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)

Whether chronic interstitial nephritis (pyelonephritis) mainly results from kidney infection is widely debated. We studies 101 patients with interstitial nephritis, selected from 320 patients with newly diagnosed chronic renal disease, for frequency of etiological factors. Eleven had no etiologic factor(s) identified; 89 had clearcut factor(s): anatomic abnormalities 31, analgesic abuse 20, hyperuricemia 11, nephrosclerosis 10, stones 9, sickle cell disease1, tuberculosis 1, multiple causes7. Bacterial infection (present in 27%) was found only with another preceding primary cause of renal damage. Analgesic abusers frequently denied drug ingestion; 15% had urinary tract infection and 20% classical papillary necrosis. Two had family histories of analgesic abuse with nephropathy. We conclude that interstitial nephritis is a common form of chronic renal disease, is seldom idiopathic, rarely results from bacterial infection alone in adults, and frequently results from analgesic abuse in the United States.
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PMID:Chronic interstitial nephritis: etiologic factors. 111 62

Survival after serum creatinine exceeded 10.0 mg/100 ml was increased if one peritoneal dialysis was performed. After one peritoneal dialysis 'survival' of 62 patients to the present time, death or the next dialysis averaged 119 days; median survival was 28 days. Characteristics of prolonged survivors were persistent reduction of serum creatinine below the predialysis concentration, tubulointerstitial diseases, i.e. polycystic kidneys, pyelonephritis or obstructive nephropathy, potentially reversibel complications such as urinary tract infection or extracellular volume depletion, and high urine volume, and low blood pressure. Occasional pateints with survival exceeding 2 years suggest the possibility of prolonged benefit after a single dialysis at least in those wiht characteristics favoring longer survival.
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PMID:Prognosis of chronic renal failure. III. Survival after one peritoneal dialysis. 112 60

Thirty-three patients seen in a urological department had taken large doses of analgesic for prolonged periods of time. In 9 cases a diagnosis of pyramidal necrosis was established, while 4 other had pyelographic evidence of pyelonephritis, and analgesic abuse was probably an important aetiological factor in their renal condition. Analgesic nephropathy is easily overlooked unless patients are questioned routinely regarding their intake of analgesic. It is important to identify the group of patients without evidence of serious renal disease who are taking excessive quantities of analgesic and to urge them to abandon the practice.
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PMID:Analgesic abuse in urological practice. 113 8

Following acceptance to a renal dialysis therapy program, 13 patients underwent serial examination of the serum complement system for periods of 6 to 12 months. Serum levels of C3 and C4 were examined at monthly intervals before the first dialysis of each month. The patients suffered from various primary renal diseases, including glomerulonephritis, obstructive uropathy with chronic pyelonephritis, nephrosclerosis and chronic nephropathy of undetermined nature. Levels of serum C3 were depressed at some time during the study period in all patients. Serum C4 levels were normal. The depression of serum C3 levels was significant and prolonged in nine patients. There seemed to be no relationship between the nature of the basic disease and the depression of serum C3 levels. Caution should be exercised in attributing depressed C3 levels to a particular type of underlying renal disease in patients on renal dialysis.
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PMID:Levels of serum complement components in patients undergoing renal dialysis. 114 Sep 50

After serum creatinine levels exceeded 10mg/100ml, median survival was 55 days (to death or dialysis) in a group of 112 patients with chronic renal disease. Renal failure was partially reversible in 29 patients, partially accounting for prolonged survival. Those with polycystic kidneys, pyelonephritis, or obstructive nephropathy survived longer,partially because of more frequent reversibility and a slower increase in serum creatinine concentration. Kiabetic nephropathy, myelomatous kidneys, and amyloidosis were associated with shorter survival, less frequent reversibility, and more rapid progression. Urinary infection and extracellular volume depletion often accounted for partially reversible renal failure and prolonged survival. Blood pressure and age were not prognostic variables, while coexistent heart failure shortened survival. Survival correlated significantly with sodium excretion.
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PMID:Prognosis of chronic renal failure. II. Factors affecting survival. 114 31

Fourteen patients with severe hypertension have been given i.v. diazoxide in a dosage of 5 mg/kg b.wt. The material comprised 2 patients with malignant nephrosclerosis, 4 with chronic nephropathy and severe reduction of renal function, 1 patient with chronic pyelonephritis, 1 with renovascular hypertension and 6 patients with essential hypertension and in malignant phase. All patients attained a controllable blood pressure. Eight patients remaining needed only one injection, while the remaining patients required 2-5 injections, and concomitant furosemide therapy. The retinopathy improved in most patients and renal function was unchanged in the azotemic patients. No serious adverse effects were seen, except one hypotensive episode. Diazoxide is easy to handle, dosage can be predetermined, monitoring is simple and we find diazoxide to be a valuable drug in severe hypertension.
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PMID:Diazoxide in the management of severe hypertension. 119 11

Renal function studies were performed in 524 gouty subjects, including follow-up studies at intervals up to 12 years in 112 of them. In 49 subjects, the glomerular filtration rate was less than 70 ml/min and Curate:glomerular filtration rate ratio tended to rise as the glomerular filtration rate decreased, reflecting a relatively stable urate excretion over varying filtered urate loads. The increment in Tsurate:glomerular filtration rate was small with spontaneous Purate between 7 and 9 mg/100 ml. It was modest with Purate up to 10 mg/100 ml. The increment in Tsurate:glomerular filtration rate became much higher beyond Purate of 10 mg/100 ml. Urinary urate levels above 800 mug/min, designated as excess urate excretion, occurred more commonly in subjects with Purate above 9 mg/100 ml, and with better preserved renal function. Tophi were more frequently observed in subjects with low glomerular filtration rate and proteinuria; but incidence of urolithiasis seemed to be less affected by a decrease in the glomerular filtration rate. Hyperuricemia alone had no deleterious effect on renal function as evidenced by follow-up studies over periods up to 12 years. Deterioration of renal function was largely associated with aging, renal vascular disease, renal calculi with pyelonephritis or independently occurring nephropathy. In only very few instances was diminished renal function ascribable to gout alone.
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PMID:Renal function in gout. IV. An analysis of 524 gouty subjects including long-term follow-up studies. 120 33

The diagnosis of hydronephrosis is made by excretory urography with late films and retrograde pyelography. Renal arteriography in hydronephrosis permits exact evaluation of vascular supply and parenchymal thickness. In three cases selective arteriography was performed because of a non-functioning kidney or suspected space-occupying lesion. The combination of arteriogram and urogram--if necessary together with percutaneous puncture--allows to differentiate between hydronephrosis, avascular tumors, renal cysts, polycystic renal disease, renal abscess, subcapsular renal hematoma, fibrolipomatosis, xanthogranulomatous pyelonephritis, and tuberculosis.
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PMID:[Angiographic differential diagnosis of hydronephrosis (author's transl)]. 120 46

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
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PMID:Vesicoureteral reflux and pyelonephritis in the monkey: a review. 143 97

A case-control study was undertaken to investigate the possible role of chronic hydrocarbon exposure and tobacco and alcohol consumption in the causation of primary glomerulonephritis. Exposure to hydrocarbons and the consumption of tobacco and alcohol were assessed blindly by telephone interview and questionnaire in 55 patients with end-stage renal disease due to biopsy-proven primary glomerulonephritis in whom there had been no evidence of systemic disease. This was compared with 55 normal subjects matched for age, sex, social class and residential area and a comparable internal control group of 45 patients with end-stage renal disease secondary to systemic disease, diabetic nephropathy or chronic pyelonephritis. Hydrocarbon exposure scores derived from the results of the questionnaires were significantly higher (p < 0.001) in the patients with primary glomerulonephritis than in the normal subjects and the internal control group. Moreover, more detailed assessment of the type of hydrocarbon exposure showed significantly greater exposure of patients with glomerulonephritis to petroleum products (p < 0.001), greasing/degreasing agents (p < 0.01) and paints/glue (p < 0.05), and a resulting estimated relative risk of developing glomerulonephritis with each type of hydrocarbon exposure of 15.5, 5.3 and 2.0. Those patients with heavy hydrocarbon exposure (hydrocarbon score > 25,000) had a significantly higher serum creatinine at presentation than those with mild to moderate exposure, suggestive of more advanced renal disease. However, there was no significant difference in tobacco and alcohol consumption among subjects in different groups. We conclude that occupational exposure to hydrocarbon is likely to play a role in the pathogenesis of primary glomerulonephritis and that the risk of developing glomerulonephritis is greatest in those subjects exposed to petroleum products.
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PMID:Primary glomerulonephritis and hydrocarbon exposure: a case-control study and literature review. 143 76


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