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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 379 records · Page 21Linked to original sources
PubMed1995

Failure of arginine-vasopressin and other pressor hormones to increase in severe recurrent dialysis hypotension.

BACKGROUND: Recurrent dialysis hypotension is common in long-term dialysis patients. Arginine-vasopressin (AVP) is a potent vasoconstrictor hormone, release of which is stimulated in hypotension. STUDY DESIGN: We measured AVP as well as adrenaline and noradrenaline in 23 patients with recurrent dialysis hypotension during severe symptomatic episodes of dialysis hypotension (BP syst. < 70 mmHg). We also tested autonomic function (amyl nitrate inhalation, cold pressor test) during the interdialytic interval. RESULTS: We observed that systolic blood pressure decreased from 127 +/- 8 (at the end of the first hour of dialysis; taken as control state) to 64 +/- 1 mmHg (symptomatic hypotension) in 23 patients. In six of the 23 patients hypotension was accompanied by nausea, which is a known direct stimulus of AVP. In these six patients, plasma AVP showed a large increase: control state, 6.2 +/- 0.9; hypotension, 130.4 +/- 51.1 pg/ml; P < 0.5). Of the remaining 17 patients without nausea, AVP fell moderately in nine and increased in eight. Taken together, this group of 17 hypotensive patients failed to show significant AVP stimulation: control state, 9.0 +/- 1.4; hypotension, 13.8 +/- 3.8 pg/ml, NS). Adrenaline and noradrenaline did not change during hypotension. During autonomic testing the patients with recurrent dialysis hypotension (compared to healthy controls) showed blunted baroreflex response (assessed by amyl nitrate inhalation) but intact sympathetic outflow (assessed by cold pressor test). CONCLUSION: The observations of AVP are taken as further evidence of defects in the afferent rather than the efferent limb of autonomic reflexes in dialysis patients with recurrent dialysis hypotension.

Acute Disease↗
PubMed1995

Anticipation of age at renal death in autosomal dominant polycystic kidney disease (ADPKD)?

It has been claimed that anticipation occurs in ADPKD, i.e. endstage renal failure at progressively earlier age in successive generations. This observation might possibly point to unstable DNA as the molecular basis of ADPKD. We analysed 74 parent-offspring pairs of 148 families in Germany and Austria in whom (i) ADPKD was verified by appropriate imaging procedures and (ii) age at renal death was accurately known. The median difference for age at renal death between parent and offspring was 0 years, range -26.3 to +27.2 years. There was no deviation from normal (Gaussian) distribution according to the Shapiro-Wilk test (P = 0.75). We conclude that systematic anticipation cannot be demonstrated with this sample which had sufficient size for meaningful biostatistical analysis.

Adult↗
PubMed1995

Chronic hypokalaemia of adults: Gitelman's syndrome is frequent but classical Bartter's syndrome is rare.

We evaluated 27 adult patients with chronic hypokalaemia (K+ = 2.9 +/- 0.2 mmol/l), documented over at least 5 years, in whom the cause of the hypokalaemia had not been clarified in spite of previous testing. In 15 patients it was possible to establish a diagnosis by a thorough outpatient workup (diuretic abuse (n = 5), surreptitious vomiting (n = 8), laxative abuse (n = 1), renal tubular acidosis (n = 1)). Commonly utilized tests such as measurements of plasma renin activity, plasma aldosterone, and urinary potassium concentration proved not to be useful in the differential diagnosis of these patients. In contrast the following were diagnostically important: in surreptitious vomiting the hypochloraemia, the mild renal insufficiency, and the extremely low urinary chloride concentration; in diuretic abuse the high urinary concentration of chloride together with repeatedly positive toxicology screens for diuretics; in laxative abuse the high stool weight and extremely low urinary sodium concentration. In the remaining 12 patients none of these diagnoses applied and further tests for suspected Bartter's syndrome were done in the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Expression of receptors for advanced glycosylated end-products in renal disease.

BACKGROUND: Advanced glycation endproducts (AGEs) are believed to mediate long-term complications in diabetes mellitus. In this context we studied the expression of the receptor for AGEs (RAGE) in the kidney of patients with a variety of different renal diseases. METHODS: RAGE was detected by immunocytochemistry in renal biopsies. We compared the staining for RAGE in nine patients with diabetic nephropathy, 20 with inflammatory and/or immune complex and 10 with non-inflammatory renal diseases. Normal renal tissue from seven patients with tumour nephrectomies served as controls. RESULTS: In controls the only cells expressing RAGE constitutively were interstitial cells and vascular smooth muscle cells (6/7), while distal tubular cells were rarely positive (1/7). Endothelial cells of arteries/arterioles, glomerular endothelial cells, podocytes, and capsular epithelial cells were consistently negative. In diabetic nephropathy, inflammatory and/or immune complex, and non-inflammatory renal diseases, all cell types mentioned above became positive for RAGE. Whilst the distribution of RAGE in the tissue was quite similar, staining intensity in inflammatory and/or immune complex diseases was higher than in diabetic nephropathy. CONCLUSION: RAGE induction in the kidney is not specific for diabetic nephropathy and occurs in other types of renal diseases as well.

Adolescent↗
PubMed1995

[Does an association between angiotensin I converting enzyme gene polymorphism and the prevalence of diabetic nephropathy in patients with diabetes type II exist?].

In type I diabetic patients association has been found between the insertion/deletion (I/D) polymorphism in the gene of angiotensin converting enzyme and the presence of diabetic nephropathy. The aim of that study was to assess this association in a cohort of type II diabetics. We examined 109 patients of more than 10 years duration of type II diabetes. Nephropathy (defined as at least confirmed albuminuria > 30 mg/24h) was present in 37 subjects. The I/D polymorphism was analyzed with PCR technique. Allele frequencies in the overall diabetic population did not differ significantly from the normal population. Distribution of genotypes was not significantly different between examined patients with and those without nephropathy. We conclude that the distribution of ACE gene polymorphism is similar in diabetic subjects and in general population and there is not association between I/D polymorphism and nephropathy in type II diabetic patients.

Aged↗
PubMed1995

Blood-pressure-independent wall thickening of intramyocardial arterioles in experimental uraemia: evidence for a permissive action of PTH.

BACKGROUND: Abnormalities in cardiovascular structures, e.g. LV hypertrophy and thickening of vessels (arteries, arterioles, veins) are hallmarks of renal failure. They are in part independent of elevated blood pressure. Parathyroid hormone (PTH) has been shown to affect cardiac function and has also been identified as a permissive factor in the genesis of cardiac fibrosis. PURPOSE OF THE STUDY: The present study in rats with experimental renal failure was designed to examine whether PTH was permissive for wall thickening of intramyocardial arterioles as well. METHODS: Male SD rats were sham operated or subtotally nephrectomized and maintained for 2 weeks. Subgroups of subtotally nephrectomized (SNX) rats were parathyroidectomized (PTX). Saline or rat 1, 34 PTH was administered by osmotic minipump. Eucalcaemia was maintained in PTX animals by a high-calcium diet (3%). Serum calcium was not statistically different between the groups. After perfusion fixation, intramyocardial arterioles were assessed using stereological techniques (wall thickness; wall/lumen ratio; minimal lumen diameter; length density). RESULTS: In random samples of the left ventricle, wall thickness of arterioles was 2.2 +/- 0.25 microns in sham-op controls and 2.76 +/- 0.41 in SNX (n = at least 8 animals per group). SNX-PTX animals+solvent did not differ significantly from sham-op controls (2.08 +/- 0.42 microns), while SNX-PTX animals+PTH had values not significantly different from SNX (2.59 +/- 0.54 microns). Differences in wall thickness were not paralleled by differences in systolic blood pressure (sham-op 110 +/- 13.3 mmHg; SNX 138 +/- 8.4 mmHg, SNX-PTX+solvent 142 +/- 5.2 mmHg; SNX-PTX+PTH 148 +/- 5.7 mmHg). PTH treated animals showed signs of marked vascular smooth-muscle cell and endothelial-cell activation. CONCLUSIONS: The data suggest that wall thickening of intramyocardial arterioles in short-term experimental uraemia is dependent upon the presence of PTH (permissive effect).

Animals↗
PubMed1994

[Acute myoglobinuric kidney failure as a consequence of autoaggressive behavior in mental retardation].

A 49-year-old female with mental retardation was admitted with suspected renal insufficiency with a raised creatinine (5.1 mg/dl), hyperkalaemia (5.6 mmol/l), and a 12-hour history of diffuse abdominal pain and persistent vomiting. On admission, she had a haematoma around the right shoulder and arm-pit, swelling of the right upper-arm, and severe limitation of movement of the right hand. These injuries were the result of trauma some 5 days previously. She was a long-term inpatient in a psychiatric clinic, with a history of autoaggressive behaviour, which had led to several fractures in the past as a result of falls. The creatinine kinase was elevated to 6680 U/l. The suspected diagnosis of acute oliguric renal failure due to rhabdomyolysis was confirmed by the presence of marked myoglobinuria (409 ng/ml). Because of the delay in diagnosis, acute renal failure developed, and the patient required haemodialysis for 20 days. Because of their many predisposing factors, psychiatric patients represent a special risk group for development of rhabdomyolysis, recognition of which is often delayed.

Acute Kidney Injury↗
PubMed1994

OACE inhibition does not interfere with acute extrarenal or renal potassium disposal in chronic renal failure.

The influence of angiotensin converting enzyme (ACE) inhibition on acute extrarenal and renal potassium elimination in stable chronic renal failure has been examined in 10 male patients median age 44 y; mean CLCR 42 ml.min-1.1.73 m-2. In a double blind, placebo-controlled cross-over study, K+ 0.3 or 0.4 mmol.kg-1 body weight was infused IV on two occasions while the patients also received an infusion either of placebo or 0.5 mg of the ACE inhibitor perindoprilat in random order. Plasma K+ levels and urinary K+ excretion were measured at regular intervals. During the study patients adhered to an isocaloric diet providing a standardised daily intake of potassium and sodium (50 mmol K+ and 40 mmol Na+). The median rise in plasma K+ was not significantly different after placebo (delta K 0.66 mmol.l-1) compared with to the infusion of perindoprilat (delta K 0.66 mmol.l-1). The median baseline urinary K+ excretion rate was 6.5 mmol.3 h-1 before the placebo infusion and 5.9 mmol.3 h-1 before infusion of perindoprilat. During the potassium load, the urinary excretion rate rose to 16.1 mmol.3 h-1 (after placebo) and 15.1 mmol.3 h-1 after perindoprilat in the first 3 h, and it returned almost to the baseline value within the next 3 h (5.6 mmol.3 h-1 after placebo and 5.7 mmol.3 h-1 after perindoprilat); the differences were not statistically significant. With perindoprilat a decrease in mean arterial blood pressure and ACE activity, an increase in renin plasma activity and a decrease in aldosterone concentrations were observed compared to the placebo infusion. There was no significant differences plasma in adrenaline or insulin levels after either infusion. Thus, ACE inhibition did not interfere either with the extrarenal or the renal disposal of an acute potassium load in patients with chronic renal failure.

Adult↗
PubMed1994

Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure. Consequence of dose adjustment.

To prevent drug accumulation and adverse effects the dose of hydrophilic angiotensin-converting enzyme (ACE) inhibitors, e.g. lisinopril, must be reduced in patients with renal failure. To obtain a rational basis for dose recommendations, we undertook a prospective clinical trial. After 15 days of lisinopril treatment pharmacokinetic and pharmacodynamic parameters were determined in patients with advanced renal failure (n = 8; endogenous creatinine clearance [CLCR]: 18 ml.min-1.1.73 m-2) and in healthy subjects with normal renal function (n = 16; CLCR: 107 ml.min-1.1.73 m-2). The volunteers received 10 mg lisinopril once daily, the daily dose in patients (1.1-2.2 mg) was adjusted to the individual CLCR according to the method of Dettli [13]. After 15 days of lisinopril treatment the mean maximal serum concentration (Cmax) in patients was lower than in volunteers (30.7 vs 40.7 ng.ml-1, while the mean area under the concentration-time curve (AUC0-24 h) was higher (525 vs 473 ng.h-1.ml-1). ACE activity on day 15 was almost completely inhibited in both groups. Plasma renin activity, angiotensin I and angiotensin II levels documented marked inhibition of converting enzyme in volunteers and patients. Furthermore, average mean arterial blood pressure in patients decreased by 5 mmHg and proteinuria from 3.9-2.7 g per 24 h after 15 days of treatment with the reduced dose of lisinopril. Adjustment of the dose of lisinopril prevents significant accumulation of the drug in patients with advanced renal failure during chronic therapy. Mean serum levels did not exceed this in subjects with normal renal function receiving a standard dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Coadministration of thiazides increases the efficacy of loop diuretics even in patients with advanced renal failure.

It is commonly assumed that thiazide diuretics are ineffective in patients with advanced renal failure (GFR < 30 ml/min/1.73 m2). Thiazides act on the nephron segment distal to the ascending thick loop of Henle, that is, the site of action of loop diuretics. Blockade of sodium reabsorption in the thiazide-sensitive segment should therefore obliterate the compensatory increase in sodium reabsorption seen after administration of loop diuretics and thus potentiate the natriuretic efficacy of loop diuretics even in advanced renal failure. In a single-blind, randomized, placebo controlled crossover study we compared the natriuretic and chloruretic effect of the loop diuretic, torasemide, given alone or in combination with the thiazide diuretic, butizid, in 10 patients with advanced renal failure (mean CIn 13.1 +/- 5.9 ml/min/1.73 m2). For two weeks patients adhered to a diet containing a standardized amount of Na+ and K+. On the 6th and 13th study days, two sham infusions were given to patients in order to assess basal 24-hour urinary electrolyte excretion. On the 7th and 14th days they were randomly allocated to receive either 50 mg i.v. torasemide in combination with a sham infusion or torasemide in combination with 20 mg i.v. butizid. Administration of torasemide alone significantly (P < 0.01) increased mean cumulative 24-hour excretion of sodium (from 154 +/- 30 to 232 +/- 59 mmol/24 hr) and chloride (from 128 +/- 21 to 233 +/- 84 mmol/24 hr) as compared with baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

PCR analysis of human renal biopsies--renin gene regulation in glomerulonephritis.

Animal studies show that the renin-angiotensin system contributes to hypertension, glomerulosclerosis and progressive chronic renal failure in renal disease. Direct data on the activity of the renal renin-angiotensin system (RAS) in human renal disease are scarce, however. The small amount of tissue in renal biopsies and insufficient sensitivity of analytical methods have precluded reliable measurements of the tissue components of the RAS in the past. Due to its highly sensitivity the quantitative polymerase chain reaction (QPCR) assay today allows the quantitation of gene transcription products in small tissue samples, for example, renal biopsies. The clinical applicability of the PCR has raised the interest in this methodology. We adopted quantitative PCR to study expression and regulation of the renin gene in patients with different forms of glomerulonephritis. For PCR a deletion mutant of the renin gene was used as an internal standard exhibiting the same primer binding sites as the human gene. The number of glomeruli per biopsy sample was counted by microscopic transillumination immediately after biopsy and was used as a reference base. Renin mRNA was expressed as fg per glomerulus. Compared to nonaffected tissue of tumor nephrectomy samples, renin gene expression was significantly lower in glomerulonephritic patients without converting enzyme inhibitor (CEI) treatment, that is, 63 +/- 20 (6) versus 250 +/- 50 (7) (P < 0.02), although plasma renin concentration was in the normal range. Significantly higher renin mRNA expression was found in patients with glomerulonephritis treated with CEI, that is, 210 +/- 50 (8) versus 63 +/- 20 (6) in patients not treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗