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Biomedical subjects

C Hasslacher

Publications and source records attributed to C Hasslacher.

At least 19 recordsLinked to original sources
PubMed1992

Effects of combined renovascular hypertension and diabetes mellitus on myocardial cells, non-vascular interstitium and capillaries: a stereological study on rat hearts.

The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive non-diabetic animals were compared to diabetic and non-diabetic controls. Hypertension was established for 12 weeks by a surgical stenosis of the left renal artery; diabetes mellitus was maintained for 8 weeks by a single intraperitoneal injection of 60 mg/kg streptozotocin. Light microscopic stereology did not reveal significant divergences between diabetic hypertensives and non-diabetic hypertensives. Hypertension induced a focal perivascular and interstitial fibrosis with increased volume densities of non-vascular interstitium and fibrosis (P less than 0.001). Capillary density (QA) was decreased in transverse sections (P less than 0.01) and increased in longitudinal sections (P less than 0.01). This indicates a three-dimensional remodelling of the capillary bed with an increased number of obliquely running capillaries. At least the length density (LV) of capillaries (mm/mm3) tends to be normalized in long-term renovascular hypertension. At the ultrastructural level, a synergism of hypertension and diabetes mellitus was observed: the volume ratio of mitochondria to myofibrils was significantly decreased in hypertensive diabetics, but not in non-diabetic hypertensives or in diabetics. This may enhance the risk of cardiac deterioration. We conclude that the primary target of the synergistic damage in hypertensive diabetic heart muscle disease is the myocardial cell and not the cardiac interstitium.

Animals↗
PubMed1992

The response of GFR to amino acids differs between autosomal dominant polycystic kidney disease (ADPKD) and glomerular disease.

We compared the glomerular filtration rate (GFR) response to amino acids in patients with glomerular disease and polycystic kidney disease. The GFR response to infusion of amino acids (75 g/12 h), of dopamine (2 micrograms/kg per min), or their combination was evaluated in nine healthy probands and in patients with two types of renal diseases at various degrees of renal function: 15 patients with ADPKD and 11 patients with glomerular disease (IgA glomerulonephritis or diabetic nephropathy). Steady-state inulin infusion technique was used. In healthy subjects amino acids increased median C(in) in response to amino acids was not found in glomerular disease. In contrast in most ADPKD patients median C(in) increased after amino acids (+6.0 ml/min; range -4 to +68), (P less than 0.05). The response to amino acids was not modified by dopamine. The results demonstrate that amino acid-induced acute changes of glomerular filtration differ in polycystic kidney disease compared with glomerular disease. These observations may have implications with respect to mechanisms of progression.

Adult↗
PubMed1992

[ACE inhibitor effects on structure and function of the glomerular basement membrane].

Metabolism of proteins which compose capillary basement membrane is altered in diabetic patients. In the kidney, this leads to an impaired permselectivity of glomerular basement membrane and consequently to onset of proteinuria. Proteinuria which is often increased by hemodynamic factors, initiates and promotes the development of diabetic glomerusclerosis. Aside from near-normal metabolic control, special antihypertensive treatment can reduce proteinuria and retard loss of kidney function in proteinuric diabetic patients. The beneficial effect of ACE-inhibitors on course of diabetic nephropathy is generally thought to be a consequence of decreased systemic and intraglomerular pressure. However, recent longterm studies in Type I and Type II diabetic patients with nephropathy showed that ACE-inhibition can reduce proteinuria independent from their hemodynamic effects and, thus, improves the filtration properties of glomerular basement membrane. This may be due to an influence of ACE-inhibition on metabolism of basement membrane proteins.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Excretion of beta-N-acetylglucosaminidase in urine in type I and type II diabetic patients with and without nephropathy].

The clinical aspects of the excretion of beta-N-acetylglucosaminidase (beta-NAG, EC 3.2.1.30) in urine of type I and type II diabetics with and without nephropathy are evaluated. Correlation between concentration of albumin and of beta-NAG activity in urine is determined and the circadian rhythm of beta-NAG excretion in urine is examined, the indication of glomerular and tubulointerstitial damage is discussed. Longitudinal studies should demonstrate, whether an increased beta-NAG activity in urine of diabetics with normoalbuminuria is an indicator of nephropathy or a predictor of nephropathy if raised albuminuria is observed.

Acetylglucosaminidase↗
PubMed1991

[Albuminuria in diabetes mellitus].

A critical overview on different procedures and methods for an early diagnosis of diabetic nephropathy is given. Genetic markers, morphology and function of glomerula, blood pressure and the metabolic state of diabetics are especially discussed. From the risk markers available today microalbuminuria (20 to 200 micrograms/min resp. 20 to 200 mg/l) is shown to be most suitable for recognizing patients developing nephropathy.

Albuminuria↗
PubMed1990

[Diagnosis and therapy of diabetic nephropathy].

Diabetic nephropathy continues to be a common complication and has an unfavorable prognosis. Metabolic and hemodynamic factors determine the natural history of the condition. Of importance for the prognosis is the detection of nephropathy at an early stage. Such early diagnosis is not possible through the detection of microalbuminuria (incipient nephropathy stage). At this stage, further progress can be reversed by optimizing the metabolic situation and initiating early treatment of increasing blood pressure. For this reason, all diabetics should be submitted to early screening for microalbuminuria. When proteinuria persists (clinically manifest nephropathy stage), renal function usually declines progressively. Vigorous treatment of hypertension, optimal metabolic management, and normalization of protein intake can slow down the rate of continued loss of renal function.

Albuminuria↗
PubMed1990

[Improved prognosis of Type I and Type II diabetics with nephropathy].

Between 1966 and 1985, 72 type I and 75 type II diabetics developed persistent proteinuria. These patients were divided into two groups according to time of onset of proteinuria (1966 to 1975 and 1976 to 1985, respectively). In these groups, we investigated both the quality of antihypertensive treatment and metabolic control as well as the course of nephropathy and life prognosis. Control of hypertension was markedly improved in type I and type II diabetics with later onset of proteinuria (1976 to 1985), compared with patients who developed proteinuria between 1966 and 1975. However, metabolic control was improved only in type I diabetics. Compared with the previous decade, prevalence of renal insufficiency was lowered by one-third in type I and type II diabetics with later onset of proteinuria (1976 to 1985). During the six-year observation period, 32% of type I and 72% of type II diabetics who developed proteinuria between 1966 and 1975 died, whereas all type I and 54% of type II diabetics with later onset of proteinuria (1976 to 1985) survived. The study shows that conservative treatment methods, especially lowering of blood pressure, may improve prognosis for proteinuric type I and type II diabetic patients.

Adolescent↗
PubMed1990

Diabetic nephropathy--are there differences between type I and type II?

It has commonly been assumed that the renal risk in type II diabetes is markedly lower than in type I diabetes since only approximately 5% of the former but 40% of the latter experience renal failure. Based on our observations in the diabetes outpatient department of the University of Heidelberg, we conclude that the cumulative risk of developing proteinuria for the nonproteinuric type II diabetic and the cumulative risk of developing renal failure for the proteinuric type II diabetic are comparable with the respective risks of the type I diabetic. This observation is noteworthy since there is no uncontroversial evidence of hyperfiltration in early type II diabetes. Type II diabetes may be an interesting model for testing the hyperfiltration theory.

Diabetes Mellitus, Type 1↗
PubMed1989

[Microalbuminuria screening in diabetics].

Nocturnal albumin excretion rate was measured in 133 diabetics and the results were compared with those in first morning urine and urine spontaneously voided later in the morning. Albumin concentrations greater than 20 mg/l in the first morning urine indicated a raised albumin excretion rate of 20-200 micrograms/min (sensitivity 86%, specificity 98%). Simultaneous creatinine measurement and calculation of the albumin/creatinine ratio did not increase sensitivity or specificity. An albumin concentration greater than 20 mg/l in spontaneously voided day urine pointed to a raised albumin excretion rate (sensitivity 90%, specificity 60%). These results suggest that determining the albumin concentration in the first voided morning urine is suitable as screening test for microalbuminuria.

Adult↗
PubMed1989

Similar risks of nephropathy in patients with type I or type II diabetes mellitus.

It is commonly assumed that in patients the risks of developing nephropathy and uraemia are high in type I and low in type II diabetes mellitus. Since type II occurs mostly in elderly individuals with limited life expectancy and high cardiovascular mortality, the true risk may have been underestimated, as many patients do not survive to experience renal complications. To assess renal risk further, we evaluated all patients with type II and type I diabetes mellitus without severe secondary disease who were followed in the outpatient clinic between 1970 and 1985. The cumulative risk of proteinuria after 20 years of diabetes mellitus was 27% in type II and 28% in type I, the findings after 25 years were 57% and 46% respectively. The cumulative risk of renal failure, i.e. serum creatinine greater than 1.4 mg/dl, after 3 years of persisting proteinuria was 41% in both type II and type I, and after 5 years of proteinuria were 63% and 59% respectively. We conclude that the renal risk is similar in patients with type II and type I diabetes mellitus.

Adolescent↗
PubMed1989

Reaction patterns of the myocardial interstitium in different models of cardiac hypertrophy--stereological investigations.

Several experimental models of cardiac hypertrophy were investigated in rats: 1. mild hypertrophy induced by physical exercise (18 weeks), 2. mild hypertrophy induced by renovascular hypertension (24 weeks), 3. moderate hypertrophy induced by renovascular hypertension in diabetic and non-diabetic animals (8 weeks), 4. moderate hypertrophy induced by renovascular hypertension in diabetic and non-diabetic animals (12 weeks), 5. moderate hypertrophy induced by thyroxin application (4 weeks), 6. mild hypertrophy in chronic uremia (5/6 nephrectomy, 3 weeks). It is concluded from quantitative stereological parameters of the left ventricular papillary muscles that 1. in hypertrophic hearts myocardial blood flow and oxygen consumption, respectively, rather than the size of muscle fibres determine the capillary supply of the myocardium, 2. interstitial fibrosis occurs in hypertrophy induced by chronic pressure overload and depends on degree and duration of hypertension, 3. the extent of interstitial fibrosis in hypertension is magnified by diabetes mellitus, and 4. the interstitial fibrosis which occurs in chronic uremia is not caused by hypertension.

Animals↗
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

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↗