Biomedical subjects
E Ritz
Publications and source records attributed to E Ritz.
[Vena cava ultrasonography for the assessment of hydration status in kidney insufficiency].
Vena cava diameter (VCD) was measured by ultrasonography in 10 acutely hypervolemic dialysis patients (6 men, 4 women; mean age 61.3 +/- 15.4 years), results being compared with the level of the central venous pressure (CVP) and, in 39 long-term dialysis patients (18 men, 21 women; mean age 56 +/- 15 years), with the plasma concentration of atrial natriuretic peptide (ANP). In 86 subjects without renal disease (43 men, 43 women; mean age 39.4 +/- 14.6 years) there was a statistically highly significant correlation between the end-expiratory VCD and heart rate (r = -0.63; P < 0.001). These data were used to construct a VCD/heart rate (HR) nomogram. In the ten dialysis patients HR-adjusted VCD correlated significantly at various hydration states (54 measurements) with the CVP (r = 0.72; P < 0.001). The steep slope for the relationship between CVP and VCD showed marked interindividual variations. However, in all patients (except one) with a raised CVP (> 12 cm H2O) the HR-adjusted VCD was above the 95th percentile. In the 39 patients on long-term dialysis (13 with, 25 without predialysis tricuspid regurgitation [TR] there occurred a parallel decrease in VCP and ANP during removal of fluid. In the 25 patients without TR, the fall in ANP concentration and VCD correlated significantly (r = 0.70; P < 0.001). These results indicate that, in patients with renal failure but normal cardiac function, measurement of the VCD by ultrasonography provides an adequate index of hydration.
1,25-dihydroxyvitamin D3 production and vitamin D3 receptor expression are developmentally regulated during differentiation of human monocytes into macrophages.
It has been well established that human mononuclear phagocytes have the capacity to produce 1,25-dihydroxy-vitamin D3 [1,25(OH)3D3] and express the vitamin D receptor (VDR). However, 1 alpha-hydroxylase activity and VDR receptor expression during differentiation of monocytes (MO) into mature macrophages (MAC) have not been previously examined. The in vitro maturation of blood MO can serve as a model for the in vivo transformation of immature blood MO into MAC. Here, when cultured in the presence of serum, MO undergo characteristic changes in morphology, antigenic phenotype, and functional activity consistent with their differentiation into MAC. We serially measured 1,25(OH)2D3 and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] synthesis, specific [3H]-1,25(OH)2D3 binding, and VDR mRNA levels during in vitro maturation of MO into MAC and correlated these functions with maturation-associated changes in the phenotype (MAX.1 and CD71) and secretory repertoire (interleukin-1 beta [IL-1 beta], neopterin) of the cells. MO showed only little conversion of 25-(OH)D3 into 1,25(OH)2D3 (1.4 +/- 0.4 pmol/10(6) cells/6 h, n = 5) that increased gradually during maturation into MAC at day 8 of culture (5.3 +/- 4.3 pmol/10(6) cells/6 h, n = 5). Interferon-gamma (IFN-gamma) increased baseline 1,25(OH)2D3-synthesis approximately twofold during all phases of differentiation. The time course of increased 1,25(OH)2D3-synthesis correlated with enhanced secretion of neopterin and expression of MAX.1 and CD71. The addition of exogenous 1,25(OH)2D3 did not influence constitutive 1,25(OH)2D3 synthesis, but IFN-gamma-stimulated production was suppressed to baseline levels. Exogenous 1,25(OH)2D3 also stimulated 24,25(OH)2D3 synthesis in freshly isolated MO (from 1.0 +/- 0.8 pmol/6 h to 5.6 +/- 0.9 pmol), whereas matured MAC showed no 24,25(OH)2D3 synthesis. Furthermore, we examined the expression of the VDR during the differentiation process. VDR mRNA and protein were constitutively expressed in MO, whereas VDR was downregulated in mature MAC on both the mRNA and protein levels. Homologous upregulation of VDR protein by 1,25(OH)2D3 occurred in MO and, to a lesser degree, in MAC. In contrast, VDR mRNA concentrations were not influenced by 1,25(OH)2D3. Taken together, our results show that MO into MAC differentiation in vitro is associated with (1) an enhanced capacity to synthesize 1,25(OH)2D3, (2) a loss of 24,25(OH)2D3-synthesizing activity, and (3) a decrease in the expression of VDR mRNA and protein. Because 1,25(OH)2D3 was shown to induce differentiation of MO into MAC, our data sugest an autoregulatory mechanism of MO/MAC generation by 1,25(OH)2D3.
[Nonocclusive intestinal ischemia as a complication of hemodialysis treatment].
A 52-year-old man on haemodialysis treatment for chronic glomerulonephritis also had a nephrotic syndrome, hypercholesterolaemia, severe arterial hypertension and peripheral vascular disease in stage IIb. He also was a heavy smoker. Following a nonspecific diarrhoeal illness, which caused haemoconcentration, he developed abdominal pain and fever. WBC count (29,000/microliter) and serum lactate level (18.2 mmol/l) were elevated, and there were clinical signs of lower abdominal peritonitis. Laparotomy revealed multiple ischaemic segments. The arteries were not thrombosed but had severe atheromatous changes. There is an increasing incidence of such nonocclusive intestinal ischaemia because there are more elderly people and more patients with high-risk factors among those requiring dialysis.
[Aluminum accumulation and deferoxamine].
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[The progression of kidney failure].
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[Acute myoglobinuric kidney failure in McArdle's syndrome. The diagnostic significance of 31P nuclear magnetic resonance spectroscopy].
A 44-year-old man developed acute renal failure, associated with reddish brown urine, after severe physical exertion. Since childhood his physical capacity was known to be limited. Muscular indurations, cramps and pains had occurred after muscular work. Serum creatinine level on the day before hospitalization was 10.0 mg/dl, creatine-kinase activity 3,790 U/l, lactate dehydrogenase activity 670 U/l, myoglobin level 701 ng/ml. Cause of the rhabdomyolysis was thought to be McArdle's disease (glycogen storage disease type V: abnormal skeletal muscle glycogen utilization). 31P-magnetic resonance spectroscopy, which gives characteristic spectra with anaerobic muscle work, provided the diagnosis, which was confirmed by measurement of myophosphorylase activity in a muscle biopsy (zero activity). After two dialysis sessions and alkalinization of the urine diuresis again occurred and the retention indicators fell to normal in the course of the subsequent 18 months. Creatinine kinase activity remained elevated.
[Why is there a type-2 diabetes?].
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Renal pressure-natriuresis relationship.
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[Isolated systolic hypertension in old age].
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[Dietary aspects and nutritional guidelines in kidney diseases].
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Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection.
The goal of this study was to quantitate the effect of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection. The study was carried out on low and normal salt intake to assess potential interaction with salt balance. Eighteen healthy normotensive volunteers were examined in a double placebo-controlled parallel group design. Subjects were randomly put on either low-salt (20 mmol/day) or normal-salt (110 mmol/day) diet. In either arm of the diet volunteers were first treated orally with placebo for 1 week and subsequently with 2.5 mg/day of the angiotensin-converting enzyme inhibitor cilazapril for another 1 week. Cumulative 24-h urinary sodium excretion was measured on the 6th day of the respective week after sham injection and on the 7th day after injection of 40 mg furosemide. Compared to pretreatment with placebo, pretreatment with cilazapril resulted in a higher cumulative sodium excretion after furosemide injection (day 7) than after the sham injection (day 6) on both salt intakes. The difference in natriuresis (cilazapril versus placebo) was evident 2 and 3 h after injection of furosemide. Neither the time of onset nor the magnitude of antinatriuresis were affected by cilazapril. Following furosemide angiotensin II increased significantly even after cilazapril pretreatment. Cilazapril tended to reduce urinary furosemide excretion. At any given urinary furosemide concentration, the increment in urinary sodium excretion was significantly greater with cilazapril irrespective of salt intake. The study shows that (a) cilazapril increases furosemide-induced natriuresis irrespective of salt intake, (b) antinatriuresis is not affected by cilazapril, and (c) angiotensin II levels rise after furosemide on cilazapril in therapeutic doses.
Survival and predictors of death in dialysed diabetic patients.
The objective of this study was to examine diabetic patients at the time of admission to maintenance haemodialysis and to follow them for 36 months in order to define predictors of cardiovascular and non-cardiovascular death. This prospective study comprised all consecutive diabetic patients admitted to 28 German dialysis centres between January 1985 and October 1987; 196 patients were examined, 67 Type 1 (insulin-dependent) diabetic (43 male, 24 female; median age 49 years, range 22-73) and 129 Type 2 (non-insulin-dependent) diabetic patients (54 male, 75 female; 64 years, range 37-82). Outcome measures were death, i.e. myocardial infarction, sudden death, cardiac death of other causes, stroke and non-cardiovascular death. Actuarial survival 36 months after the beginning of dialysis was similar in Type 1 (40%) and Type 2 diabetic patients (43%) despite the age difference. Causes of death were myocardial infarction (18%), sudden death (18%), other cardiac causes (18%); stroke (6%); septicaemia (17%) mostly originating from diabetic foot problems; and interruption of therapy. Survival rates and the proportion dying from cardiac causes were similar in patients with diabetic nephropathy or with other primary chronic renal disease and coincidental diabetes. On dialysis, de novo amaurosis or de novo amputation was not observed in any patient. The strongest predictor of myocardial infarction or sudden death was serum lipids on admission. Duration of hypertension, blood pressure at the time of admission to dialysis, left ventricular hypertrophy or end-diastolic diameter by echocardiography, Sokolow index and average predialysis blood pressure, smoking, interdialytic weight gain and type of dialysis were not predictive of cardiovascular death or death by all causes.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension in diabetic nephropathy: prevention and treatment.
Hypertension is the major determinant of morbidity and mortality in diabetic patients. In type I diabetes hypertension develops in parallel with the evolution of nephropathy, whereas in type II diabetes hypertension precedes the onset of manifest diabetes mellitus by years or decades. Nephropathy is equally common in types I and II diabetes. Strong genetic determinants for nephropathy have been recognized, but it is unclear whether a genetic predisposition to hypertension and elevated sodium-lithium countertransport are involved. In epidemiologic studies hypertension is related to the risk and rate of evolution of diabetic nephropathy, retinopathy, and cardiovascular complications. The relationship appears to be causal, because antihypertensive treatment attenuates the rate of loss of glomerular filtration. In this respect angiotensin-converting enzyme inhibitors appear to be superior (renal protective action). Calcium channel blockers have been promising in experimental studies, but clinical information is currently incomplete.
Morbidity and mortality due to hypertension in patients with renal failure.
The incidence of, and the mortality from, cardiac disease is strikingly increased in dialysis patients. Coronary disease existing prior to the onset of dialysis is an important determinant of ischemic heart disease (IHD) on dialysis. Death from IHD on dialysis is higher by factor 5-20 than in the general population. In several studies either a marginal or no relation between blood pressure on admission to renal replacement therapy, or average predialysis blood pressure and cardiac death has been noted. In other studies blood pressure was, however, predictive of IHD. Such discrepancies may be explained by a low-risk threshold, a nonlinear relationship, and the necessity to examine large patient cohorts to document the effect. Of great importance may be the potentially increased susceptibility of the heart to hypertensive injury and ischemia. This may be related to factors like left ventricular hypertrophy, cardiac fibrosis and altered cardiac mechanical properties, diminished coronary reserve, and reduced ischemia tolerance, particularly during intradialytic hypotensive episodes due to compromised microcirculation and disturbed insulin-induced glucose uptake and abnormalities of autonomous neural innervation of the heart.
Hypertension and the kidney--an overview.
The kidney plays a major role in the genesis of any type of hypertension, as demonstrated by experiments which show that hypertension can be "transplanted" when the kidney itself is transplanted. Hypertension is common in patients with renal disease, and may occur even at normal glomerular filtration rates. The mechanisms that promote hypertension and are involved in renal disease comprise both activation of pressor mechanisms and failure of depressor mechanisms, the latter having been considerably less well studied. The major pressor mechanisms are an abnormal pressure-natriuresis relationship and inappropriate activity of the renin-angiotensin system.
Scleroderma renal crisis as a presenting feature in the absence of skin involvement.
A 56-year-old man was admitted to the nephrology unit with a short (6-week) history of severe hypertension that necessitated renal replacement therapy within 7 days after admission. Renal biopsy showed features of thrombotic microangiopathy in arterioles and small arteries with occluding thrombi. The skin was unremarkable at the time of admission. Progressive skin lesions with scleroderma, telangiectasia, sclerodactyly, and generalized cutaneous sclerosis developed within 4 weeks and the specific skin changes were found on skin biopsy. On admission antinuclear antibody titers were high (1:10, 240) with a nucleolar pattern, and PM-Scl antibodies (1:5, 120) were present. In the present case the diagnosis of scleroderma renal crisis was made in vivo by renal biopsy. Renal and skin biopsies documented that renal lesions may precede the clinically manifest skin lesions of progressive systemic sclerosis.
Stimulation of mononuclear cells by contact with cuprophan membranes: further increase of beta 2-microglobulin synthesis by activated late complement components.
Contact of mononuclear cells (MNC) with cuprophan membranes in vitro causes an increase in beta 2-microglobulin (beta 2m) synthesis. Since in vivo the dialyzer membrane is rapidly coated with plasma proteins, contact activation of MNC was tested in the presence of normal human serum (NHS). After contact with cuprophan, deposition of C5b-9 on the cells was seen, followed by an increase in beta 2m synthesis and cytokine release, exceeding that seen after contact activation in the absence of serum. Inactivated serum or serum deficient in C8 did not increase beta 2m production, indicating that the additional activation was due to complement C5b-9. The results suggest that there are two cuprophan-related mechanisms of cell activation: one by contact of cells with the membrane, the other by the complement activation products. Both might synergistically contribute to an increased beta 2m synthesis in hemodialysis patients.