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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 37 records · Page 2Linked to original sources
PubMed2003

ACE-inhibitors but not endothelin receptor blockers prevent podocyte loss in early diabetic nephropathy.

AIMS/HYPOTHESIS: It was the aim of our study to investigate the influence of a selective ET-A receptor antagonist LU 135252 alone and in combination with the ACE-inhibitor, trandolapril on podocyte number and morphology in streptozotocin diabetic rats. METHODS: Male Sprague-Dawley rats were injected with 65 mg streptozotocin i.v. and subsequently developed diabetes. Animals were left untreated or received daily either trandolapril (0.3 mg/kg body weight), LU 135252 (50 mg/kg body weight) or a combination of both. After 6 months the experiment was terminated. Glomerular geometry and cellularity were assessed by stereological techniques. Protein expression of TGF-beta, ET-1, PDGF-AB, fibronectin, desmin and alpha-smooth muscle cell actin was investigated by immunohistochemistry. RESULTS: The mean number of podocytes per glomerulus was lower (86+/-17 vs. 138+/-25; p<0.05) and mean podocyte volume was higher in untreated diabetic animals than in non-diabetic controls. Only ACE-i alone and in combination, but not ET(A)-RB alone prevented loss of podocytes and podocyte hypertrophy. In diabetic rats, increased numbers of PCNA positive and p27(kip1) positive cells (mainly podocytes) were reduced by all treatments, but only ACE-i decreased numbers of desmin positive podocytes and tubulointerstitial expression of TGF-beta. Albuminuria was increased in untreated diabetes and was prevented only by ACE-i and combination treatment. CONCLUSION/INTERPRETATION: Podocyte hypertrophy and degeneration is an early event in diabetic nephropathy leading to a loss of podocytes. Treatment with an ACE-i, but not with an ET(A)-RB, prevented the development of albuminuria as well as damage and loss of podocytes. The well known anti-proteinuric effect of ACE-i is presumably due at least in part to conservation of podocyte structure. Increased plasma endothelin-1 (ET-1) concentrations and urine excretion of ET-1 have been documented in patients with diabetes and proteinuria [1]. It has been shown that experimental diabetes mellitus increases renal ET-1 gene transcription [2]. To assess the relevance of the ET-system in the pathogenesis of renal structural changes in the model of the STZ-induced diabetic rat we compared the effect of an ET(A)-receptor specific antagonist with the well known beneficial effect of an ACE-i, especially on podocyte cell number and morphology.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

[Acute renal failure and hypertension crisis after a technoparty].

HISTORY: A 22 year old patient had noted progressive flank pain without recognizable urinary abnormalities for five days. INVESTIGATIONS: A urologist had noted increased serum creatine (2.1 mg/dl), hypertension (180/100 mmHg) and microhematuria. A post-renal cause was excluded by excretory urography. An interview revealed that the patient had consumed cocaine on weekends since age 19; the acute episode was preceded by a rave party with consumption of a total of 3 g of street quality cocaine. DIAGNOSIS AND TREATMENT: Because of microhematuria with a suggestive nephritic urinary sediment, the patient underwent renal biopsy. It showed acute tubular necrosis and interstitial edema, but no signs of glomerulonephritis and negative immunohistology. The patient received antihypertensive treatment. This led to rapid reversal of elevated serum creatinine and microhematuria was noted, but hypertension persisted. Currently the patient receives ACE inhibitors. CONCLUSION: Similar to what is seen in the US, cocaine use has to be considered in the differential diagnosis of acute renal failure with hypertension.

Acute Kidney Injury↗
PubMed2003

[Uremic patients--late referral, early death].

BACKGROUND AND OBJECTIVE: A number of reports from various countries document that patients with renal failure who are referred late to renal units, have more complications e. g. lack of vascular access when dialysis has to be started as well as longer hospitalisation and have also a higher risk of early death. No data on these points are available from Germany. PATIENTS AND METHODS: In a retrospective analysis the timing of referral to the nephrologists was studied in two Departments of Medicine, e. g. Heidelberg and Vienna, for all patients who started renal replacement therapy. For patients in Heidelberg the relation between timing of referral and survival on dialysis was analysed using the Kaplan-Maier-technique. RESULTS: In Heidelberg 280 patients were analysed, 174 men, 106 women, age 61.8 +/- 14.5 years; 136 diabetic patients (9 type 1). They had been referred from GPs (n = 131), specialists (diabetologists, cardiologists; n = 20), emergency departments (n = 33), other hospitals (n = 90) or other institutions (n = 16). The measured median creatinine clearance at the time of referral was 14 ml/min (5-34). The median interval between referral and start of dialysis was 17 weeks. 137 patients had been referred < 17 weeks and 143 patients > or = 17 weeks prior to the start of dialysis. 97 of the 111 patients referred < or = 4 weeks prior to dialysis and 59 of the 169 patients referred > 4 weeks had to be dialysed with a central catheter. There were clear differences in patient survival. In patients referred < 17 weeks before the start of dialysis, the actuarial risk of death during the first 12 month was 34.2 % compared to 5.5 % (p < 0.0001) in patients referred > or = 17 weeks. Even the mortality in the interval between 12 and 24 months after the start of dialysis was clearly higher (15.3 %) in patients with late compared to early referral (11.4 %). CONCLUSION: Late referral of patients with impaired renal function to renal units causes more frequent problems of vascular access, longer hospitalisation, more medical complications, higher costs and higher mortality. Early referral of patients with renal failure is indispensable to improve dialysis outcomes.

Adult↗
PubMed2003

[Aim, design and methods of the "Hypertension and diabetes screening and awareness" -- (HYDRA) study].

Aim of the study is a comprehensive clinical-epidemiological description of the prevalence of arterial hypertension and diabetes among primary care patients along with an assessment of doctor's recognition rates and prescription behaviour. The paper describes methods and design of the study and provides background information on the sampling process, instruments used as well as characteristics of doctors and patients. The study is based on a nationally representative sample of 1,912 primary care doctors and 45,000 patients that attended the doctors' office on the target days. The patients were also characterized by laboratory tests. The first stage of study consisted of a comprehensive description of the doctors' characteristics in terms of psychosocial, qualification- and provider aspects as well as attitudes towards hypertension and diabetes and their management. In the second stage all patients completed a questionnaire to describe their health behaviour and attitudes as well as the treatment history and therapy. In the third stage all patients were characterized by their doctors in terms of their diagnostic status and their past and current interventions.

Adolescent↗
PubMed2003

[Management of diabetes and hypertension: how do primary care physicians judge their performance?].

With regard to the management of hypertension and diabetes, HYDRA reveals that doctors report multiple problems in their everyday practice. Being confronted with an average of 73 patients a day, with almost every second having either diabetes or hypertension, frequently associated with multiple comorbid conditions, the core obstacle is the time factor. Doctors do not have sufficient time to perform diagnostic tests and especially no time for non-drug interventions of any type. Further available treatment guidelines are only used in 1 out of 2 doctors. Further they seem not to affect doctors performance significantly.

Adult↗
PubMed2003

[Hypertension, diabetes mellitus and comorbidity in primary care].

Almost every second patient seeing a primary care doctor suffers from arterial hypertension and about every fifth has diabetes mellitus. These diseases often occur at the same time. They are associated in more than 80% of the cases with other severe concomitant and subsequent diseases (heart attack, stroke, renal failure, neuropathy etc.). The magnitude especially of subsequent and concomitant diseases, the dimension of the personal suffering and the immense diagnostic and therapeutic challenges for the doctors have been massively underestimated so far. The article informs about the prevalence of the above disease, and structure of the problem. Before the background of an extremely high patient load seen by German General Physicians, the mainstay challenge is highlighted how to achieve further improvements of the quality of care on the basis of scientific guidelines alone, without a concomitant change in the system structure.

Adolescent↗
PubMed2003

[Microalbuminuria is an early marker for increased morbidity and mortality].

Recent studies have shown the beneficial effects of a blockade of the renin-angiotensin system (RAS) not only for blood pressure reduction but also end organ protection. One of the markers that is closely correlated with the increased cardiovascular risk is microalbuminuria. A common mediator for the development of both, microalbuminuria and end organ damage seems to be Angiotensin II, the blockade of which apparently reduces microalbuminuria as well as end organ damage. Therefore we had a closer look into pathophysiology of microalbuminuria and the relevance for end organ damage and discuss current medical strategies to alleviate these diseases.

Albuminuria↗
PubMed2003

[Diabetes, hypertension and microalbuminuria in primary care].

Microalbuminuria has been widely appreciated in recent years to be a valuable risk marker for an increased cardiovascular disease morbidity and mortality. Thus guidelines for the treatment of type-2-diabetes in Germany and the US recommend an annual screening as soon as the diagnosis of diabetes is established and a quarterly control when microalbuminuria is present. While nationally representative epidemiologic data from the US have been available, data from Germany, especially from the primary care sector are missing. This is especially important in light of the gatekeeper function of the primary care physician. The "Hypertension and Diabetes Risk Screening Study" (HYDRA) has been identifying 37.8% of patients with hypertension and diabetes to have a positive dipstick test for microalbuminuria on the study day while only 12.5% of these are diagnosed by the doctor as having nephropathy. These patients additionally show a high burden of associated comorbidities and thus call for early detection and intervention especially because effective therapy is available. Although screening for microalbuminuria is recommended in the guidelines the value of a routine screening for microalbuminuria in primary care is under recognized.

Adult↗
PubMed2003

[Nephropathy: an overview for daily practice].

The examination of renal function in the daily practice may give important information on the risk status of a given patient. For example, the diagnosis of microalbuminuria carries high predictive value for a future cardiovascular risk of patients with hypertension, diabetes, congestive heart failure, as well as myocardial infarction. The findings of the Hypertension and Diabetes Screening and Awareness Study (HYDRA) indicate that screening for microalbuminuria is performed not often enough in patients with diabetes or hypertension, respectively, and a positive screening finding often does not trigger necessary consequences as for additional diagnosis or therapy.

Adult↗
PubMed2003

Hypertension after renal transplantation.

With current immunosuppression elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this finding are impairment of renal function, secondary to chronic allograft nephropathy or (less frequently) recurrence of primary renal disease, the use of calcineurin inhibitors as immunosuppresants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenos- ing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia and (genetic predisposition to) hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, ACE inhibitors are indicated in the treatment, but, given the causal role of sodium retention in graft vasoconstriction, diuretics and calcium channel blockers remain main stays of antihypertensive treatment in the renal allograft recipient.

Antihypertensive Agents↗
PubMed2003

Special characteristics of atherosclerosis in chronic renal failure.

Cardiovascular complications are a major clinical problem in patients with chronic kidney disease and end stage renal failure. Death from cardiac causes accounts for 40%-50% of all deaths in these patients and is thus up to 20 times more common in uremic patients than in the general population. Cardiovascular pathology in patients with renal failure is complex, but accelerated atherosclerosis has repeatedly been discussed as one major cause. The prevalence of coronary atheroma in uremic patients is approximately 30% by autopsy and coronary angiography studies. Not only is the prevalence of atherosclerotic lesions very high, but also the case fatality rate of myocardial infarction. Recently, excess mortality in uremic patients having had a myocardial infarct was noted; the one year mortality was 55.4% and 62.3% in uremic patients with and without diabetes, respectively, compared to about 10-15% in non-uremic patients. This study goes beyond the well-known notion that urea is associated with more severe atherosclerosis and shows that, in addition, the adaptation to coronary perfusion deficits is inappropriate. Recent clinical and autoptical studies in pre-dialysis and dialysis cohorts have documented increased intima and media thickness which appear early in the course of renal disease; Vascular wall thickening in renal failure seems to be modified at least in part by parathyroidhormone (PTH) and endothelin-1 (ET-1) which are both elevated in patients with renal failure. In experimental renal failure a direct effect of high phosphorus diet in arterial wall thickening was also documented. In addition to thickening of the vascular wall marked structural alterations were noted in renal failure i.e. a decrease in elastic fibre content and an increase in extracellular matrix. Furthermore, increased calcification of coronary atherosclerotic plaques and of the media of the aorta and some peripheral arteries has been documented in patients with renal failure. Factors contributing to this increased calcification process may be deposition of abundant circulating calcium, microinflammation, oxidative stress, de novo expression of bone morphogenous proteins and lack of inhibitors of calcifcation. These changes in vascular wall composition may alter vessel elasticity and thus contribute to impaired vessel function in renal failure. It is obvious from the above mentioned facts that cardiovascular disease in the renal patient is certainly multifaetorial in origin. There are, however, important issues to adress in the future, like (I) the characterization of vascular morphology in the different vascular beds, (II) the pathomechanisms of vascular and plaque calcification as well as the potential beneficial effect of rigorous control of non-classical risk factors (i.e. high P or Ca x P, inflammation, oxidative stress, etc.), (III) an additive or supraadditive effect of various classical and non-classical risk factors and (IV) the role of diabetes mellitus in modifying these vascular alterations.

Animals↗