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

Analgesic nephropathy, its morphology, development and pathogenesis are described. The earliest analgesic-caused lesion is capillary sclerosis of the urinary tract mucosa. Later focal necroses can be found in the papillae surrounding the collecting ducts. Foci of necrosis progress and become confluent, resulting in complete papillary necrosis. Later renal cortical lesions develop due to retained areas of papillary necrosis. The cortical changes include chronic interstitial nephritis with cortical atrophy in the suprapapillary region as well as hypertrophy of the columnae Bertini with segmental, focal glomerulosclerosis. The analgesic-related lesions are the result of toxic damage to endothelial, tubular and interstitial cells. Analgesic-induced kidney and urinary tract changes are quite specific. Frequent complications include hypertension, pyelonephritis, hydro- or pyonephrosis and urinary tract tumors. The clinical picture is characterized by the consequences of distal tubular damage: impairment of urine concentrating capacity, acidosis, electrolyte loss. Analgesic nephropathy is an example of an absolutely preventable drug induced nephropathy. It is the most important single manifestation of the analgesic syndrome. It is recommended that prescriptions for mixed analgesics (multi-component analgesics) should be made obligatory. Monocomponent analgesics could be sold over-the-counter.
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PMID:[Analgesic nephropathy]. 355 93

An 18-month-old girl presenting with anorexia and failure to thrive, was referred for adenoidectomy. Arterial hypertension was discovered on physical examination. Laboratory results revealed hyperkalaemic, hyperchloraemic, metabolic acidosis, with slight azotemia. Urinary aldosterone excretion and plasma renin were decreased. Renal biopsy showed idiopathic interstitial nephritis. The diagnosis of type 4 renal tubular acidosis, sub-type 2, i.e. primary hyporeninaemic secondary hypoaldosteronism was proposed. According to our knowledge, this disease has not previously been reported in young children, but is well known in azotaemic adults. We therefore propose the inclusion of this uncommon renal disease in the differential diagnosis of failure to thrive in childhood.
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PMID:Type 4 renal tubular acidosis (sub-type 2) associated with idiopathic interstitial nephritis. 355 88

In the present study, the frequency and the mechanism of hypertension associated with unilateral hydronephrosis (UHY) were investigated in 115 patients. Hypertension (blood pressure greater than 140/90 mm Hg) was found in 20% of 101 consecutive patients with UHY. Twenty-six patients with UHY and hypertension were followed for 35 months and the effect of surgery on blood pressure was analyzed. Blood pressure fell from 178 +/- 4/108 +/- 4 to 135 +/- 2/84 +/- 2 mm Hg after surgery. Hypertension was cured in 62%, improved in 19% and unchanged in 19%. In 73% of the cured patients the PRA-ratio was greater than or equal to 1.5, while all unchanged patients had a value of less than 1.5. Hypertensive patients were significantly older than normotensive patients, but did not differ in kidney function, underlying cause of hydronephrosis, incidence of urinary tract infection or frequency of interstitial nephritis. We conclude that in UHY the incidence of hypertension is not particularly high. However, in a substantial number of patients, high blood pressure is reversible by surgery. In most of these patients the renin-angiotensin-aldosterone system seems to play an important role in sustaining high blood pressure, although in some patients other mechanisms might be operative as well. Since the overall incidence of hypertension is not particularly high in UHY, this secondary form of hypertension appears to be rare.
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PMID:Unilateral hydronephrosis and hypertension: cause or coincidence? 355 76

We reviewed our 10-year experience with neonatal hypertension. Fifty-three cases were identified, which represented 0.7% of all neonatal tertiary care admissions. Causes were identified in 23 (43%) neonates. These included acute tubular necrosis (n = 7), renal vascular abnormalities (n = 8), renal structural abnormalities (n = 4), interstitial nephritis (n = 2), and coarctation of the aorta (n = 2). No cause was identified in 30 (57%) infants. If the two neonates with coarctation are excluded, infants who had normal urinalyses, blood urea nitrogen (BUN), serum creatinine and plasma renin activity (PRA), had non-malignant hypertension that tended to be short-lived and always resolved spontaneously. In contrast, a cause of hypertension was found in 68% of those having an abnormal urinalysis, BUN, serum creatinine or PRA. There were two hypertensive deaths in this group. While the hypertension was usually more prolonged, it still generally resolved spontaneously by 1 year of age or following corrective surgery. Our experience indicates that diagnostic studies can be postponed if the urinalysis, BUN, serum creatinine and PRA are normal and if coarctation of the aorta has been excluded. If these preliminary studies are abnormal, however, a renal cause is likely and further studies are indicated.
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PMID:Hypertension in the first month of life. 379 27

Based on the clinico-laboratory and intravital morphological examination of 104 patients and the reported data the authors recognize 6 versions of chronic tubulo-interstitial nephritis (TIN): idiopathic, drug-induced, dysplastic, dysmetabolic, secondary TIN associated with primary glomerulopathies and vasorenal hypertension, secondary TIN in the presence of a long-term ischemia. Discuss the features of each form, diagnostic criteria, a possible importance of TIN for the development of arterial hypertension. Emphasize the importance of recognizing TIN in patients with primary glomerulopathies to early specify the causes of the deterioration of the disease course. Discuss the problems of therapy.
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PMID:[Chronic tubulointerstitial nephritis (structure, pathogenesis, clinical picture and morphology)]. 407 8

Seven cases of acute renal failure consecutive to haemorrhagic fever with renal syndrome (HFRS) due to the Hantaan virus or to a serologically related virus are reported. These cases were observed in north-eastern France between March, 1983 and January, 1984. All patients were of rural origin and had been in contact with field mice. The predominant initial clinical symptoms were signs of infection and diffuse muscle pain, without evidence of haemorrhage. However, massive proteinuria was noted, and acute anuric renal failure unaccompanied by oedema or arterial hypertension developed. Renal biopsy performed in 2 patients showed tubular and interstitial nephritis but no glomerular or vascular lesions. Two patients only required haemodialysis. All patients recovered within 2 to 8 weeks without sequelae. Antibodies directed against the Hantaan virus were detected by indirect immunofluorescence tests, and seroconversion could be demonstrated in 2 patients seen at a sufficiently early stage. The risk of epidemics suggested by this small outbreak of HFRS can only be evaluated after an exhaustive epidemiological study.
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PMID:[Hemorrhagic fever with renal syndrome due to Hantaan virus or a serologically related virus]. 615 Nov 76

A case of acute renal failure associated with captopril administration is reported. A woman, age 57, with a two-year history of hypertension presented with a generalized maculopapular rash preceded by pruritus after three weeks of captopril therapy. Her serum creatinine level on admission was 11.0 mg/dl. Renal biopsy was compatible with acute tubular necrosis without evidence of interstitial nephritis. A skin biopsy did not show any evidence of vasculitis. Captopril was discontinued, and her renal failure reversed over the course of nine days. A year later, the patient has good blood pressure control with stable renal function. Captopril has been associated with renal failure in patients with preexisting renovascular hypertension, and with acute interstitial nephritis in one case. The presentation of this case was similar to the latter case, but the renal biopsy did not show any evidence of acute interstitial nephritis.
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PMID:Acute renal failure, skin rash, and eosinophilia associated with captopril therapy. 622 49

In a patient with severe renovascular hypertension, nonoliguric acute renal failure developed after she received captopril treatment. We believe this to be a previously unreported complication. Urine volume ranged from 1,640 to 2,260 mL/24 hr, and serum creatinine level rose from 2.3 to 8.3 mg/dL. There was no evidence of renal hypoperfusion or interstitial nephritis. Acute renal failure most likely was secondary to the nephrotoxic effect of captopril on chronically hypoperfused kidneys. Renal function improved rapidly after withdrawal of the drug therapy.
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PMID:Nonoliguric acute renal failure after captopril therapy. 634 31

Hypertension, phosphate retention, hyperfiltration hyalinosis and the natural course of the underlying are well known factors leading to progression of chronic renal failure. Acute bacterial interstitial nephritis occurring in a previously diseased kidney, although well documented in experimental animals, has not been shown to aggravate chronic renal failure in man. We report on 3 cases of acute suppurative interstitial nephritis, due to E. coli urinary infection complicated by septicemia. All had rapid aggravation of previously mild renal failure secondary to chronic interstitial nephritis. Sepsis originated from the urinary tract which in 2 instances had been temporarily obstructed. Renal biopsy disclosed a diffuse interstitial infiltrate containing numerous polymorphonuclear leukocytes. This was superimposed on chronic tubular and interstitial lesions. In 1 case there were glomerular lesions with crescents and mesangial C3 deposits. A 2nd biopsy performed in 2 cases was of prognostic interest. In one case it showed active lesions and the necessity of continuing the treatment and in the other a satisfactory healing allowing cessation of therapy. Treatment was guided by antibiograms, the clinical and urinary signs of activity, renal biopsy findings and antibiotics known to be concentrated in renal tissue. The duration of treatment seemed important for the regression of acute renal lesions. Hematogenous bacterial interstitial nephritis should be considered as a possible cause of aggravation in chronic renal failure.
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PMID:[Acute hematogenic interstitial nephritis of urinary origin: an unrecognized factor in the exacerbation of chronic kidney failure]. 634 71

The CaNa2EDTA lead mobilization test permits identification of lead nephropathy in a variety of situations in which past-exposure is uncertain and acute symptoms of lead poisoning are lacking. In addition to lead workers and moonshiners, lead nephropathy has been identified in gout patients with renal failure and in hypertensives with renal failure. The presence of excessive mobilizable lead in these patients and its absence in control patients with comparable renal dysfunction suggests that unrecognized lead poisoning is sometimes responsible for renal failure in gout and hypertension. Use of the EDTA lead-mobilization test may thus permit prevention and sometimes treatment of renal failure in patients who might otherwise enter the End-Stage Renal-Disease Program. The controversies surrounding interstitial nephritis in lead poisoning, gout and hypertension may in part be explained by the surreptitious role of lead.
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PMID:The role of lead in renal failure. 675 98


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