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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

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
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PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

Study of case-notes and autopsy reports of patients with renal disease suggests that analgesic nephropathy is responsible for at least 12 per cent of cases of chronic renal failure, Between 1970 and 1975 eight new cases of analgesic nephropathy were seen annually in a population of three-quarters of a million. This is equivalent to an incidence of 490 new cases per year in England and Wales. Fifty-five patients with analgesic nephropathy were followed from one to 84 months for a total of 190 patient years. Changes in renal function were correlated with bacteriuria, hypertension and analgesic consumption. One-third of the cases had been misdiagnosed and analgesic abuse was only revealed by thorough examination of case-notes and autopsy records, together with careful questioning of patients and relatives. A number of cases had been classified as chronic pyelonephritis. The calculated survival rate at five years was 44 per cent. Mortality was related to the level of analgesic consumption and the degree of renal failure at the time of diagnosis. The prognosis was poor if serum creatinine at presentation was greater than 400 mumol/l. There was no significant correlation between deterioration in renal function and bacteriuria or hypertension. Forty-two per cent of the patients were taking analgesics for arthritis; 27 per cent had rheumatoid arthritis. Most had been taking large quantities of analgesic mixtures containing phenacetin. Renal papillary necrosis was present in only 26 per cent on intravenous urography but was found in all those examined at autopsy. Twenty thousand, two hundred and twenty-nine autopsy reports were examined for the presence of renal disease. Renal papillary necrosis was found in 0.41 per cent, and could be attributed to analgesic nephropathy in 24 per cent. In patients under 65 years of age analgesic nephropathy appeared to be a more frequent cause of death than chronic pyelonephritis. The report indicates the need for careful enquiry about analgesic consumption in all patients with renal disease, and emphasizes the importance of early diagnosis and cessation of analgesics in suspected cases of analgesic nephropathy.
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PMID:Analgesic nephropathy: an important cause of chronic renal failure. 67 50

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

Diagnostic criteria of analgesic nephropathy with well-defined sensitivity and specificity are not available. During a 2-year period all new patients (n = 273) starting renal replacement therapy in 13 Belgian dialysis units were investigated aiming to select diagnostic criteria of analgesic nephropathy with acceptable performance. Using several interview techniques, a history of analgesic abuse was found in 31% of the patients. Analgesic abusers presenting a clear non-analgesic-related renal diagnosis were excluded from analysis (n = 25). Comparing the remaining abusers (n = 60) and patients without a history of analgesic abuse (n = 188) it was found that renal imaging investigations (sonography plus tomography), showing a decrease in length combined with bumpy contours of both kidneys, presented a sensitivity of 90% and a specificity of 95%. The additional finding of signs of renal papillary necrosis resulted in an overall sensitivity of 72% and a specificity of 97%, giving a positive predictive value of 92%. Other signs frequently mentioned in the literature (hypertension, anaemia, sterile pyuria, bacteriuria, proteinuria) showed insufficient sensitivity and/or specificity to be of help for diagnosing analgesic nephropathy in end-stage renal failure (ESRF) patients starting renal replacement therapy.
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PMID:Diagnostic criteria of analgesic nephropathy in patients with end-stage renal failure: results of the Belgian study. 132 Feb 26

Experimental renal papillary necrosis induced by 2-bromoethylamine hydrobromide (BEA) results in hypertension in the rat. The haemodynamics of this increase in blood pressure were investigated with radiolabelled microspheres, thus enabling individual organ blood flows to be evaluated. Total peripheral resistance was raised in BEA-treated rats (3.6 +/- 0.3 mmHg ml-1 min X 100 g) compared with control rats (2.87 +/- SEM 0.2, P less than 0.05) whilst cardiac index remained similar (39.9 +/- 3.6 vs 39.2 +/- 3.1 ml min-1 100 g-1). Heart and brain from BEA rats demonstrated a significant rise in vascular resistance with a normal blood flow. In the kidneys vascular resistance increased still further and here there was a reduction in renal blood flow despite an increase in kidney size. These findings are compatible with a loss of renomedullary vasodepressor mechanisms acting directly or indirectly on the resistance vessels.
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PMID:Haemodynamic consequences of experimental papillary necrosis in the rat. 358 86

Five ambulatory children with various types of chronic arthritis developed renal papillary necrosis (RPN), as documented by intravenous pyelography. Each child was being treated with nonsteroidal anti-inflammatory drugs (NSAIDs) at the time of diagnosis of RPN and had had episodes of gross or microscopic hematuria for several months prior to diagnosis. In each child hematuria was associated with more than one NSAID, and three of the five children also had ingested acetaminophen intermittently. Glomerular function has remained normal and hypertension has not developed, but management of these children has necessitated reduction or elimination of NSAIDs. As evidenced by these five cases, microscopic or gross hematuria in a child with chronic arthritis treated with anti-inflammatory drugs should raise the possibility of RPN.
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PMID:Renal papillary necrosis in children with chronic arthritis. 394 2

Since phenacetin was removed from the Drug Tariff in New Zealand in 1974 there has been a decrease in the number of patients with analgesic nephropathy entering dialysis-transplant programmes. Since then there has been an increase in the consumption of non-steroidal anti-inflammatory agents. Experimental work in animals has shown that these drugs can cause renal papillary necrosis. We report two men with sever osteoarthritis who regularly ingested anti-inflammatory agents and developed papillary necrosis with renal insufficiency and hypertension. One patient consumed 0.5 kg of indomethacin over 10 years and the other 3.5 kg of ibuprofen, 200 g of naproxen and an uncertain amount of ketoprofen over 13 years. The increased chronic usage of non-steroidal anti-inflammatory drugs could bring about an upsurge in the incidence of papillary necrosis.
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PMID:Renal papillary necrosis following regular consumption of non-steroidal anti-inflammatory drugs. 695 56

Three patients who developed renal papillary necrosis while receiving long-term, high-dose aspirin therapy for juvenile rheumatoid arthritis are presented. It appears that aspirin alone or aspirin in combination with other drugs is the causative agent. The incidence and biologic significance of renal papillary necrosis are insufficient to alter the use of aspirin as the drug of choice in management of JRA. It is recommended that all children with JRA be encouraged to drink ample fluids and be followed with periodic urinalysis and blood pressure measurements. Those children who develop hematuria or hypertension should be evaluated by excretory urography.
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PMID:Renal papillary necrosis in juvenile rheumatoid arthritis. 738 45

While the relative incidence of serious nephrotoxicities in the population consuming nonsteroidal anti-inflammatory drugs (NSAIDs) is very low, the frequency of adverse events in patients at risk has considerably increased due to the rising popularity of the use of the drugs in recent years. Under normal conditions, NSAIDs have relatively little effect on the kidney because of low renal production of prostaglandins. However, in the presence of renal hypoperfusion in which local synthesis of vasodilator prostaglandins is increased to protect the glomerular hemodynamics and to maintain appropriate renal tubular transport of fluid and electrolytes, inhibition of prostaglandin synthesis by NSAIDs can lead to vasoconstrictive acute renal failure as well as fluid and electrolyte disorders such as sodium retention and resistance to diuretics, hyponatremia and hyperkalemia. Conditions that increase the risk for NSAID-induced nephrotoxicities include volume depletion from diuretics and other causes, edematous states such as congestive heart failure and cirrhosis of the liver, old age and underlying renal disease, especially in the presence of renal functional impairment. In addition, renal parenchymal diseases may develop in susceptible patients taking NSAIDs. These include acute tubulointerstitial nephritis, frequently associated with nephrotic syndrome, and chronic progressive renal disease, with or without renal papillary necrosis. Rare cases of vasculitis and glomerulonephritis have also been reported. Finally, NSAIDs may aggravate hypertension by interacting with antihypertensive drugs, especially with diuretics and beta-blockers. Withdrawal of NSAIDs in patients at risk can frequently reverse or improve the nephrotoxicities. It is recommended that physicians be aware of the clinical settings that increase the risk for NSAID-induced nephrotoxicities and take preventive or therapeutic measures accordingly.
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PMID:Nephrotoxicities of nonsteroidal anti-inflammatory drugs. 908 Jul 53


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