Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report renal biopsy findings in 109 patients with unexplained renal impairment (serum creatinine greater than 0.15 mmol/l) and normal-sized non-obstructed kidneys. The most common histological lesions were interstitial nephritis, rapidly progressive glomerulonephritis and a variety of other types of glomerulonephritis. The groups could not be distinguished by the presence or absence of hypertension, haematuria, proteinuria, or features of systemic disease. However interstitial nephritis was found more frequently in patients presenting with one or none of these features and rapidly progressive glomerulonephritis in patients presenting with three or more. All four patients with none of these features had interstitial lesions. Fifty-two per cent of patients with interstitial nephritis improved and 60 per cent of the patients with rapidly progressive glomerulonephritis who received immunosuppressive treatment improved or remained stable with treatment. The benefits of a biopsy diagnosis were almost wholly confined to these two groups. Complications were recorded in nine patients - prolonged macroscopic haematuria in six and symptomatic perirenal haematomata in three. Six required blood transfusion. One required nephrectomy to control haemorrhage and subsequently died. Percutaneous renal biopsy is not without risk in patients with renal impairment but the benefits of diagnosing interstitial nephritis and rapidly progressive glomerulonephritis outweigh the disadvantages.
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PMID:Renal biopsy in patients with unexplained renal impairment and normal kidney size. 260 35

Triamterene (TA) is a mild 'potassium-sparing' diuretic usually employed in combination with other more potent diuretics in the treatment of hypertension. TA pharmacokinetics and pharmacodynamics in normal volunteers, elderly subjects and in patients with renal and hepatic dysfunction are reviewed. A variety of adverse renal effects, such as abnormalities in urinary sediment, nephrolithiasis, interstitial nephritis and acute renal failure, has been reported to occur and is also reviewed. Of particular concern with the increased availability of 'over-the-counter' nonsteroidal anti-inflammatory medications (NSAID) is the adverse interaction between TA and NSAID which may culminate in acute renal failure. Although a rare occurrence, the clinician should be aware of potential adverse reactions associated with the use of TA.
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PMID:Triamterene and the kidney. 266 34

Tubular functions and the state of renal parenchyma were evaluated in 45 patients with primary aldosteronism (PA) in order to assess morphological and functional characteristics of PA-associated endocrine nephropathy. Data on acid excretion and concentration activities were compared to morphologic findings in renal biopsy specimens, obtained at adrenalectomy. It is demonstrated that endocrine nephropathy may be manifested clinically in two ways: 1) increased secretion combined with a reversibly depressed maximum osmotic urinary concentration; and 2) persistent depression of both functions. The first variant can be seen in cases of high aldosteronemia, marked hypokalemia and recent disease. The morphological substrate of these disorders is hypokalemic tubulopathy, reflected in tubular epithelium vacuole dystrophy of varying degrees. The other variant is seen in cases of moderate aldosteronemia and hypokalemia and long duration of the disease, involving severe hypertension. The morphologic substrate of these tubular disorders is nephropathy with a marked tubulo-interstitial component (chronic tubulo-interstitial nephritis).
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PMID:[Morphofunctional characteristics of endocrine nephropathy in primary aldosteronism]. 267 77

Over a 15-year period we observed seven children (four girls, three boys) who presented within the first months of life with severe renal failure and acidosis, associated with hypertension in five patients and polyuria in four. In addition, one patient had a severe cholestatic liver disease. In two families, a similarly affected sibling had died previously. Four patients were referred with the clinical diagnosis of polycystic kidney disease because of moderate enlargement of kidneys, but renal imaging (intravenous pyelography and ultrasonography) did not confirm this diagnosis. A renal biopsy, performed in all patients, showed similar features characterized by a diffuse chronic tubulo-interstitial nephritis (TIN) and particularly by the presence of microcystic dilatation of proximal tubules and Bowman's space. Liver pathology was normal in two patients, including one with hepatomegaly. However, in the patient with cholestasis there was inflammatory portal fibrosis with mild duct proliferation. Progression of the renal disease was extremely rapid and all patients reached end-stage renal failure (ESRF) before the age of 2 years (11-22 months). Two children had successful renal transplants. Although this chronic TIN shares some features with nephronophthisis, we suggest that it represents a distinct entity both on clinical and morphological grounds. The specific clinical features of this disease are its early onset and rapid progression to ESRF. Pathologically, it differs from nephronophthisis by the absence of medullary cysts and thickened tubular basement membranes and by the presence of cortical microcysts.
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PMID:Infantile chronic tubulo-interstitial nephritis with cortical microcysts: variant of nephronophthisis or new disease entity? 270 88

Host kidneys may contribute considerably to hypertension after renal transplantation. Their role in sustaining hypertension is more prominent if glomerulonephritis (GN) than if interstitial nephritis (IN) is the original renal disease. We compared the antihypertensive effect of beta-blockade in IN (n = 10) and GN (n = 19) hypertensive renal transplant recipients with host kidneys in situ with those who had undergone bilateral nephrectomy (BN, n = 10). Pretreatment blood pressures were comparable in BN, IN, and GN patients, being 165 +/- 6/108 +/- 3, 172 +/- 5/104 +/- 3, and 161 +/- 3/104 +/- 1, mmHg, respectively. Blood pressure did not change on beta-blockade in BN patients, whereas it decreased significantly more (P less than 0.001) in GN than in IN patients, changes of mean arterial pressure being -107 +/- 1.0, -14.9 +/- 1.3, and -6.8 +/- 1.6%, respectively. This failure to respond to beta-blockade in patients without host kidneys may be related to low activity of the renin-angiotensin system or to functional denervation of the grafted kidney. Further investigations of this phenomenon may clarify the mechanism of antihypertensive action of beta-blockade as well as the nature of hypertension after renal transplantation.
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PMID:Antihypertensive effect of beta blockade in renal transplant recipients with or without host kidneys. 290 May 64

The prevalence of hypertension was studied in renal transplant recipients followed for at least 1 year. Twenty-eight patients with a transplant renal artery stenosis, all with hypertension, were excluded from further study. Hypertension was present at 1 year after transplantation in 48.3% of 329 cadaveric renal graft recipients, treated with azathioprine. These hypertensive patients had experienced more rejection episodes. The prevalence of hypertension was higher in patients with (n = 237) than in those without (n = 92) host kidneys in situ (57.8% and 23.9% respectively, P less than 0.001). In patients with host kidney, the prevalence of hypertension was higher in patients with glomerulonephritis (n = 108) than in those in whom interstitial nephritis (n = 63) was the original renal disease (71.3% and 42.8 respectively, P less than 0.001). In 41 patients initially treated with cyclosporin and in 42 recipients of a kidney from a living donor, the prevalence of hypertension was not clearly lower than in the azathioprine-treated patients. In 30 patients without host-kidneys who did not experience acute rejections, only three had hypertension. In all three patients a specific cause for the hypertension was found. In hypertensive patients, blood pressure decreased gradually in the years following transplantation. In conclusion, besides transplant renal artery stenosis, the main determinants of the prevalence of hypertension after renal transplantation are host kidneys original renal disease, and rejection.
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PMID:Factors determining the prevalence of hypertension after renal transplantation. 311 Jun 95

The acute renal side-effects of nonsteroidal anti-inflammatory drugs are well documented. These include interstitial nephritis, hyperkalaemia, renal tubular acidosis, fluid retention, hypertension and nephrotic syndrome. The long-term effects are less well known. We have carried out a cross-sectional survey of an unselected out-patient population with definite or classical rheumatoid arthritis to determine the prevalence of renal problems in this group. Thirty-four patients (20%) were shown to have an abnormality as defined by our criteria but in the majority this was transient or had been previously recognised. Thirteen patients (8%) had a persistent unexplained abnormality but only 1 had merited renal biopsy using established criteria (Patient 1). We conclude that the long-term use of NSAID's is associated with relatively few renal side-effects.
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PMID:A survey of renal function in outpatients with rheumatoid arthritis. 326 30

A 51-year-old man with diabetes mellitus and mild hypertension developed acute interstitial nephritis 4 days after starting a course of co-trimoxazole for bronchopneumonia. Following initial symptoms of overt hypersensitivity, he developed azotemia and renal tubular dysfunction with malaise and anorexia requiring hospitalization. Renal pathology demonstrated an acute granulomatous interstitial nephritis superimposed on chronic diabetic renal disease.
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PMID:Acute granulomatous interstitial nephritis due to co-trimoxazole. 326 85

Non-steroidal anti-inflammatory drugs (NSAIDs) may produce acute renal failure, papillary necrosis and interstitial nephritis. These adverse drug reactions are rare but have been reported in patients with congestive heart failure, cirrhosis, renal parenchymal disease, lupus nephritis and hypertension. All these conditions may be associated with hypovolaemia and an activated renin-angiotensin system, when renal blood flow and glomerular filtration depend on local renal prostaglandin biosynthesis. A severe impairment of renal function may occur when this synthesis is inhibited by NSAID treatment. It is possible that 1 in 100 of elderly patients have renal parenchymal disease, 1 in 100 arteriolar nephrosclerosis, 1 in 200 unilateral or bilateral renal artery stenosis and an unknown number suffer from atheroembolic renal disease. Fortunately, only a small proportion of 'at risk' patients given NSAIDs appear to develop renal failure. Perhaps bilateral renal disease or salt depletion are necessary factors? Whatever the explanation, NSAIDs should be used with caution in the elderly.
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PMID:Pharmaco-epidemiological considerations in patients with arthritis and vascular disease of the kidney. 349 36

The origin of free cells in urine is difficult to determine in the absence of cellular casts. Using fluorescein-conjugated antibody to human Tamm-Horsfall protein (THP), it was demonstrated that some free cells in urine are coated with THP. To evaluate the usefulness of this observation in the differentiation of upper from lower urinary tract disease, the presence of THP coating of cells was correlated with the clinical diagnosis in 141 subjects. The percentage of THP-coated cells for each group (mean +/- SD) was Healthy volunteers (n = 10), 4% +/- 2%; hospitalized controls (n = 20), 3% +/- 3%; glomerulonephritis (n = 21), 61% +/- 6%; chronic interstitial nephritis (n = 26), 56% +/- 5%; other renal parenchymal diseases (n = 14), 50% +/- 8%; bladder disease (n = 14), 8% +/- 2%; and hypertension (n = 36), 24% +/- 33%. Based on the results from the bladder disease group, 12% coating was set as the 95% confidence limit for lower urinary tract disease. The results in this group were not different from control subjects. By analysis of variance and chi 2 analysis, subjects with renal parenchymal disease could be distinguished from those with hypertension and bladder disease (P less than .001 and P less than .0001, respectively). The presence of cellular coating by THP in renal parenchymal disease and its absence in bladder disease suggests that this simple test may be of use in determining the origin of free cells observed in the routine microscopic urinalysis.
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PMID:Tamm-Horsfall protein coating of free cells in urine. 354 23


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