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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a consecutive series of 88 cases of carcinoma of the kidney and upper urinary tract seen at one hospital, 31 had malignant urothelial tumours of the renal pelvis or ureter. Forty-two per cent of these transitional-cell carcinomas occurred in patients with renal papillary necrosis following upon prolonged and heavy analgesic ingestion. Other possible aetiological factors were heavy cigarette smoking (61% of cases), long standing urinary obstruction or infection (23%) and possible occupational exposure (6%); in only four cases (13%) was there no identifiable aetiological factor. Those cases with analgesic nephropathy were characterised by renal functional impairment, hypertension and interstitial nephritis, but there was no difference in the clinical behaviour or pathological appearances of the tumours in the two groups. The clinical and experimental evidence that certain metabolites of phenacetin are carcinogenic is reviewed.
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PMID:Analgesic abuse, renal parenchymal disease and carcinoma of the kidney or ureter. 27 65

"Outpatient hyperkalemia" is a new clinical syndrome in which high serum potassium levels (SK) are found in the outpatient condition returning toward normal without any specific treatment after admission to the hospital. We report here of six patients with high blood pressure of various origin (chronic glomerulonephritis, interstitial nephritis, diabetic nephropathy, Gordon syndrome) in whom dietary and postural factors were found to be responsible for the outpatient hyperkalemia. The Na content of the "ad libitum" outpatient diet was definitely higher than that of the regular hospital diet. Increasing the Na intake from 120 mEq to 300 mEq induced a marked elevation of SK (from 5.21 +/- 0.16 to 6.34 +/- 0.40 mEq/l; p less than 0.001) in two hospitalized, recombent patients. On the other hand, Na restriction induced a dramatic improvement in hyperkalemia (from 5.89 +/- 0.11 mEq/l to 4.79 +/- 0.08 mEq/l:; p less than 0.001) in 4 patients in whom the effect was studied in the outpatient state. Although the mean plasma aldosterone (PA) was significantly lower in the patient group than in the healthy group, during normal Na intake there was a considerable overlap. A clearer distintion was made by using the new index of PA per SK ratio expressing the diminution in the apparently normal PA when related to the abnormally high SK. During high Na intake, PA was definitely suppressed and during Na restriction there was a dramatic relief from suppression. The present studies confirmed the previously described phenomenon of "upright hyperkalemia" which may have played an additional role in the development of outpatient elevation of SK. The knowledge of the clinical syndrome of "outpatient hyperkalemia" may be important to single out certain cases of easily correctable insufficient (suppressed) aldosterone production.
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PMID:"Outpatient hyperkalemia" syndrome in renal and hypertensive patients with suppressed aldosterone production. 28 14

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
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PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.
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PMID:Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections. 97 63

The rare occurrence of lead nephropathy in widely differing circumstances has suggested that additional causative factors might be required for its production. Seventeen cases of interstitial nephritis associated with severe chronic lead poisoning were reviewed in an attempt to identify these. Data suggested that alcoholism and preexistent hypertension, and also previous or minor urinary tract disease, may potentiate the injurious effects of lead. We recommend that the diagnosis of lead nephropathy should be a positive one, not one of exclusion, and that stored lead should be removed, particularly in persons with hypertension or previous urinary tract diseases.
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PMID:Etiologic factors in lead nephropathy. 101 39

Because of epidemiological, clinical, pathomorphological, and etiological criteria the Balkan-nephropathy is suggested to be a particular form of chronic interstitial nephritis with super-imposed pyelonephritis in about 30 p.c. of the patients. A basic scheme illustrates the origin and the development of the endemia as well as etiology and clinical course of the disease. Another scheme shows pathogenesis and pathomorphogenesis of the nephritis. This analysis about the characteristics of the endemic Balkan-nephropathy allows for the clarification of the triad: endemic occurrance, familial susceptibility, and mosaik like morbidity. The following important aspects of the disease are given: rarely occuring hypertension, facultative leukuria, and bacteriuria, smooth nephrocirrhosis. Prophylactic and therapeutic prospects are given.
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PMID:[Balkan-nephropathy, a particular form of interstitial nephritis (author's transl)]. 109 38

Prolonged ingestion of mixed analgesics containing phenacetin has been associated significantly with the development of a chronic interstitial nephritis frequently associated with papillary necrosis. This disease is frequently underdiagnosed. If an adequate history of headache and/or backache (of which most of these patients complain) is not taken, the central causative effect of phenacetin ingestion may never be appreciated. Laboratory tests show the usual abnormalities seen in any form of chronic interstitial nephritis such as poor urinary concentration, renal failure with large urine output, and no hypertension. Papillary necrosis is helpful but not pathognomonic. The type of medications ingested appears to be changing to prescription compounds. The with significant improvement in renal function.
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PMID:Phenacetin nephritis. 114 22

To define interstitial nephritis without preselection bias, 25 consecutive renal biopsy specimens from patients with tubular damage, interstitial damage and interstitial inflammation were analyzed in detail. In four patients (all with acute renal failure), tubulitis, and interstitial eosinophil and lymphocyte infiltration were found, but no glomerular abnormalities. In four others, the findings were similar but some glomerular abnormalities were noted. Two patients had probable healed interstitial nephritis. The clinical presentation varied from transient renal insufficincy to oliguric renal failure. Three of the patients with glomerular abnormalities had significant proteinuria. When the 10 patients with interstitial nephritis were compared with the other 15 serving as controls, striking features in the former group were skin rash, eosinophilia, the absence of hypertension and the frequency of administration of penicillin and its analogs. Serum immunoglobulin E (IgE) levels were elevated in three of the patients. The striking eosinophilia, interstitial eosinophil infiltration and increased IgE levels suggest that allergen-reaginic complexes may be involved in the pathogenesis of the lesion.
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PMID:Acute interstitial nephritis. A clinical and pathologic study based on renal biopsies. 120 34

Renal artery aneurysms were diagnosed in 11 patients (9 boys) aged 1 to 14. The examinations were carried out for vasorenal hypertension in 4 cases, for bladder-ureter reflux, hematuria, nephroptosis in 4, ureterohydronephrosis in 2 cases, and for interstitial nephritis. Aneurysms of the major trunk of the renal artery, mostly oval-shaped, 11 x 14 to 25 x 28 mm in size, were detected in 4 patients, intrarenal aneurysms 2 x 3 to 5 x 6 mm in size in 7 cases. The share of aneurysms among uronephrologic conditions in children was found to be 1.54%, among vasorenal hypertension cases, 4.3%. Vasorenal hypertension is the main optional sign of aneurysms of the main trunk of the renal artery, whereas for intrarenal aneurysms such sign is hematuria.
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PMID:[Renal artery aneurysms in children]. 130 2

Dipeptidyl peptidase IV (EC 3.4.14.5) and angiotensinase A (EC 4.4.11.7) were purified to homogeneity from pooled urine concentrate of patients with renal damage, using ultrafiltration, ammonium sulphate precipitation, lectin affinity chromatography, FPLC-ion-exchange(Mono-Q-)chromatography, and FPLC-gel filtration (Superdex). Based on the specific enzyme activity of the starting material, dipeptidyl peptidase IV was enriched 1629 fold, angiotensinase A 1183 fold. The relative molecular masses, Michaelis constants and isoelectric points were determined. Negative staining of the purified enzymes revealed globular proteins (5-7 nm). Antisera raised against dipeptidyl peptidase IV and angiotensinase A reacted specifically with tubular and, in the case of anti-angiotensinase A sera, with tubular and glomerular structures. In addition, urinary membrane vesicles of proximal tubule origin were eluted with the void volume (Superdex-gel filtration), indicating heavy epithelial cell disintegration. Both soluble tissue enzymes (dipeptidyl peptidase IV, angiotensinase A) and vacuolar blebs shed from epithelia contribute to proteinuria, as was shown in patients with glomerulonephritis, interstitial nephritis, diabetic nephropathy and, for angiotensinase A, in patients with essential arterial hypertension.
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PMID:Biochemical and immunological properties of urinary angiotensinase A and dipeptidylaminopeptidase IV. Their use as markers in patients with renal cell injury. 136 94


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