lead to colonization of the perineum in girls and of the prepuce in boys (if uncircumcised). Nephropathogenic bacteria ascend the urinary tract because of the P-fimbriae of Escherichia coli which adhere to a specific urothelial cell glycolipid. The endotoxin effect on ureteral peristalsis leads to intrarenal reflux, adherence in the kidney and acute pyelonephritis. Complement activation then causes granulocytic aggregation in capillaries with renal ischemia and activates granulocytes to produce the respiratory burst of phagocytosis, which releases superoxide into both phagosomes and the tubular lumen. Bacteria are thus killed as are renal tubules, leading to nephron loss. Untreated, the ischemia and respiratory burst lead to a loss of renal function and scar formation ending as chronic pyelonephritis (or reflux nephropathy).
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PMID:Norwich-Eaton lectureship. Pathogenesis of nonobstructive urinary tract infections in children. 237 23

Chronic pyelonephritis (c.p.) is by definition an infectious tubulo-interstitial nephritis. It has to be differentiated from other etiologic forms of tubulo-interstitial nephritis. Therefore strict morphological criteria are needed for diagnosis. The characteristic lesion is a large cortico-medullary scar overlying a dilated chronically inflammed calyx. The macroscopic aspect and the histologic survey picture are more important than histologic details. A diagnosis on renal biopsies is therefore not warranted. Vesico-renal reflux and papillary morphology play an important pathogenetic role. Beside the more common focal scar a diffuse form of scarring can be observed. A limited number of conditions only have to be considered in differential diagnosis. The Ask-Upmark kidney seems to be a special form of c.p. related to urinary tract infection and reflux in early infancy. Pelvi-calyceal lithiasis without superimposed infection causes a picture very similar to a pyelonephritic scar. A reliable differentiation between c.p. and analgesic nephropathy may cause problems in endstage kidneys with sloughed off papillae. Various mechanisms of renal damage such as bacterial infection, immunological mediated inflammation, leakage of urinary constituents into the interstitium especially Tamm-Horsfall-protein and ischemia have to be considered. Despite the frequency of urinary tract infections chronic progressive pyelonephritis is rare. Predisposing factors are needed for progression of the disease. These include congenital or acquired urinary tract obstruction, vesico-renal reflux and papillary damage with intrarenal obstruction to the urinary flow. Other important factors are focal and segmental glomerulosclerosis and hypertension.
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PMID:[Chronic pyelonephritis and its differential diagnosis. A disease changing with time]. 248 12

During the 1970s renal biopsies were obtained after blood pressure had been controlled in 41 black patients in Memphis who had severe hypertension plus excretory renal failure. An additional 13 binephrectomy specimens were also studied. This material yielded significant information on the state of the renal arteries--arterioles under these circumstances. Fibrinoid necrosis of the afferent glomerular arteriole and proliferative glomerulitis were not noted. Rather, the vascular lesion characterized by the accumulation of smooth muscle cells and mucopolysaccharide in the intima attended by a marked narrowing of the lumen was dominant. This lesion caused pronounced ischemia associated with obsolescence of glomeruli, atrophy, and fibrosis (end-stage kidney). This lesion has been renamed musculomucoid intimal hyperplasia as a result of changes revealed by electron microscopic and histochemical studies. Since this study the incidence of this severe vascular disease of the kidney in the same geographic area has been markedly reduced. There are a number of possible reasons for this change in incidence, but a major one appears to be improved treatment of hypertension and better compliance with antihypertensive therapy. Why such extreme changes occur in a subset of hypertensive blacks is not known. It is apparent that without improved antihypertensive treatment, this type of end-stage renal disease due to severe vascular damage will continue to be encountered.
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PMID:Histopathology of severe renal vascular damage in blacks. 262 Apr 72

An abnormal filtration fraction or a significant divergence between a kidney's ability to extract Tc-99m dimercaptosuccinic acid (DMSA) and other function parameters, such as the glomerular filtration rate (GFR) or the effective renal plasma flow (ERPF), could lead to different estimates of relative or absolute renal function, depending on the radiopharmaceutical administered. To evaluate this possible divergence, we measured the relative GFR (I-125 iothalamate), ERPF (I-131 hippurate), and Tc-99m DMSA accumulation in adult male Sprague-Dawley rats with unilateral ureteral obstruction or unilateral ischemia at various times after renal injury. The relative ERPF of the obstructed kidney was significantly greater than the relative GFR at all time periods studied; significant but less dramatic differences were noted comparing DMSA with GFR in obstruction and DMSA and ERPF with GFR in ischemia. In evaluating renal disease, it is important to consider the functional parameter reflected by the administered radiopharmaceutical as well as the underlying disease state.
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PMID:Differential renal function in unilateral renal injury: possible effects of radiopharmaceutical choice. 298 2

To avoid the center effect and the possible hidden interactions of multicenter studies, the validity of the Cox Proportional Hazards Model for the analysis of a single-center kidney transplant program was tested, considering 287 renal transplants performed in a 10-year period. The inclusion of type of donor and main immunosuppressive drug as covariates in the model did not violate the proportionality assumption of the Cox model. According to this method, the following covariates were significant in predicting graft survival: cyclosporine, type of donor, good human leukocyte antigen (HLA)-A and HLA-B match (DR data were not considered), highest percentage of reactive antibodies against panel cells, and nephroangiosclerosis as a primary renal disease. Cyclosporine did not significantly improve graft survival in living related donor transplants. Pretransplant blood transfusions, cold ischemia time, and donor ABO blood group were initially significant but dropped out in the step-down procedure. Recipient's age at transplant, cyclosporine, HLA-A and HLA-B match, and nephroangiosclerosis were significant in predicting patient survival. It was concluded that using long-term data of cadaveric and living related renal transplants either on azathioprine or cyclosporine is a valid way to perform multivariate analysis of single-center transplant programs that do not have large samples.
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PMID:An alternative approach for statistical analysis of kidney transplant data: multivariate analysis of single-center experience. 305 83


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