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

Psychosocially stressed male mice competing in a Henry-Stephens complex population cage develop hypertension, cardiovascular damage, and chronic interstitial nephritis. Their plasma renin, noradrenaline, corticosterone, and adrenal-catecholamine synthetic enzymes are increased and they die prematurely. Adding 3.3 mg of caffeine a day per kilogram of mouse body weight (the equivalent of 20 micrograms/ml decaffeinated coffee) to their drinking water significantly intensifies most of these changes. A dose of 90 mg/kg of caffeine (the equivalent of 560 micrograms/ml, i.e., brewed tea or coffee) further increases the effects. The drug-induced enhancement of competitive social stimulation of the neuroendocrine system resulted in a further increase of plasma renin and corticosterone levels as well as blood pressure and adrenal weight. These effects together with accelerated mortality and increased pathology indicate that chronic consumption of caffeinated liquids adds to the risks of psychosocial stress.
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PMID:Caffeine as an intensifier of stress-induced hormonal and pathophysiologic changes in mice. 700

1. A double-blind crossover trial comparing the antihypertensive effect of tienilic acid and hydrochlorothiazide was conducted in thirty-eight patients with mild to moderate hypertension. 2. Tienilic acid was shown to be as effective as hydrochlorothiazide in controlling blood pressure. 3. Tienilic acid acid significantly lowered serum uric acid levels compared with both placebo and hydrochlorothiazide. 4. Tienilic acid was generally well tolerated but one patient developed acute renal failure due to acute allergic interstitial nephritis whilst taking the drug.
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PMID:Tienilic acid in the treatment of mild to moderate hypertension. 700 78

The renal biopsy technique has made it possible to classify lupus nephritis into its varied forms. Utilizing light histology, immunofluorescence microscopy, and ultrastructural techniques, the following renal morphological manifestations of systemic lupus erythematosus can be identified: mesangial abnormalities; focal proliferative, diffuse proliferative and membranous glomerulonephritis; glomerular sclerosis; interstitial nephritis; vascular sclerosis and necrotizing renal vasculitis. Each of the morphological forms is associated with distinctive clinical features and prognosis. Mesangial and focal proliferative lupus nephritis may occur in the absence of clinical abnormalities, and in general have a favorable prognosis. Diffuse proliferative lupus nephritis often is manifested by the nephrotic syndrome and renal functional impairment which proves to be irreversible and progressive. Transition from the milder forms to diffuse proliferation occurs in about one-sixth of patients. Membranous lupus nephritis is characterized by the nephrotic syndrome, which often is persistent, but renal functional impairment develops slowly and is rarely severe. Necrotizing vasculitis, which supervenes on occasion during the course of diffuse proliferative lupus nephritis, produces the clinical picture of malignant hypertension and progresses rapidly to uremia. Interstitial nephritis usually occurs in combination with one of the glomerular forms, but at times may be the predominant renal lesion both morphologically and clinically. Glomerular sclerosis, often associated with hypertension and vascular sclerosis, commonly develops in the course of lupus nephritis, especially in the more severe forms, and may progress even though active disease has remitted. An awareness of clinico-pathologic correlations in lupus nephritis provides a basis for intelligent management and critical assessment of therapy.
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PMID:Clinical usefulness of the morphological classification of lupus nephritis. 710 64

A history of ingestion of large quantities of analgesics in patients having clinical and radiographic features of chronic interstitial nephritis leads to the diagnosis of analgesic nephropathy. In analgesic nephropathy the renal damage possibly occurs from a high concentration of analgesics and/or their metabolites. Since urinary concentrations of analgesics and their metabolites are also high, urinary bladder wall may be similarly damaged. Bladder urothelium was examined in 20 patients. Ten control patients with uremia, hypertension, or bladder neck obstruction showed normal histology. Two of the 5 patients with analgesic nephropathy had brownish pigmentation of bladder. All 5 analgesic nephropathy patients showed chronic inflammation similar to that found in 5 patients with bacterial infections. It is suggested that pigmentation of bladder wall and/or chronic inflammation of bladder mucosa of unknown etiology when found in a patient with chronic interstitial nephritis, would support the diagnosis of analgesic nephropathy.
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PMID:Bladder urothelium in nephropathy associated with analgesics. 740 25

Six members of kindred with only one surviving male in three generations, a history of an unusual combination of precocious gout in a girl of nine and rapidly progressive renal disease in young women, have been investigated. Sensitive indicators of the familial defect were the early development of hyperuricemia, an inability to concentrate the urine, and a patchy non-specific interstitial nephritis at biopsy. All these features were disproportionately severe for the young age and sex of affected subjects, and the relatively moderate reduction of GFR in some. Identification of these characteristics enabled the recognition of an early stage of the disease in one young family member whose renal function had previously been normal. The histopathology of the renal lesion in this normotensive teenage girl was similar to that frequently attributed to ageing or hypertension in the archetypal middle-aged gouty male, indicating that neither age nor vascular lesions are necessarily implicated in the latter. Allopurinol has halted further progression of the renal lesion in this young girl over two years. It is thus possible that early diagnosis may benefit the subsequent clinical course and may be important since the number of such families in our experience suggests that precocious familial gout with renal failure is more prevalent than currently recognized.
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PMID:Familial gout and renal failure in young women. 742 92

High dosages of nephrotoxic drugs in elderly patients might be correlated with an increase in the number of patients with tubulo-interstitial nephritis (TIN). In patients with acute TIN, marked fever, back or flank pain, CVA tenderness, skin rash, arthralgia, eosinophilia, and eosinouria are observed. Clinical symptoms might be induced by glomerular, proximal tubular or distal tubular dysfunction in chronic TIN. Mild to moderate proteinuria, edema, hypertension, azotemia, glucosuria, aminoaciduria, polyuria and polydipsia are characteristic findings in patients with chronic TIN. These findings are slowly progressive in such patients. It appears that the marked fibrosis with lymphocyte infiltration in the interstitium is a poor clinical marker in patients with TIN. Furthermore, it is important to differentiate TIN from glomerulonephritis.
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PMID:[Symptoms in patients with tubulo-interstitial nephritis]. 756 29

Hereditary interstitial nephritides are a heterogeneous group of disorders comprising medullary cystic disease, several varieties of Alport's syndrome and also one familial disorder with a distinct clinical syndrome and without characteristic ultrastructural glomerular basement membrane changes. Our family consisted of 11 members, 5 of which presented with renal dysfunction of varying degrees. Clinically, the affected siblings presented with long-standing hypertension, minimal proteinuria and no hematuria. All known causes of a secondary diffuse interstitial nephritis, Alport's syndrome and medullary cystic disease have been excluded. An HLA association is suggested between the affected and unaffected members of the family. Renal biopsy subsequently showed the typical features of a chronic interstitial nephritis without basement membrane changes.
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PMID:Hereditary interstitial nephritis without basement membrane changes. 777 6

Virtually all diseases affecting the native kidney recur in the kidney transplant with the exception of Alport syndrome, polycystic kidney disease, hypertension, chronic pyelonephritis, and chronic interstitial nephritis. Fortunately, in the majority of patients, recurrence of the original disease has minimal clinical impact, with only approximately 5% of all graft loss occurring as a result of recurrent disease. The primary renal diseases that commonly recur include membranoproliferative glomerulonephritis type II, IgA nephropathy, and focal and segmental glomerular sclerosis. The most common systemic disease that recurs is diabetic nephropathy. Living-related transplantation should be used with caution in patients with the hemolytic uremic syndrome, recurrent focal and segmental glomerular sclerosis, and membraneous glomerulonephritis. Fabry disease and primary hyperoxaluria type I are no longer absolute contraindications to kidney transplantation.
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PMID:Recurrent diseases in the kidney transplant. 802 19

Microscopic haematuria is a common clinical finding, with reported prevalences of up to 22%. The role of renal biopsy in the investigation of this condition is still debated. Currently urological investigation including cystourethroscopy is often regarded as adequate. We investigated 165 patients (94 male, 71 female; mean age 37.5 years, range 10-71) referred with isolated microscopic haematuria, using renal biopsy and cystourethroscopy. All patients were normotensive with normal serum creatinine, no proteinuria, sterile urine and a normal IVU. Renal biopsy abnormalities were found in 77/165 (46.6%): IgA nephropathy (49), global or segmental mesangial proliferative glomerulonephritis without IgA deposits (16), thin membrane nephropathy (7), vascular changes suggestive of hypertension (3), interstitial nephritis (1), and membranous nephropathy (1). Only five abnormalities were found on cystourethroscopy (cystitis 3, urethral stricture 1, bladder stone 1). Two patients with cystitis also had IgA nephropathy. Biopsy abnormalities were commonest under the age of 20 (69.2%), but 40% of biopsies were abnormal even in the seventh decade of life. Because renal biopsy abnormalities are very frequent in patients with isolated haematuria, renal biopsy is indicated in patients over 45 years of age if renal imaging and cystoscopy are normal. In those under 45 years, renal biopsy should replace cystoscopy as the investigation to follow normal renal imaging.
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PMID:Glomerular disease as a cause of isolated microscopic haematuria. 795 7

Reduced renal length is widely used to diagnose chronicity in patients with renal impairment. A length of 9 cm or less measured ultrasonographically is considered to indicate irreversible disease. However, some patients with normal renal length have thin parenchyma. The aim of this study was to determine the relationship between ultrasonographically measured parenchymal thickness and renal length and to correlate parenchymal thickness with the histology obtained at renal biopsy. Sixty-four patients, aged 16-74 years, who had had a renal biopsy were evaluated retrospectively. Histology was considered in five categories: I, interstitial nephritis (n = 13); II, glomerulonephritis (28); III, diabetes mellitus/metabolic/other (8); IV, chronic renal disease (CRD) (11); V, hypertension/vascular disease (4). There was a good linear correlation between renal length and renal parenchymal thickness (r = 0.64, P < 0.001). Both were reduced most in patients with CRD. Sixty-four per cent of patients with CRD had renal parenchymal thickness 1.5 cm or less, compared to 38% in group I, 25% in groups II and V, and 7% in group II. Although 11/37 (30%) of patients whose serum creatinine had increased 3 months post-biopsy had parenchymal thickness 1.5 cm or less, so did 6/27 (23%) whose creatinine decreased. Like renal length, parenchymal thickness gives an indication of the chronicity of renal failure. However, some patients with parenchymal thickness 1.5 cm or less still have potential for improvement. This measurement alone should not be used to obviate renal biopsy.
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PMID:What is the value of measuring renal parenchymal thickness before renal biopsy? 829 31


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