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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 73 records · Page 4Linked to original sources
PubMed2000

[The quality of the treatment of diabetics in kidney failure in Germany].

BACKGROUND AND OBJECTIVE: In recent years there has been a rapid increase in the number of dialysis-dependent diabetics in Germany. Survival on dialysis is not satisfactory and damage acquired in the preterminal stage of renal failure is thought to play an important role. Late referral to a nephrologist and insufficient quality of medical management are thought to contribute importantly to poor outcome. This hypothesis was evaluated in the present study. PATIENTS AND METHOD: The data of all 173 diabetic patients (16 with type 1, 157 with type 2 diabetes, 90 men, 83 women, mean age 63.3 [31-95] years), who had been referred in 1996 for the first time to five renal units, were retrospectively assessed using a structured protocol. RESULTS: Patients were usually referred in advanced renal failure (median creatinine clearance 29 ml/min, range 1-216) with insufficient control of systolic (170 [120-260] mmHg) and diastolic blood pressure (90 [60-180] mmHg), insufficient antihypertensive therapy (without treatment 32 of 173 patients; median number of classes of antihypertensive agents used 2 [range 1-6]; ACE inhibitors 79 of 173 patients), high HbA1c (7.9 [4.9-15.7]%) and LDL cholesterol (176 [67-307] mg/dl). Immediate dialysis was required in 45 patients. CONCLUSION: The data document insufficient quality of treatment and late incorporation of a nephrologist into the medical team involved in the care of diabetic patients. Changes in the structure of diabetes care are necessary to improve treatment quality.

Adult↗
PubMed2000

Atherosclerotic complications after renal transplantation.

Death with functioning graft, the most frequent cause being cardiac death, continues to be the most frequent cause of long-term graft loss. The risk of cardiovascular death in the transplanted patient is lower than in patients with other modalities of renal replacement therapy, but continues to be substantially higher than in the general population. Amongst the factors predicting patient and graft survival are hypertension, dyslipidemia, smoking and possibly hyperhomocysteinemia. It is concluded that lowering of blood pressure to levels far lower than levels accepted in the past, more widespread administration of statines, cessation of smoking and possibly administration of folate should reduce cardiovascular mortality and possibly also influence chronic allograft vasculopathy.

Arteriosclerosis↗
PubMed2000

Circadian rhythm of blood pressure in renal disease.

Ambulatory blood pressure (BP) measurement has added a new dimension to the evaluation of abnormal BP in patients with various stages of renal disease. Although there is not complete consensus concerning the definition of normal values, a high prevalence of an abnormal circadian BP profile is noted in patients with essential hypertension with renal involvement (ie, microalbuminuria), in diabetic patients (particularly those with microalbuminuria or overt proteinuria), and in patients with primary chronic renal disease. Studies in diabetic patients point to an important role of both hypervolemia and disturbed autonomic innervation in the genesis of an abnormal circadian BP profile. In both patients with diabetic renal disease and patients with nondiabetic renal disease, retrospective studies suggest that an abnormal nocturnal decline in BP is associated with more rapid progression independent of 24-hour mean arterial pressure. The abnormal circadian BP profile persists in dialyzed patients, is ameliorated by long and frequent dialysis sessions, but is not completely normalized after successful renal transplantation.

Blood Pressure↗
PubMed2000

[Diuretics and kidney diseases].

The main indications for diuretic treatment of renal patients are edema and hypertension. Pharmacokinetics and pharmacodynamics of diuretics are altered in patients with proteinuria and/or impaired renal function. These patients exhibit avid sodium retention. Diuretics are partially inactivated by binding to proteins in tubular fluid. The natriuretic response to diuretics is limited by counter-regulation, specifically increased proximal tubular reabsorption in response to hypovolemia and increased distal tubular sodium reabsorption in response to increased sodium load. At higher serum creatinine values, thiazides are no longer sufficiently effective in monotherapy. The diuretics of first choice are then loop diuretics, potentially in combination with thiazide diuretics. Potassium-sparing diuretics are contraindicated. The most important side effects of diuretics are hypovolemia with orthostatic hypotension, hypokalemia, metabolic alkalosis, increase of creatinine concentration and (rarely) hyponatremia. Diuretic treatment should be accompanied by reduction of dietary sodium intake. Important points are selection of an adequate dose (in problematic cases dose-finding via urine sodium measurements) and selection of proper dosing intervals. If cases do not respond to loop diuretic monotherapy, combination with thiazide diuretics or intravenous administration of loop diuretics should be considered.

Benzothiadiazines↗
PubMed2000

Effects of ACE inhibition and bradykinin antagonism on cardiovascular changes in uremic rats.

BACKGROUND: Cardiovascular death continues to be a major problem in renal failure. Structural abnormalities of the heart and the vasculature contribute to the increased cardiovascular risk. They are ameliorated by angiotensin-converting enzyme (ACE) inhibitors, but because of the nonspecifity of ACE inhibition, it is uncertain whether the beneficial effect is mediated by interfering with angiotensin II (Ang II) or by modulating other effector systems, for example, bradykinin. METHODS: To assess a potential role of bradykinin, subtotally nephrectomized Sprague-Dawley rats (SNX) received either the ACE inhibitor Ramipril (Rami, 0.2 mg/kg body weight p.o.), the specific B2 bradykinin receptor antagonist Hoe140 (0.2 mg/kg body weight, s.c.), or a combination of both, and were compared to sham-operated controls. To separately assess the effect of Ramipril on development and reversal of structural abnormalities, animals were either treated from the third day after SNX or from the fourth week after SNX onward (0.01 mg/kg body weight, p.o.). RESULTS: Heart and aorta were evaluated by morphometric and stereologic techniques. The weight of the perfused left ventricle, as an index of cardiac hypertrophy, was significantly higher in untreated SNX. While it was significantly lower in animals with early and late Ramipril treatment, the beneficial effect was completely antagonized by Hoe140. The wall-to-lumen ratio of intramyocardial arterioles was significantly higher in untreated SNX compared with controls, but failed to be modified by administration of either Ramipril or Hoe140. In the heart, the intercapillary distance was significantly higher in SNX, but it was not lowered by either early or late Ramipril or Hoe140 treatment. Treatment of SNX with Hoe140 alone, however, resulted in a marked further increase in intercapillary distance. The wall thickness of the aorta was significantly higher in SNX than in controls; early and late Ramipril treatment prevented such increase, and this effect was antagonized by Hoe140. CONCLUSION: These findings illustrate that bradykinin plays an important role for the beneficial effect of Ramipril in preventing (and potentially reversing) abnormal cardiovascular structure in uremic hypertensive rats.

Adrenergic beta-Antagonists↗
PubMed2000

Counteracting progression of renal disease: A look into the future.

It is the very nature of research, including medical research, that truly novel results are not predictable. Nevertheless, some predictions concerning the understanding and management of progression of renal disease are plausible. It is very likely that in the future, exploding health budgets will force authorities and nephrologists to more effectively apply existing knowledge in this field to patients with early renal disease, particularly diabetics. We hope that this optimistic note is justified, although experience admittedly indicates that it is very much against human nature to behave rationally. With the powerful methodological tools available today, it is safe to predict that insight into the mechanisms underlying progression will also increase. Although pharmacological blockade of the renin-angiotensin system has been one of the great success stories of the past two decades, in many patients, progression is seen despite administration of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers. Fortunately, additional targets for intervention, such as endothelin-1, inflammatory cascades, chemokines, etc., are on the horizon. A particularly fertile target for prevention of progression will be kidney grafts, since it has become increasingly clear that factors unrelated to allo-immunity play an important role in chronic allograft nephropathy.

Disease Progression↗
PubMed2000

Microvascular disease--the Cinderella of uraemic heart disease.

It has been known for a long time that atherosclerosis, particularly plaques in the epicardiac coronary conduit arteries, are more frequent in patients with chronic renal failure than in non-uraemic patients. It has been only recently, however, that modification of post-stenotic remodelling of cardiac arteries as well as abnormalities of the arterioles and the capillaries in the myocardium of uraemic animals and uraemic patients have been recognized and analysed. These lesions can be dissociated from changes in blood pressure and may be an important cause contributing to reduced ischaemia tolerance and cardiac malfunction (pump failure, arrhythmia) thus predisposing to cardiac death. Recent insights into angiogenesis, particularly adaptive angiogenesis in response to hypoxia, may potentially provide novel approaches to the understanding and management of cardiac microangiopathy in renal failure.

Animals↗