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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial hypertension is frequent among chronically dialyzed patients. The kidney obviously plays a major role in arterial blood pressure control. There is a large number of experimental data emphasizing different factors (in addition to renin important in renal hypertension prognosis) such as: sodium balance, angiotensin, etc [1-8]. Sympathetic activity disorders or lack of vasodilatory prostaglandins and quinine may also play a certain role. In uremic patients peripheral arteriolar resistance is increased, unlike normotensive uremic patients or those who prove to be normotensive upon clinical examinations [8, 11-15]. Hypertension occurs in approximately 80% of patients with chronic renal failure, producing a number of complications primarily affecting the CNS and systemic circulation [5-8, 10, 11, 13]. The study concerned patients on chronic dialysis, with a male to female ratio of 69.9%:32.1%. In most of them the underlying disease, which caused chronic renal failure, was glomerulonephritis (60.0%), then pyelonephritis (17.0%) and nephrosclerosis, nephrolithiasis, polycystic kidney and, finally, renal tumours. The effect of permanent haemodialysis during the first year of treatment, was efficacious on hypertension in 1704 (65.1%) patients; in 672 (25.7%) patients therapeutical effects were achieved by dialysis and antihypertensive drugs, while in 240 (9.2%) subjects there was no improvement. General observations suggest that two types of arterial hypertension persisted in patients with chronic renal failure: volume-dependent arterial hypertension which is more frequent (90-95%) among haemodialyzed patients and renin-dependent hypertension. Such findings are of utmost importance indicating that hypervolaemia is one of the major factors in the development of arterial hypertension in patients with chronic renal failure, with renin playing the secondary role. Salt-free diet should be used in the treatment of arterial hypertension for years, a well conducted haemodialysis is highly effective in the control of arterial hypertension among these patients. In our series of patients dialysed three times a week; normalization of blood pressure was faster with lower incidence of hypertensive crises during haemodialysis and with few complications. Water and sodium excess was reduced by frequent haemodialyses and sudden changes in electrolyte, hydrostatic and other metabolic effects were minimized. Increased values of plasma renin activity were observed in a small number of patients. Ultrafiltration is insufficient for normalization of blood pressure. Hypertensive crises were frequent in these patients. Their response to medicaments such as methyldopa, beta-adrenergic blockers or other antihypertensive drugs, was good. Severe changes in blood vessels, especially in fundus oculi blood vessels were frequent in these patients. The life of hypertensive glomerulonephritis patients was especially endangered (graphs 1-6). In addition to the mentioned factors arterial hypertension during haemodialysis may also be of cardiac origin, including increase in cardiac output due to arteriovenous anastomosis, disequilibrium syndrome, changes in osmotic gradient of both extra- and intracellular spaces with resultant arteriolar wall oedema, erythrocyte amount, hypoxia, composition of dialysis fluid (sodium concentration), plasma osmotic pressure, metabolic acidosis and other factors. More recently, natriuretic hormone has also been indentified as a cause of vascular refraction. Peripherial arteriolar resistance as a cause of arterial hypertension among uremic patients must not be forgotten, because the genesis of arterial hypertension in patients with chronic renal failure is multifactorial. The highest percentage refers to volume-dependent arterial hypertension, whereas the percentage of other aetiologic factors is lower. Haemodialysis enables the normalization of blood pressure in most of hypertensive patients.
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PMID:[Arterial hypertension in patients on chronic hemodialysis]. 910 57

The action of indirect electrochemical blood oxidation with 0.06% solution of sodium hypochlorite on kidney and urinary inflammation was studied in experiments on 60 non-inbred rat females of 200-250 g body weight. The animals were intravesically infected through the catheter with E. coli and Ps. aeruginosa. 3 days later, after histological verification of acute pyelonephritis, ureteritis, cystitis, the animals were injected intraperitoneally 1.0 and 2.0 ml daily of sodium hypochlorite solution (control animals) or 0.89% solution of sodium chloride. Though no reliable decrease of the bacterial contamination was achieved, histologically, there was a marked reduction in morphological signs of the inflammation in the kidneys, ureter and urinary bladder on the first day after beginning of electrochemical blood oxidation with solution of sodium hypochlorite in experimental groups. In experimental group rats morphological signs of urinary and renal inflammation for both infections disappeared on days 7 and 10, respectively. In the control animals morphological signs of the inflammation remained after 10 days. Moreover, purulent inflammation was registered in the controls infected with Ps. aeruginosa.
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PMID:[Effects of indirect electrochemical blood oxidation by sodium hypochlorite solution on the course on inflammatory process in the kidneys and urinary tract]. 964 85

Endoscopic subureteric injection of tissue-augmenting substances has become an alternative to long-term antibiotic prophylaxis and open surgery in the treatment of children with vesico-ureteric reflux. Successful elimination of reflux in about 80% of patients after a single injection (and in 90% after a repeat) has been achieved using the foreign-body non-degradable substances Teflon and silicone. Few patients have required open surgery and recurrence of reflux after initial successful treatment has occurred in only 5-10%. Concern has arisen, however, about possible distant migration and granuloma formation after injection of particulate plastic materials. Cross-linked bovine collagen is a biodegradable alternative substance, but with a lower response rate of 60% after the first treatment and a recurrence rate of 10-20%. Dextranomer in sodium hyaluronan is a new biological substance with microparticles with a response rate of 69% after the first injection. Biological substances have caused few complications. Present literature on injection treatment unfortunately focuses on elimination of reflux, with little attention to subsequent frequency of pyelonephritis or to the long-term development of the kidneys. Furthermore, there are no controlled, randomized studies with subureteric injection as one of the treatment alternatives. Thus, although having the advantage of being a minimally invasive procedure that can be performed on an outpatient basis, this technique needs to be tested in a large prospective study with the long-term renal outcome as the main end-point.
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PMID:Endoscopic treatment of children with vesico-ureteric reflux. 1058 73

Acute renal insufficiency (ARI) complicated the course of the underlying process, including primary and secondary glomerulonephritis, interstitial nephritis, pyelonephritis, dysmetabolic nephropathies, urolithiasis, tubulopathies, renal congenitae defects and injuries in 136 of 1695 children with nephrological diseases hospitalized at Republican Pediatric Renal Center during the last decade. In 69.1% cases ARI developed by the renal type, in 23.5% cases was caused by prerenal factors, and rarely (in 7.4% cases) by postrenal factors. Renal ARI in children was caused by 5 causes, including glomerulonephritis (47%), acute tubular necrosis (19%), interstitial nephritis (14%), vascular disorders (11%) resultant from vasculitis, renal vein thrombosis, and acute crystalluria (9%) which developed in the presence of grave dysmetabolic nephropathy. Among three clinical variants of ARI the most severe was observed in renal ARI leading to grave endogenous intoxication and pronounced decompensation of renal function. More benign course of renal ARI caused by acute tubular necrosis or acute crystalluria differed significantly from prerenal ARI by a more pronounced endogenous intoxication, increased fractionated sodium excretion, and renal insufficiency index higher than 1.
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PMID:[Diagnosis of acute renal failure in pediatric nephrology]. 1133 30

Pyelonephritis is a risk factor for renal tubular epithelial cell damage in children. The inter- and intracellular regulator nitric oxide (NO) plays a role in the modulation of cellular viability in urinary tract infections, but the role of the NO pathway in renal proximal tubular-cell death remains unclear. The present study demonstrates that, in renal epithelial cells undergoing death mediated by Escherichia coli strain ARD6 serotype O6K13H1 (O6), levels of the phosphorylated extracellular signal-regulated kinase (ERK) 1/2 and inducible NO synthase (iNOS) proteins are up-regulated, but levels of endothelial NO synthase are down-regulated. When NO synthase (NOS) activity is inhibited by the specific inhibitor of NOS or mitogen-activated protein kinase kinase, cells are prevented from death. Moreover, down-regulating protein 53 (p53) does not prevent the cells from dying, although p53 is up-regulated in O6-exposed cells. Up-regulation of heme oxygenase (HO)-1 by sodium nitroprusside or by the specific activator hemin inhibits cell death. In conclusion, the activation of ERK mediates O6 toxin-mediated renal cell death via induction of iNOS. Stimulation of HO-1 protects cells against death.
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PMID:Activation of extracellular signal-regulated kinase mediates apoptosis induced by uropathogenic Escherichia coli toxins via nitric oxide synthase: protective role of heme oxygenase-1. 1519 52

A 27-year-old gravida was referred to an other hospital complaining of left lumbago and pyrexia, and she was diagnosed with acute pyelonephritis. Left lumbago increased and magnetic resonance imaging of abdomen demonstrated a low intensity area like hematoma around the left kidney. Then the patient was transported to our hospital under the diagnosis of high-risk graviditas. She was performed cesarean section. High-grade inflammation still continued after the operation and computerized tomography revealed the increase of high density area. We performed angiography of the left kidney for hemostasis, but the tumor in the left renal upper pole revealed hypovascularity. We started medication of imipenem/cilastatin sodium (IPM/CS). Inflammation and pyrexia did not improve until we changed antibiotics from IPM/CS to amikacin sulfate. Seven days after that high density area around the left kidney disappeared and a renal cyst was recognized by computerized tomography for the first time. Finally, the current case was diagnosed as spontaneous rupture of infectious renal cyst.
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PMID:[A case of spontaneous rupture of infectious renal cyst with difficulty in diagnosis]. 1591 85

Ion transport is essential for maintenance of transmembranous and transcellular electric potential, fluid transport and cellular volume. Disturbance of ion transport has been associated with cellular dysfunction, intra and extracellular edema and abnormalities of epithelial surface liquid volume. There is increasing evidence that conditions characterized by an intense local or systemic inflammatory response are associated with abnormal ion transport. This abnormal ion transport has been involved in the pathogenesis of conditions like hypovolemia due to fluid losses, hyponatremia and hypokalemia in diarrhoeal diseases, electrolyte abnormalities in pyelonephritis of early infancy, septicemia induced pulmonary edema, and in hypersecretion and edema induced by inflammatory reactions of the mucosa of the upper respiratory tract. Components of membranous ion transport systems, which have been shown to undergo a change in function during an inflammatory response include the sodium potassium ATPase, the epithelial sodium channel, the Cystic Fibrosis Transmembrane Conductance Regulator and calcium activated chloride channels and the sodium potassium chloride co-transporter. Inflammatory mediators, which influence ion transport are tumor necrosis factor, gamma interferon, interleukins, transforming growth factor, leukotrienes and bradykinin. They trigger the release of specific messengers like prostaglandins, nitric oxide and histamine which alter ion transport system function through specific receptors, intracellular second messengers and protein kinases. This review summarizes data on in vivo measurements of changes in ion transport in acute inflammatory conditions and in vitro studies, which have explored the underlying mechanisms. Potential interventions directed at a correction of the observed abnormalities are discussed.
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PMID:Changes in ion transport in inflammatory disease. 1657 Nov 16

The authors present the case of a 3-year-old girl with a history of myelomeningocele repair, ventriculoperitoneal (VP) shunt placement for hydrocephalus, and shaken baby syndrome who presented in a hypernatremic state as a result of dehydration. At the time of presentation, the patient had experienced a 1-week-long history of diarrhea associated with antibiotic agents used to treat a coexisting pyelonephritis. On admission, the patient exhibited signs and symptoms of dehydration and was discovered to have profound hypernatremia with a serum sodium level of 180 mmol/L. A computerized tomography (CT) scan of the head revealed ventricular enlargement compared with previous imaging findings. A shunt tap revealed intracranial hypotension with good proximal flow. The child was treated for her hypernatremic state, and her neurological condition returned to baseline level. Subsequent CT scans of the head demonstrated a return of the ventricular system to its premorbid size. On the basis of the initial radiographic presentation and subsequent evaluation, the authors hypothesize that the ventricular enlargement was a result of hypernatremia. The signs and symptoms were similar to those found in patients with a VP shunt obstruction; however, a shunt tap revealed intracranial hypotension and excellent proximal flow. To the authors' knowledge, there has not been a radiographically documented case of reversible ventricular enlargement associated with hypernatremia.
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PMID:Transient ventriculomegaly in a child presenting with hypernatremia. Case report. 1657 37

The role of the kidney in the control of blood pressure has been convincingly demonstrated by several studies. Recent evidence has suggested that subtle acquired tubulointerstitial injury may cause a defect in sodium excretion function, thus leading to salt-sensitive hypertension. There are no reports, however, examining the effect of experimental chronic pyelonephritis on renal sodium handling and arterial pressure. Thus, to examine the influence of salt intake and unilateral nephrectomy, unanesthetized, unrestrained rats were randomly assigned to one of two separate groups: sham-operated rats (CO) or chronic unilateral pyelonephritic rats (CP). After twenty one days, the pyelonephritic group was subdivided in two: one subgroup continued with water intake (CPw), while the other was changed to 0.9% NaCl intake (CPs), like the control group (COs). After seven days, all rats were submitted to unilateral nephrectomy of the left normal kidney. Data presented herein show that chronic pyelonephritis produced an increase in mean arterial pressure (CO: 121.4 +/- 1.0 mmHg to CP: 127.0 +/- 0.9 mmHg, p = 0.000) that was enhanced by saline ingestion (COs: 121.6 +/- 1.4 mmHg; CPw: 127.0 +/- 1.8 mmHg; CPs: 132.1 +/- 1.2 mmHg, p = 0.000) and further aggravated by unilateral nephrectomy (CO: 125.2 +/- 2.6 mmHg; CPw: 127.5 +/- 0.9 mmHg; CPs: 139.2 +/- 1.1 mmHg, p = 0.000). Unchanged blood pressure measurements (120.2 +/- 2.3 mmHg) were observed beyond 21 days in control rats maintained on water regimen when compared with saline-drinking groups. These changes in mean arterial pressure were observed despite an increased fractional sodium excretion in the CPs group compared to the other groups before uninephrectomy (COs: 0.125 +/- 0.025%; CPw: 0.045 +/- 0.013%; CPs: 0.292 +/- 0.046%; p = 0.000), as compared to CPw after uninephrectomy (COs: 0.249 +/- 0.077%; CPw: 0.062 +/- 0.011%; CPs: 0.363 +/- 0.195%, p = 0.019). In addition, it was shown that daily liquid intake was higher in CPs than in CPw but similar to COs, both before uninephrectomy (COs: 42.8 +/- 2.6 ml/d; CPw: 34.3 +/- 3.5 ml/d; CPs: 51.8 +/- 3.7 ml/d, p = 0.006) and after uninephrectomy (COs: 40.9 +/- 5.5 ml/d; CPw: 33.8 +/- 1.4 ml/d; CPs: 53.0 +/- 3.5 ml/d, p = 0.004). The current data suggest that chronic pyelonephritis promotes an inability of renal tubules to handle sodium excretion when exposed to sodium overload and aggravated by uninephrectomy, thus constituting a model for salt-sensitive hypertension.
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PMID:Development of hypertension in a pyelonephritis-induced model: the effect of salt intake and inability of renal sodium handling. 1692 20

Most physical illness in vertebrates involves inflammation. Inflammation causes disease by fluid shifts across cell membranes and cell layers, changes in muscle function and generation of pain. These disease processes can be explained by changes in numbers or function of ion channels. Changes in ion channels have been detected in diarrhoeal illnesses, pyelonephritis, allergy, acute lung injury and systemic inflammatory response syndromes involving septic shock. The key role played by changes in ion transport is directly evident in inflammation-induced pain. Expression or function of all major categories of ion channels like sodium, chloride, calcium, potassium, transient receptor potential, purinergic receptor and acid-sensing ion channels can be influenced by cyto- and chemokines, prostaglandins, leukotrienes, histamine, ATP, reactive oxygen species and protons released in inflammation. Key pathways in this interaction are cyclic nucleotide, phosphoinositide and mitogen-activated protein kinase-mediated signalling, direct modification by reactive oxygen species like nitric oxide, ATP or protons and disruption of the cytoskeleton. Therapeutic interventions to modulate the adverse and overlapping effects of the numerous different inflammatory mediators on each ion transport system need to target adversely affected ion transport systems directly and locally.
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PMID:Ion channels in inflammation. 2127 80


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