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Biomedical subjects

R S Nanra

Publications and source records attributed to R S Nanra.

At least 19 recordsLinked to original sources
PubMed1992

Pattern of renal dysfunction in analgesic nephropathy--comparison with glomerulonephritis.

Comprehensive renal function tests were performed in 84 patients with analgesic nephropathy, 33 glomerulonephritis patients matched for creatinine clearance, and 30 control subjects. A system of 1-day renal function tests including urine microscopy, creatinine clearance, phenolsulphonphthalein excretion, urine concentration and acidification, and electrolyte excretion, was used. Patients with analgesic nephropathy were found to have significant sterile pyuria and haematuria, even those with mild renal insufficiency, significantly reduced concentrating ability and a distal acidifying defect, and a tendency to impaired sodium conservation. These function defects are consistent with the primary lesion of renal papillary necrosis in analgesic nephropathy; the detection of these defects have implications in patient management.

Adult↗
PubMed1991

Use of the fistula assessment monitor to detect stenoses in access fistulae.

Twenty-three unselected hemodialysis patients with functioning access arteriovenous fistulae were studied prospectively to determine the best technique for detecting stenoses within the fistulae. Combined clinical assessment and fistula assessment monitoring were compared with transbrachial angiography. Fistula assessment monitoring was more accurate (96%) than combined clinical assessment (accuracy, 52%) in stenosis detection. Complications of angiography occurred in 17% of patients; there were no complications of fistula assessment monitoring. Fistula assessment monitoring was better than combined clinical assessment in predicting clinical outcome for arteriovenous fistulae over 6 months and was as good as angiography. Routine fistula assessment monitoring could reduce inappropriate angiography and detect clinically significant silent stenoses. It is an ideal method for monitoring arteriovenous access fistulae.

Angiography↗
PubMed1991

Acute renal failure due to acute pyelonephritis.

We report a case of biopsy-proved acute pyelonephritis which caused acute renal failure. Despite appropriate antibiotic therapy, recovery of renal function was slow and incomplete. Renal papillary necrosis was an apparent complication, which the patient may have been predisposed to by alcoholism. Although rare, acute pyelonephritis is an important consideration in the differential diagnosis of acute renal failure because of the need for specific therapy.

Acute Kidney Injury↗
PubMed1989

Xanthogranulomatous pyelonephritis in a renal allograft: a case report.

We report a case of xanthogranulomatous pyelonephritis in a renal allograft. The kidney was not removed and there was an initial response to antibiotic therapy, with amelioration of toxicity and improvement in renal function. However, the kidney failed 10 months later in association with histological changes of chronic rejection.

Anti-Infective Agents, Urinary↗
PubMed1984

Gangrenous colitis in the haemolytic-uraemic syndrome.

The cases of two children with the haemolytic-uraemic syndrome (HUS) in whom clinical signs of intussusception necessitated emergency surgical intervention are reported. Both patients had bilateral renal cortical necrosis and haemorrhagic gangrenous colitis; both subsequently died. The early recognition and appropriate management of HUS is advocated.

Child, Preschool↗
PubMed1983

Renal effects of antipyretic analgesics.

Most antipyretic analgesics can cause acute nephrotoxic effects, including acute tubular necrosis, acute interstitial nephritis, glomerular toxicity, and functional changes, such as "salicyl edema," following large doses of sodium salicylate. Most functional changes are related to acute suppression of prostaglandin synthesis, "the acute prostaglandin-effect," and have been primarily noted with the use of indomethacin. The association between prolonged and excessive consumption of compound analgesics and the development of renal disease and renal failure, characterized by renal papillary necrosis, is now well established. Studies in several countries have shown that the incidence of analgesic nephropathy as an indication for dialysis and transplantation corresponds to the per capita consumption of phenacetin in compound analgesics. Analgesic nephropathy, which is part of a wider clinical syndrome, the analgesic syndrome, is uncommon following the use of single analgesics. Analgesic nephropathy and the analgesic syndrome are discussed in detail, including the development of uroepithelial tumors.

Animals↗
PubMed1983

Post-obstructive diuresis.

A patient with post-obstructive diuresis is described. Inappropriate losses of salt and water occurred, with urine volume exceeding half the glomerular filtration rate. Additionally, excessive urinary excretion of potassium, bicarbonate, calcium, phosphate, magnesium and urate took place in the presence of subnormal blood levels. Transient proteinuria was also observed. This case demonstrates that serious electrolyte disturbances can occur after relief of urinary tract obstruction and the evidence suggests these may be due to disordered proximal tubule function.

Diuresis↗
PubMed1982

Unusual radiological changes associated with probable Bartter's syndrome.

We report 2 cases that fulfill some of the criteria for the diagnosis of Bartter's syndrome and were associated with marked radiological changes. Both patients demonstrated distortion of the caliceal pattern with medullary cavities and loss of cortical substance in the absence of vesicoureteral reflux. However, the glomerular filtration rate was well preserved. It seems unlikely that known organic renal disease was responsible for these changes and the potassium-losing state. These radiological findings also do not appear to be a consequence of hypokalemia and their pathogenesis remains uncertain.

Adult↗
PubMed1981

Consequences of legislative restriction on the sale of compound analgesics in Newcastle (N.S.W., Australia).

In June 1979 legislation was enacted in New South Wales to restrict the sale of compound analgesics. The consequences of this legislation were assessed by a household survey in Newcastle, New South Wales, during November 1979. This survey followed an identical survey in the same community in November 1977. After legislation, a marked decrease was found in the proportion of homes having compound analgesics. A small decrease in total analgesic usage was also observed, though this was not necessarily related to the legislative restrictions. The legislative restrictions did not result in any substantial increase in use of the doctor to obtain prescriptions for compound analgesics, or any substantial increase in reported health problems. The results suggest that legislation is an effective method of inducing rapid change in health-related behavior.

Adolescent↗
PubMed1980

Analgesic nephropathy induced by common proprietary mixtures.

Renal papillary necrosis has been induced in 36.4% to 75% of rats which were gavage-fed with analgesic mixtures containing proprietary combinations of aspirin, paracetamol, phenacetin, phenazone, salicylamide and caffeine. These findings support the recent recommendations of the National Health and Medical Research Council which suggest that the free availability of analgesic mixtures be restricted.

Acetaminophen↗
PubMed1980

Clinical and pathological aspects of analgesic nephropathy.

1 Analgesic nephropathy is part of the analgesic syndrome which has gastrointestinal, haematological, cardiovascular, psychological and psychiatric, and pregnancy and gonadal manifestations; premature ageing may also be a feature. 2 Analgesic nephropathy is a form of renal disease characterized by renal papillary necrosis, secondary chronic interstitial nephritis and renal failure with features of predominant tubulointerstitial dysfunction. 3 The percentage of patients with analgesic nephropathy who present with terminal renal failure is 12%. With appropriate management, 17% of analgesic nephropathy patients improve, 50% remain stable and 23% deteriorate. The 6 year cumulative survival is 70%. The major factors influencing deterioration are malignant hypertension, persistent proteinuria and small initial renal size. 4 The risk of renal papillary carcinoma in patients who regularly take analgesics is 8 per 100,000 patients per year. 5 Renal papillary necrosis is a consequence of the chronic toxicity of all non-steroidal anti-inflammatory drugs and results from medullary ischaemia secondary to suppression of prostaglandin E2 synthesis and from direct cellular toxicity. 6 Analgesic nephropathy is a preventable form of renal disease and renal failure. It can be prevented by limiting the abuse potential of analgesics rather than by making minor modifications in the composition of analgesic mixtures.

Analgesics↗
PubMed1979

Double-blind trial of antihypertensive effect of chlorothiazide in severe renal failure.

A randomised double-blind crossover trial was done to assess the efficacy of chlorothiazide as an antihypertensive drug in patients with severe renal failure. There was a significant reduction in standing (mean drop 13/6 mm Hg) and supine (mean drop 13/5 mm Hg) blood-pressure, without postural hypotension. Chlorothiazide has a place in the management of hypertension in patients with severe renal failure and its antihypertensive effect is probably due to a change in peripheral vascular resistance and not to volume contraction.

Adult↗