Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of progression of early renal failure was evaluated in three groups of adult patients with renal disease of diverse etiology on dietary protein and phosphorus restriction (about 0.6 g/kg of protein, 700 mg of phosphorus) and in a control group of 22 patients with the same renal disease, retrospectively studied, on a free diet. Group 1 had 33 patients with chronic glomerulonephritis (CG), initial serum creatinine (Scr) of 1.4 to 4.3 mg/dl (mean, 2.20), followed for 5 to 94 months (mean, 44). Group 2 had 17 patients with polycystic kidney disease (PKD), Scr 1.3 to 4.7 mg/dl (mean, 2.40), followed for 8 to 81 months (mean, 42). Group 3 had 28 patients with primary chronic pyelonephritis (CP), Scr of 1.5 to 4.5 mg/dl (mean, 2.57), followed for 9 to 92 months (mean, 41). The control group had 22 patients (11 with CG, five with PKD, and six with CP), with Scr 1.7 to 4.1 mg/dl, followed for 6 to 72 months (mean, 24). In the regression analysis between reciprocal creatinine and time, the slopes were -0.0017, -0.0025, and -0.00016 dl/mg/month in the three patient groups on a protein-restricted diet, respectively. The difference between both groups 1 and 2 and group 3 was statistically significant (P less than 0.05). The slopes in patients on a free diet were significantly greater than those found in patients on a protein-restricted diet. The actuarial survival probability at 72 months, assuming as "renal death" a Scr of 10 mg/dl, was 45% in patients with CG, 44% in those with PKD, and 67% in those with CP on a protein-restricted diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progression of renal failure in patients with renal disease of diverse etiology on protein-restricted diet. 399 43

R-R variations in the ECG were studied as a sign of autonomic dysfunction in 44 non-diabetic patients with terminal uraemia treated with intermittent haemodialysis. A severe impairment of this parasympathetic vagal reflex was found though there were only mild signs of diffuse polyneuropathy. No acute effect was associated with haemodialysis. There was no correlation between either the R-R variations and the polyneuropathy-index or the total dialysis time. Patients with chronic glomerulonephritis, pyelonephritis and polycystic kidney disease were equally affected.
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PMID:Autonomic dysfunction in non-diabetic terminal uraemia. 400 36

Autopsies of all uraemic patients in Leningrad for three years, and materials of the City Nephrological Service have demonstrated that the structures of nephrological diseases in their early and terminal stages were different. Chronic glomerulonephritis has been noted in patients with normal renal function just as often as chronic pyelonephritis but the former prevails considerably among the causes of uraemia. The proportion of polycystic kidney disease, amyloidosis, and diabetic nephropathy increases in patients with chronic renal failure. Due to these changes and the difference in the death age of patients with various diseases the majority of patients suitable for treatment with long-term dialysis suffer from chronic glomerulonephritis and only 14.89-20.5% from chronic pyelonephritis.
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PMID:Epidemiology of chronic renal diseases. 622 4

Bone mineral content (BMC) was measured annually over a three year period in 31 consecutive patients on maintenance hemodialysis (HD). No patient had received treatment with vitamin D derivatives, anticonvulsants or corticosteroids, nephrectomy or a renal transplant. Initial median BMC value in per cent of sex and age matched normal mean was significantly decreased to 91.0% (P less than 0.01), indicating bone mineral loss in chronic renal failure prior to HD. During HD a highly significant fall in mean BMC (in per cent of initial value) continued to 95.1%, 92,7% and 90.8% after 1, 2 and 3 years, respectively, with no influence of age, sex or initial BMC value. The interindividual variation in BMC changes, however, was considerable: the BMC loss over 3 years exceeded 10% in 13 (42%) patients ("rapid losers") while 12 (39%) patients had a BMC loss below 5%, or no loss at all. The "rapid loser" group had significantly higher serum levels of parathyroid hormone and alkaline phosphatases and, moreover, developed a lower serum phosphate and calciumXphosphorus product than the other group of patients ("slow losers"). The mean BMC loss over 3 years of HD was pronounced and significant (P less than 0.02) in patients with chronic pyelonephritis (9.8%) and polycystic kidney disease (14.2%), but much smaller, and not significant, in patients with chronic glomerulonephritis (4.8%). It is concluded that a selection of patients with a high degree of bone mineral loss during HD is not possible by means of sex, age, initial BMC, biochemical parameters, or diagnosis (2 patients with chronic glomerulonephritis appeared to be "rapid losers"). For that purpose a high-precision BMC method is mandatory.
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PMID:Bone mineral content in patients on prolonged maintenance hemodialysis: a three year follow-up study. 664 Oct 32

Plasma concentrations of middle molecule (MM) fractions were quantitatively assessed by use of combined gel filtration and ion exchange chromatography in 82 non-dialyzed azotemic patients. "Sick" patients exhibiting uremic symptoms were compared with symptom-free azotemic patients with regard to plasma levels of individual MM fractions. The patients with edema, pericarditis and intercurrent infections had significantly higher plasma concentration of MM fraction 7c than symptom-free controls. The results confirm our earlier anecdotic observations that high plasma concentration of fraction 7c often associated with uremic symptoms. In the symptom-free group, the patients with polycystic kidney disease showed a significantly lower concentration of fraction 7b in plasma than those with pyelonephritis; the patients on protein restricted diet had higher plasma concentrations of fractions 7b and 7c than those on diets with daily protein intake of 60 g or more. Slight correlations between some biochemical parameters and MM fractions in plasma were found in the total patient material; the highest correlation between albumin and fractions 7c (r = -0.36), and 7d (r = 0.36), respectively. Statistical analysis of this survey has shown that the accumulation of MM fractions, especially fraction 7c, is associated with uremic "sickness", i.e. edema, pericarditis and intercurrent infection.
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PMID:Uremic middle molecules in non-dialyzed azotemic patients: relation to symptoms and clinical biochemistries. 706 71

Eight cases of acquired cystic disease of the kidney (ACDK) associated with chronic renal failure and hemodialysis are described. No patient had a family history or clinical evidence of congenital adult polycystic kidney disease (CAPKD). Glomerulonephritis was the cause of renal failure in 6, and pyelonephritis in 2. Massive renal and perirenal hemorrhage necessitated 3 nephrectomies in 2 patients. Single kidney weights did not exceed 280 Gm., a major feature in the distinction of ACDK from CAPKD. Morphologically, in addition to the usual stigmata of end-stage kidneys, 40 to 80 per cent of the renal parenchyma was replaced by small cysts. Continuity of cysts with tubules was established by nephron dissection.
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PMID:Acquired cystic disease of kidney in chronic dialysis patients. 721 Mar 78

Circulating antibody to Tamm-Horstall protein (THP) was measured using a radioimmunoassay in forty-five patients on maintenance hemodialysis and compared to levels of antibody titers measured in sera from ten healthy controls. The etiology of the end-stage kidney disease in the patient population was polycystic kidney disease in thirteen, glomerulonephritis in fourteen, diabetic nephropathy in nine, interstial nephritis and chronic pyelonephritis in three each, multiple myeloma in two, and urinary tract obstruction in one. Four patients had significantly elevated titers of antibody to THP but shared no other unifying characteristics. The results also indicate that none of the groups studied had mean antibody titers significantly different from controls. Furthermore, no general trend was apparent between levels of antibody to THP and number of months on dialysis. Observations made during the study revealed that heparinized samples of blood had lower titers of antibody to THP than did non-heparinized samples from the same patient. This finding was repeated when other anti-coagulants, i.e., ethylenediaminetetraacetate (EDTA) and sodium citrate, were used. Titers returned toward normal when CaCl2 was added back to samples anticoagulated with EDTA and sodium citrate. This suggests that clotting factors, probably fibrinogen, interfered with the measurement of antibody titers. Therefore, only serum should be used in further investigations of THP antibody using this assay.
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PMID:Tamm-Horsfall protein antibody in patients with end-stage kidney disease. 739 72

The urographic nephrogram is an important indicator of underlying functional and structural renal disease. With expansions in use of cross-sectional imaging, the computed tomographic (CT) nephrogram (ie, contrast material enhancement within the renal parenchyma) has assumed a greater role in the evaluation of urinary tract disorders. Both quantitative and qualitative nephrographic abnormalities are well demonstrated by CT, including global or segmental absence or persistence of the nephrogram, slowed temporal progression, striated pattern, and rim pattern. Global absence is nearly always unilateral and is most often seen with blunt abdominal trauma with renal pedicle injury. Segmental absence is attributable to focal renal infarction, most likely due to arterial emboli. Global persistence, which is much more common than segmental persistence, may be unilateral (caused by renal artery stenosis, renal vein thrombosis, or urinary tract obstruction) or bilateral (due to systemic hypotension, intratubular obstruction, or abnormalities in tubular function). Striated nephrograms may be unilateral or bilateral and are caused by ureteric obstruction, acute pyelonephritis, contusion, renal vein thrombosis, tubular obstruction, hypotension, and autosomal recessive polycystic kidney disease. The rim pattern is most often associated with renal infarction and occasionally with acute tubular necrosis and renal vein thrombosis. Careful evaluation of the CT nephrogram is an integral part of the abdominal CT examination.
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PMID:The CT nephrogram: implications for evaluation of urinary tract disease. 750 51

This study was carried out to determine the prevalence of hepatitis C virus (HCV) antibodies and the epidemiologic factors associated with HCV infection in patients with chronic renal failure before the onset of ESRD. Sex, age, type of renal disease, level of renal function, and history of blood transfusions and invasive procedures were analyzed in 226 patients with renal disease, compared with a population of 1,244 normal subjects and 124 patients with impaired immunity (patients having autoimmune diseases and receiving chemotherapy treatment). Eighteen seropositive patients with renal disease (prevalence, 7.9%) were found, which was significantly higher than the prevalence in the normal population (1.03% in blood donors, 0.98% in pregnant women; P < 0.001, chi 2). There was no significant association of sex, number of blood transfusions, or history of invasive procedures with the presence of HCV antibodies. The prevalence of HCV antibodies was higher (16.6%) in patients with glomerulonephritis compared with patients diagnosed with interstitial nephritis, pyelonephritis, nephrosclerosis, diabetes mellitus, polycystic kidney, and miscellaneous renal diseases (P < 0.01, chi 2). There was a higher prevalence of HCV antibodies in patients with creatinine clearance lower than 30 mL/min (13%) compared with patients with creatinine clearance higher than 30 mL/min (2.7%) (P < 0.01, chi 2). These data suggest that HCV infection may be associated with the pathogenesis of glomerulonephritis. Alternatively, glomerulonephritis or severe renal insufficiency may increase the likelihood of HCV infection.
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PMID:Epidemiology of hepatitis C virus infection in patients with renal disease. 752 63

During the past decade, experimental and clinical evidence has indicated an important role for the renin-angiotensin system in the progressive destruction of nephrons in a wide variety of chronic renal diseases. Studies have indicated that in the subtotally nephrectomized rat model of progressive glomerulosclerosis, in experimental diabetes mellitus, in the chronic phase of puromycin aminonucleoside-induced nephrotic syndrome and in Heymann's nephritis, angiotensin-converting enzyme (ACE) inhibitors dramatically preserve both nephron structure and function. Clinical studies have similarly noted that chronic administration of ACE inhibitors inhibits progression of renal failure in type I diabetes and type II diabetes as well as primary glomerulopathies, sickle cell nephropathy, systemic lupus erythematosis, chronic pyelonephritis and adult polycystic kidney disease. Current evidence suggests that the beneficial effect of ACE inhibitors is primarily due to inhibition of angiotensin II production, and there is strong suggestive evidence for increases in local intrarenal activation of the renin-angiotensin system in these conditions. In obstructive uropathy, activation of the renin-angiotensin system has also been shown to be an important aspect of the early functional changes and may be of importance in the subsequent generation of interstitial fibrosis. In the obstructed kidney, renin and angiotensinogen production increase and type I angiotensin receptors decrease. Inhibitors of angiotensin II production and angiotensin II action partially reverse the vasoconstriction and the reduced renal blood flow, and abolish the changes in expression of AT1 MRNA induced by obstruction. Studies suggest that the angiotensin-mediated increases in tubulointerstitial fibrosis may be mediated by increased production of transforming growth factor-beta.
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PMID:Angiotensin II-mediated renal injury. 756 81


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