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M Aurell

Publications and source records attributed to M Aurell.

At least 19 recordsLinked to original sources
PubMed2001

A historical cohort study of kidney damage in long-term lithium patients: continued surveillance needed.

BACKGROUND: Insufficient knowledge on the longitudinal fate of renal function in lithium patients incited this retrospective study of 149 patients. METHOD: Medical record review of a lithium cohort (N = 149), 8--12 years after an initial renal function study. RESULTS: Twenty-one patients had died, one from uremia probably not caused by lithium, and 42 had discontinued lithium. Reduced urinary concentrating capacity (Umax) or glomerular filtration rate (GFR) was not more frequent among deceased or off-lithium patients than among the 86 patients who were on lithium at follow-up. In 63 of the latter patients, Umax had been re-examined after the initial study, and GFR in 29 patients. Reduced Umax and GFR had become twice as common, and average Umax and GFR had decreased significantly. The reduction of GFR was associated with lithium treatment duration and age, and reduced Umax with treatment duration only. CONCLUSIONS: Reduced renal function is not a major cause of treatment discontinuation but becomes increasingly common with treatment duration.Limitations. Missing data rendered the interpretation difficult in some respects. Clinical relevance. The increased proportion of patients with reduced GFR and Umax with time implies an increased risk of potentially lethal dehydration and lithium intoxication. Continued surveillance of urinary output and GFR is therefore necessary.

Adult↗
PubMed2001

The effects of an ACE inhibitor and a calcium antagonist on the progression of renal disease: the Nephros Study.

BACKGROUND: The renoprotective effect of ACE inhibition in chronic renal disease is well established but the studies on effects of calcium antagonists on progression of renal disease and on proteinuria have given varying results. METHODS: We conducted an open long-term randomized prospective multi-centre study comparing the combination of ramipril and felodipine ER (F) with either drug alone in non-diabetic renal disease. Included were patients with uncontrolled hypertension (diastolic blood pressure (DBP)) > or =95 mmHg on treatment with a diuretic and a beta-blocker. Fifty-one patients received the combination of R and F, 54 patients R, and 53 patients F. The treatment goal was a DBP <90 mmHg and a similar BP reduction in the three groups. Mean doses at the last visit were 5+5, 10 and 9 mg, respectively, after a mean treatment time of nearly 2 years. The progression of renal impairment was studied by serial measurements of serum creatinine, iohexol clearance, and albuminuria. RESULTS: The reduction in supine systolic (S) BP and DBP expressed as median values were -19.0/-14.5,-14.3/-15.0 and -13.5/-13.3 mmHg in the R+F, R, and F groups, respectively. There was no significant difference between the groups. When correction for the acute drug effect was performed the R+F group had a slower progression rate of the renal disease (loss of glomerular filtration rate (GFR) ml/min/year) compared with the F group (P<0.05) but not to the R group (P>0.20). There was a rise in albuminuria after 2 years in the F group (P<0.05), but no significant change was found in the other groups. CONCLUSIONS: In patients with non-diabetic renal disease the combination of an ACE inhibitor and a calcium antagonist in reduced doses used in addition to baseline therapy with beta-blockers and diuretics, tended to cause a better BP reduction as each drug per se. The R+F treatment also caused a slower progression of the renal disease compared with F alone. The combination treatment seems to afford better BP control and appears to be a favourable therapeutic option in patients with renal disease and hypertension.

Adult↗
PubMed2000

Evaluation of duplex ultrasound and captopril renography for detection of renovascular hypertension.

BACKGROUND: Renovascular hypertension is the most common form of curable secondary hypertension and, if untreated, may lead to end-stage kidney disease. Given that renal function and hypertension may improve after renal angioplasty, it is pertinent to identify patients with renal artery stenosis. The aim of the present study was to evaluate both duplex ultrasound and captopril renography for detection of renal artery stenosis among hypertensive patients. METHODS: To avoid selection bias, all patients referred to our center for evaluation of renovascular hypertension were asked to participate in the study. Patients were examined by intra-renal duplex ultrasound (N = 121), measuring pulsatility index and acceleration of the blood flow during early systole. In 98 patients, 99mTc-DTPA captopril renography was performed in conjunction with duplex ultrasound. Renal angiography was performed in all patients regardless of the results of the noninvasive tests. RESULTS: The prevalence of renal artery stenosis was 19%. In the 98 patients examined by both duplex ultrasound and captopril renography, sensitivity and positive predictive values for detection of a renal artery stenosis of 50% degree or more were 84 and 76%, respectively, for duplex ultrasound, whereas captopril renography was associated with a sensitivity and positive predictive value of 68% for both (P = NS). Specificity and negative predictive values were 94 and 96%, respectively, for duplex ultrasound, whereas the corresponding values for captopril renography were 92% for both (P = NS). Specificity and negative predictive values were 94 and 96%, respectively, for duplex ultrasound, whereas the corresponding values for captopril renography were 92% for both (P = NS). CONCLUSIONS: Both duplex ultrasound and captopril renography are associated with high specificity and negative predictive values for detection of renal artery stenosis. Sensitivity and positive predictive values are at least as good for duplex ultrasound compared with captopril renography. Given that duplex ultrasound is easier to perform and more cost effective, we propose that it should be the method of first choice when screening for renal artery stenosis in a hypertensive population.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Angiotensin-converting enzyme gene I/D polymorphism in malignant hypertension.

BACKGROUND: The mechanism of the rapid transition of a stable benign hypertensive disease to a severe and devastating malignant hypertension is not fully understood. However, the renin angiotensin system, which is highly activated in malignant hypertension, is established as an important pathogenetic factor in different cardiovascular and renal diseases. Over the last decade, a polymorphism in genes regulating this system has been found. This includes the 287 bp sequence deletion (D)/insertion (I) polymorphism in the angiotensin-converting enzyme (ACE) gene and the methionine (M) to threonine (T) point mutation polymorphism in the angiotensinogen (AGT) gene. These gene polymorphisms have been associated with various cardiovascular and renal diseases and the aim of this study was to investigate whether they were linked to malignant hypertension. METHODS: Forty-two patients with malignant hypertension (mean age 55 years), 42 patients with non-malignant hypertension (mean age 57 years) and 85 normotensive control subjects (mean age 42 years) were investigated with respect to ACE I/D and AGT M/T genotypes. DNA was prepared by standard methods from isolated white blood cells and analysed by the PCR technique. The PCR reaction used in the detection of the ACE I/D polymorphism was optimized for an equal amplification of the I and D alleles. RESULTS: The frequency of the DD genotype was significantly increased in patients with malignant hypertension (43%) compared with patients with non-malignant hypertension (14%) and normotensive control subjects (18%) (p <0.01) for both. The frequency distribution of AGT M/T genotype did not differ between patients with malignant and non-malignant hypertension. CONCLUSION: The DD genotype of the ACE gene occurred more than twice as often in malignant hypertension than in non-malignant hypertension and indicates that ACE gene polymorphism is a significant risk factor for initiation of malignant hypertension.

Adult↗
PubMed1999

[A 100-year perspective on renal function and hypertension. Anti-renin therapy has made hypertensive renal failure a rarity].

One hundred years ago, in 1898, Professor Robert Tigerstedt, Karolinska institutet, Sweden, discovered renin. The subsequent elaboration in 1960 of the renin-angiotensin-aldosterone system signalled the start of modern hypertension research. The kidney takes part in blood pressure regulation in a number of ways. Indications are that increased renovascular resistance due to increased renin-angiotensin activity is of importance for the barostatic function of the kidneys and for the pathogenesis of human hypertension. Several commonly used, efficacious and well tolerated antihypertensive agents act by blocking the renin-angiotensin system, thus normalising kidney function. A number of current large-scale trials--utilising ACE inhibitors and angiotensin receptor antagonists--will, it is hoped, elucidate the proper role of 'anti-renin therapy' in the treatment of hypertension. Thanks to effective modern management of hypertension, renal failure due to hypertensive kidney disease is rare in Sweden today.

Acute Kidney Injury↗
PubMed1999

Drug-induced diabetes insipidus: incidence, prevention and management.

Drug-induced diabetes insipidus is always of the nephrogenic type, i.e. unresponsiveness of the kidneys to the action of antidiuretic hormone. This condition is easily diagnosed by measuring urinary concentrating capacity during a thirst test (e.g. 12 hours of water deprivation) or by administration of a modified antidiuretic hormone, desmopressin, to demonstrate the renal unresponsiveness. Drug-induced nephrogenic diabetes insipidus is not a common disorder except in patients receiving treatment with lithium salts for affective disorders where it may affect about 10% of patients treated long term (15 years). Drug-induced nephrogenic diabetes insipidus caused by other drugs usually occurs in critically ill patients in intensive care units receiving a multitude of drugs dominated by antimicrobials and cytostatics. A search of the World Health Organization's adverse effect database revealed 359 reports of drug-induced diabetes insipidus. Lithium was the most common cause (159 reports) followed by foscarnet (15) and clozapine (10). Treatment is symptomatic in most patients and the offending drug should be stopped. If urine volumes exceed 4 L/day, treatment with thiazides and amiloride has been advocated, and nonsteroidal anti-inflammatory drugs, such as indomethacin, may be tried in severe cases. Prevention of lithium-induced nephrogenic diabetes insipidus is an important aspect of the treatment of affective disorders. In patients treated long term it appears to be only partly reversible upon lithium discontinuation. Close monitoring of the treatment aiming at 12-hour trough value of 0.4 to 0.6 mmol/L is recommended. Yearly measurement of the urinary volume/day is effective in making both the patient and the physician aware of the development of the drug-induced nephrogenic diabetes insipidus. The condition is a serious adverse effect because of the risk of developing dehydration and aggravation of drug intoxications.

Animals↗
PubMed1998

[Renal artery stenosis--an underestimated cause of hypertension and renal failure?].

Although renovascular hypertension is associated with substantial cardiovascular morbidity, ultimately it is a curable disease. Early identification and appropriate treatment of renovascular hypertension may save years of antihypertensive therapy, reduce the morbidity associated with long-standing hypertension, and help to minimise the risk of renal failure. However, the main problem is to identify patients with renovascular disease suitable for treatment. This requires alertness in the clinician, and renographic screening of renal function or duplex-ultrasound scanning of renovascular circulation to augment the yield of angiographic procedures. The predominant treatment of renovascular disease today is percutaneous transluminal angioplasty, which can be used as a repeat procedure or in combination with endoluminal stenting of the stenotic renal artery.

Angioplasty, Balloon↗
PubMed1998

GFR measurement with iohexol and 51Cr-EDTA. A comparison of the two favoured GFR markers in Europe.

BACKGROUND: The aim of the present study was to compare the most commonly used GFR markers for clearance measurements, 51Cr-EDTA and iohexol, using two different methods for iohexol analysis, HPLC and X-ray fluorescence, referring both to the multiple-sample and single-sample calculations, using 51Cr-EDTA as the reference method. METHODS: Forty-nine patients with an estimated GFR >40 ml/min were included. 51Cr-EDTA and iohexol were injected simultaneously and blood samples were taken 150, 195 and 240 min after injection of the respective marker. RESULTS: The multiple-point clearances, determined from HPLC and X-ray fluorescence, compared to 51Cr-EDTA correlated highly (r=0.92 and 0.95 respectively). The results from single-point clearance comparison, iohexol measured by HPLC vs 51Cr-EDTA, yielded a correlation of r=0.91, while single-point clearance from iohexol, analysed by X-ray fluorescence, obtained a correlation of 0.93 and an intercept statistically different from origo. CONCLUSIONS: Iohexol and 51Cr-EDTA are comparable as GFR markers for multiple-point clearance measurements. The single-sample method for GFR >40 ml/min can be used with a high accuracy. The precision and accuracy of X-ray fluorescence analysis of low concentrations of iohexol were less than those of HPLC. Care should therefore be taken when using X-ray fluorescence that the injected dose of iohexol should result in a plasma concentration level of iodine of at least 0.06 mg/ml at the time of blood sampling.

Adult↗
PubMed1997

Enalapril versus metoprolol in primary hypertension--effects on the glomerular filtration rate.

BACKGROUND: Hypertension is a significant cause of end-stage renal failure and effective treatment of hypertensive will reduce the progression rate of chronic renal failure in various kidney disorders. Different classes of drugs may be more effective than others in this respect. In this study we compared the effects on the glomerular filtration rate (GFR) of the ACE-inhibitor enalapril and the betablocker metoprolol in patients with mild and moderate primary hypertension during 6 years. METHODS: Patients with GFR in the normal range (> or = 80 ml/min/1.73 m2 BSA) were included after a placebo treatment period of 4-8 weeks if diastolic blood pressure was 100-120 mm Hg. Target blood pressure was set to < 90 mm Hg diastolic. One hundred and thirty patients were randomized in an open parallel study to receive either enalapril or metoprolol. No placebo group was included. GFR was measured using the 51CR-EDTA clearance method and 81 patients completed the study. RESULTS: At inclusion, there were no significant differences regarding GFR or blood pressure between the groups. The blood pressure treatment goal was reached in all patients and was maintained during the whole observation period. A small but significant fall in GFR by 4 ml/min/1.73 m2 BSA was noted in both groups after the first year of treatment but thereafter GFR decreased by only 1 ml/min/year/1.73 m2 BSA, in both groups. Body weight, serum uric acid and triglycerides increased slightly with metoprolol treatment but no other differences between the two treatments were noted. CONCLUSIONS: With the blood pressure maintained at the same level using either enalapril or metoprolol during a 6-year study period, GFR decreased to the same extent in the two groups both during the first year and thereafter. The overall magnitude of the GFR decline approached that of the normal age-related decrease of kidney function, i.e. GFR decreased only about 1 ml/min/year. Thus, treatment with an ACE-inhibitor, enalapril, and a beta-blocker, metoprolol, protected the kidney function to the same extent in this 6 year long study in mild and moderate primary hypertension.

Adrenergic beta-Antagonists↗