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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 613 records · Page 34Linked to original sources
PubMed1989

Specific binding of angiotensin II and atrial natriuretic factor in non-nephropathic type I diabetes mellitus.

We examined ten patients with type I diabetes mellitus and ten age- and sex-matched healthy controls. Median duration of diabetes was 7 years (range 0.5-24). None of the diabetic patients had hypertension, microalbuminuria, or proliferative retinopathy. Maximal specific binding capacity for angiotensin II to thrombocytes was significantly increased in diabetics (Bmax 11.9 +/- 1.6 sites per cell vs 7.0 +/- 0.9 in controls; P less than 0.01). In contrast, maximal binding for atrial natriuretic factor tended to be lower in type I diabetics (8.84 +/- 1.25 sites per cell vs 16.8 +/- 2.97; P less than 0.07). There was no difference of apparent dissociation constant (KD) for either receptor. Angiotensin II values (RIA) were greater in diabetics (16.2 +/- 1.5 pg/ml vs 8.5 +/- 1.4 in controls; P less than 0.02) and concentrations of atrial natriuretic factor (RIA) were not significantly different. The data suggest increased angiotensin II binding despite high angiotensin II concentrations in non-nephropathic type I diabetic patients. These findings may be relevant when considering the evolution of hypertension and microangiopathy lesions.

Adult↗
PubMed1989

Effects of WY 47987 (atrial natriuretic factor 102-126) in patients with renal insufficiency: a placebo-controlled, randomised study.

We studied renal, hormonal and cardiovascular effects of ANF 102-126 (WY 47987) in seven patients with chronic renal failure (serum creatinine 25-68 mg/l) and in four normal volunteers. ANF or placebo bolus injections were given at 1, 2, and 3 micrograms/kg i.v. (each dose on separate days). As compared to placebo, ANF did not induce changes of renal excretory parameters, of plasma renin and aldosterone or of blood pressure and heart rate in patients. In healthy volunteers, however, the same dose of ANF increased urinary excretion of sodium, potassium, calcium, chloride and phosphorus as well as water, and creatinine clearances, and decreased plasma aldosterone. The data suggest blunted effectiveness of ANF bolus injections in patients with renal insufficiency.

Aldosterone↗
PubMed1989

Detection and clinical implication of anti-neutrophil cytoplasm antibodies in Wegener's granulomatosis and rapidly progressive glomerulonephritis.

The specificity of anti-neutrophil cytoplasm antibodies (ACPA/ANCA) was investigated in patients suffering from Wegener's granulomatosis (WG), various forms of systemic diseases including vasculitides (non-WG), and different types of biopsy-proven glomerulonephritides. In particular, the diagnostic significance of ACPA/ANCA was assessed in patients affected by rapidly progressive glomerulonephritis with and without systemic manifestations. From 25 patients with active Wegener's granulomatosis 22 showed the classical diffuse finely granular cytoplasmic staining of neutrophils as did 4/31 patients with idiopathic rapidly progressive glomerulonephritis. One patient with biopsy confirmed Wegener's granulomatosis, six patients with microscopic polyarteritis and 3/31 patients with idiopathic rapidly progressive glomerulonephritis showed a focal cytoplasmic staining exhibiting a rosette-like pattern. One further patient with Wegener's granulomatosis displayed a prominent fluorescence of the outer nuclear membrane as well as a punctate-diffuse nuclear staining resembling that of granulocyte specific antibodies. Another patient with active Wegener's granulomatosis did not react in the ACPA/ANCA-test. These findings demonstrate different staining patterns of neutrophils which are related to different clinical entities within the spectrum of small vessel vasculitis. Moreover, they point out that different antigens are involved in the various types of vasculitis. In classical cases of Wegener's granulomatosis, but not in other forms of vasculitis, the titer of ACPA/ANCA showed a close relationship to the number of organs involved.

Adolescent↗
PubMed1989

The acute effect of growth hormone on GFR is obliterated in chronic renal failure.

Recombinant human growth hormone (rhGH) has become available for treatment of growth failure in uremic children. Since GH raises the glomerular filtration rate (GFR) in healthy individuals, there has been concern that treatment with rhGH, by its action on glomerular hemodynamics, may adversely affect the progression of renal failure. To further address this issue, inulin clearance (enzymatic steady-state infusion technique) was measured in 7 healthy normotensive adult volunteers and 7 patients with chronic renal failure from glomerular or non-glomerular causes. Subjects were given 4.5 U bid of rhGH by s.c. injection for 3 days. In volunteers, a significant increase in Cin was noted 72 h after start of rhGH administration from 120 ml/min/1.73 m2 (range 91-158) to 133 (108-167) (p less than 0.02). In contrast, no significant increase in Cin was noted in patients with chronic renal failure (baseline Cin 21 ml/min/1.73 m2, 15-32; after rhGH 22 ml/min/1.73 m2, 15-32) despite pronounced effects of GH on S-cholesterol and urea excretion rate. The results show that stimulation of GFR by short-term administration of rhGH is obliterated in chronic renal failure.

Adult↗
PubMed1989

Impact of hypertension on prognosis in IDDM.

In Type I diabetes, hypertension is usually associated with the development of diabetic nephropathy. In proteinuric patients hypertension has a deleterious effect on the progression of microangiopathy and macroangiopathy, which in turn impairs their quality of life and long-term prognosis. As shown in numerous studies, hypertension accelerates loss of renal function. After kidney transplantation, the percentage of functioning grafts is much lower in diabetic patients who remain hypertensive. Furthermore, the rate of development of proliferative retinopathy, a common complication in proteinuric diabetics, increases in the presence of hypertension. Finally, hypertensive blood pressure values at the start of maintenance hemodialysis are significant predictors of cardio-vascular death among diabetics of renal replacement therapy. It has recently been demonstrated that during the last two decades blood pressure control has improved in proteinuric Type I diabetic patients. These results are associated with better renal prognosis and higher life expectancy.

Cardiovascular Diseases↗
PubMed1988

[Calcium antagonists in chronic renal failure. Undesirable effects on glomerular hemodynamics?].

Seven patients with glomerular proteinuria and hypertension (six with biopsy confirmation of glomerulonephritis, one with proteinuria after unilateral nephrectomy) were randomly given, for 14 days each, a calcium antagonist and then a conversion enzyme inhibitor, or vice versa, following a 14-day pause of all medication. Fractional albuminuria rose significantly during administration of calcium antagonists (P less than 0.05), while it decreased significantly during administration of converting enzyme inhibitor (P less than 0.05). The explanation for this finding may be that calcium antagonists raise glomerular capillary pressure by dilating the afferent arterioles, while converting enzyme inhibitors predominantly cause dilatation of the efferent arterioles.

Adult↗
PubMed1988

[The renin-angiotensin system in diabetic patients].

We review available data on the activity of the renin-angiotensin system (RAS), responsiveness to angiotensin II (ANG II), ANG II receptor number, and effects of inhibition of the RAS by angiotensin I converting enzyme (ACE) inhibitors in patients with diabetes mellitus. Most authors, including ourselves, observed a normal or enhanced activity of the RAS in metabolically stable diabetics. Increased but also reduced activity of the RAS was described in nephropathic diabetes. This is in contrast to the common suggestion that the RAS of diabetics is generally suppressed and functionally inactive. The last assumption was mainly based on the finding of reduced ANG II receptor numbers in anorectic, severely hyperglycemic rats. These findings could not be reproduced in man, and a higher ANG II receptor concentration on platelets of diabetics goes in parallel with the frequent finding of an enhanced pressor response to infused ANG II in diabetes. This increased responsiveness is most probably of functional importance since the RAS is not suppressed - as one would expect - in the face of a supranormal body sodium content. A number of data also indicate that renal resistance vessels display increased responsiveness to ANG II in diabetics. This may be a reason for hyperfiltration. This notion is further supported by the reduction of albuminuria which is usually observed following inhibition of the RAS with ACE inhibitors, and which may be an index of reduction of glomerular capillary pressure in human diabetes.

Diabetes Mellitus, Type 1↗
PubMed1988

Role of diuretics, hormonal derangements, and clinical setting of hyponatremia in medical patients.

Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid intake--conditions which have not been addressed sufficiently in published literature--we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Since a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (less than 0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35 +/- 0.15 l. In the presence of stimulated vasopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1988

Mechanism of cephalosporin-induced hypoprothrombinemia: relation to cephalosporin side chain, vitamin K metabolism, and vitamin K status.

The mechanism of cephalosporin-induced hypoprothrombinemia has been investigated in hospitalized patients, with respect to cephalosporin structure, vitamin K metabolism, and vitamin K status. Cephalosporins containing side chains of N-methylthiotetrazole (latamoxef, cefmenoxime, cefoperazone, cefotetan, cefamandole) or methyl-thiadiazole (cefazolin) all caused the transient plasma appearance of vitamin K1 2,3-epoxide in response to a 10-mg intravenous dose of vitamin K1, whereas two cephalosporins without a heterocyclic side chain (cefotaxime and cefoxitin) did not. The plasma accumulation of vitamin K1 2,3-epoxide was qualitatively similar to, but quantitatively less than, that produced by the oral anticoagulant phenprocoumon. Patients eating normally had plasma vitamin K1 concentrations (176 to 1184 pg/mL) that were within the normal range (150 to 1550 pg/mL) and their clotting tests remained consistently normal for all antibiotics tested. Patients on total parenteral nutrition had lower plasma vitamin K1 concentrations (50 to 790 pg/mL) but normal clotting before starting antibiotic therapy. Of 19 parenterally fed patients, all seven treated with latamoxef developed hypoprothrombinemia, PIVKA-II and a decrease of protein C within four days whereas 12 patients treated with cefotaxime or cefoxitin showed no clotting changes. Latamoxef-associated hypoprothrombinemia was readily reversible by 1 mg of vitamin K1 given intravenously, but hypoprothrombinemia and sub-normal plasma vitamin K1 could recur within two to three days. The data suggest that NMTT-cephalosporins are inhibitors of hepatic vitamin K epoxide reductase and that a lower nutritional-vitamin K status predisposes to hypoprothrombinemia.

Adult↗