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Biomedical subjects

M Zeier

Publications and source records attributed to M Zeier.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1999

HIV type 1 V3 domain serotyping and genotyping in Gauteng, Mpumalanga, KwaZulu-Natal, and Western Cape Provinces of South Africa.

More than 20.8 million people are living with HIV/AIDS in sub-Saharan Africa, with southern Africa the worst affected area and accounting for one of the fastest growing AIDS epidemics worldwide. Samples from 81 patients, including 25 from KwaZulu-Natal, 26 from Gauteng, 5 from Mpumalanga, and 25 from Western Cape Province, were serotyped using a competitive V3 peptide enzyme immunoassay (cPEIA). Viral RNA was also isolated from serum and the V3 region amplified by reverse transcriptase polymerase chain reaction (RT-PCR) to obtain a 240-bp product for direct sequencing of 29 samples. CLUSTAL W was used to make multiple sequence alignments. Distance calculation, tree construction methods, and bootstrap analysis were done using TREECON. Subtype C-like V3 loop sequences predominate in all provinces tested in South Africa. Discordant sero- and genotype results were observed in one patient only. The correlation between sero- and genotyping was 96% (24 of 25) in KwaZulu-Natal and 100% in Gauteng and Mpumalanga. In Western Cape Province 18% of patients were identified as sero/genotype B and 82% as sero/genotype C. Our data show that results of the second-generation V3 cPEIA correlated well with V3 sequencing and would be a rapid and affordable screening test to monitor the explosive southern African HIV-1 epidemic.

Adolescent↗
PubMed1999

Antihypertensive therapy in renal patients - benefits and difficulties.

High blood pressure values, diastolic and systolic, are associated with decreased renal function. This is particularly true when the diastolic blood pressure is higher than 90 mm Hg. Several studies showed that lowering of the blood pressure within the range of normotension according to the WHO causes a reduction in the rate of progression to terminal renal failure. These studies have led to recommendations to aim at a target blood pressure of approximately 125/75 mm Hg in the treatment of patients with glomerular diseases and particularly diabetic nephropathy with proteinuria >1 g/day. In contrast to these results, blood pressure values corresponding to the recommendation (</=125/75 mm Hg) of the JNC VI (see text) were achieved in 15% of the patients only. It has also been shown that at any given level of an average 24-hour blood pressure, patients with an insufficient decrease of the blood pressure during nighttime have a higher risk to progress to terminal renal failure. Thus it is very important to lower the nighttime blood pressure and to detect nighttime blood pressure increases using ambulatory blood pressure measurements.

Aged↗
PubMed1998

Effects of testosterone on glomerular growth after uninephrectomy.

BACKGROUND: Renal functional prognosis is consistently more adverse in male individuals with renal disease. Male animals develop more marked proteinuria and glomerulosclerosis in several models of renal damage. Renal and glomerular growth are important permissive factors for progression of renal failure. PURPOSE OF THE STUDY: To investigate the influence of testosterone on renal and glomerular growth. DESIGN: Renal compensatory growth after uninephrectomy (UNX) was chosen as a model of renal growth. The effect of testosterone was assessed in control male, in orchidectomized (OX) male, and in ovariectomized (OV) female SD rats. Observation time was 10 months. MEASUREMENTS: Albuminuria by nephelometry; glomerular diameter, glomerular tuft area, renal zonal analysis by quantitative stereology. Testosterone and dihydroxytestosterone by gas chromatography and RIA. RESULTS: In sham-operated male rats, testosterone administration did not change the (left) kidney:body-weight ratio after uninephrectomy. In contrast, in OX male rats, testosterone administration caused a significant increase in kidney:body-weight ratio and in albuminuria. In these animals, glomerular diameter and outer stripe width were significantly lower in OX rats than in sham-operated controls. Glomerular volume and outer stripe width in OX animals were significantly higher after uninephrectomy (UNX) and were further increased in OX-UNX animals by administration of testosterone. Similar effects on glomerular diameter, cortical width (single) kidney:body-weight ratio were seen when OV female rats were treated with testosterone. CONCLUSION: After gonadal ablation, administration of testosterone amplifies compensatory glomerular and tubular growth in uninephrectomized male and female rats, i.e. testosterone is a permissive factor. Stimulation of glomerular growth may favour development of glomerulosclerosis.

Adaptation, Physiological↗
PubMed1998

Hypertension in the transplanted patient.

Hypertension is a common finding after renal transplantation, and it has a variety of underlying mechanisms. One reason is the type of immunosuppressive therapy, with a higher prevalence of hypertension in cyclosporine-treated patients. Cyclosporine interferes with several humoral and neural systems which are involved in blood pressure regulation such as the renin-angiotensin system, endothelins, nitric oxide, prostaglandins and the sympathetic nervous system. Other pathomechanisms for posttransplant hypertension are uncontrolled renin secretion of the native kidneys, polycythemia, recurrence of renal disease in the graft and renal failure. Renal transplant artery stenosis is a potentially treatable cause of post-transplant hypertension and several techniques such MRT angiography, Doppler sonography and conventional angiography are available. The diagnosis and treatment of hypertension are of high importance in general for the transplanted patient, and especially for the long-term prognosis of graft function.

Female↗
PubMed1997

[The clinical significance of renal cell carcinoma in dialysis dependent patients in comparison with kidney transplant recipients].

The clinical relevance of de novo Renal Cell Cancer was compared in chronic hemodialysis patients and renal allograft recipients. Clinical course of these patients was followed for 15 years. 21 of 788 patients who underwent radical nephrectomy were suffering from renal insufficiency at the time of surgery. Evaluated data included clinical symptoms; tumor histology and clinical course. 19 patients received chronic hemodialysis treatment. 7 patients demonstrated stable function of the allograft. 92% of patients receiving hemodialysis treatment did not show metastasis and none died of renal cell carcinoma. On the contrary, 71% of patients who underwent renal transplantation showed advanced tumor disease or metastasis. 3 patients have died of RCC. Aggressive tumor growth of RCC requires close follow up in patients who received a renal allograft.

Adult↗
PubMed1997

Aortic changes in experimental renal failure: hyperplasia or hypertrophy of smooth muscle cells?

Cardiovascular complications are a well-known feature of chronic renal failure. Increased wall thickness of intramyocardial arterioles and elastic (aorta) and peripheral (mesenteric) arteries is seen even after normalization of blood pressure. It is currently unknown whether such increases result from hyperplasia of vascular smooth muscle cells, hypertrophy, or a combination of both or from an increase in aortic extracellular matrix. Using a recently developed unbiased stereological technique (the dissector), we investigated the aortas of subtotally nephrectomized rats and sham-operated controls after perfusion fixation. We determined aortic wall thickness, cross-sectional area of aortic media, total number of vascular smooth muscle cells per unit aortic length (1 mm), mean cell and nuclear volumes, volume density of elastic fibers, extracellular matrix, vascular smooth muscle cells, and total volumes of these structures per unit of aortic length (1 mm). Blood pressure was not significantly increased in subtotally nephrectomized rats. In contrast, wall thickness, cross-sectional media, total number of aortic vascular smooth muscle cells, and volume of extracellular matrix including collagen were significantly increased after subtotal nephrectomy, whereas cellular hypertrophy was only modest and an increase in elastic fibers did not occur. In conclusion, increased aortic wall thickness in experimental renal failure results primarily from an increase in aortic extracellular matrix. In addition, however, proliferation of aortic vascular smooth muscle cells resulting in cell hyperplasia also contributed to aortic wall thickening to a minor degree. It appears that aortic wall thickening is caused by secretory stimulation of the proliferating vascular smooth muscle cells, resulting in increased matrix production. The nature of the underlying stimulus requires further investigation.

Animals↗
PubMed1996

Autosomal dominant polycystic kidney disease--the patient on renal replacement therapy.

In Europe approximately 6% of all patients on chronic renal replacement therapy suffer from polycystic kidney disease. Survival of patients with polycystic kidney disease on renal replacement therapy is better than for other primary renal diseases, despite a similar cardiovascular risk profile. We documented a significantly higher erythropoietin level in polycystic patients even in advanced uraemia and on dialysis. A better haemoglobin level seems to improve long-term survival because of a possible beneficial effect on cardiac function. There is no increased risk of renal cell carcinoma in patients with autosomal dominant polycystic kidney disease. Polycystic patients on dialysis should be followed for cardiac valve abnormalities and cerebral aneurysms.

Cardiovascular Diseases↗
PubMed1996

Arteriolar wall thickening, capillary rarefaction and interstitial fibrosis in the heart of rats with renal failure:the effects of ramipril, nifedipine and moxonidine.

In experimental renal failure, increased intramyocardial arteriolar wall thickness, reduced myocardial capillary density, and increased cardiac interstitium are found. The extent to which such alterations can be modified by therapeutic interventions has not been investigated to date. The purpose of this study was to examine the effects of Ramipril, Nifedipine and Moxonidine on these structural changes. Sham-operated and subtotally nephrectomized (SNX) 300-g male Sprague-Dawley rats (N = 7 to 11) were left untreated (N = 9) or treated with Ramipril (0.5 mg/kg body wt per day; N = 7), Nifedipine (30 mg/kg body wt per day; N = 9), or Moxonidine (10 mg/kg body wt per day; N = 8) for 8 wk. After perfusion fixation, heart and aorta were examined by stereological techniques. Aortic wall thickness was significantly higher in SNX than in sham-operated control rats and was similarly lowered by all three interventions. In contrast, the wall thickness of intramyocardial arterioles was significantly higher in SNX; this was prevented by Ramipril and Nifedipine, but not by Moxonidine. Intramyocardial capillary length density (Lv) was significantly lower and interstitial volume density (Vv) significantly higher in untreated SNX. Reduction of capillary length density was completely prevented by Moxonidine and in part by Ramipril. The increase in cardiac interstitial volume density was completely prevented by Ramipril and was partially prevented by Moxonidine or Nifedipine treatment. The following conclusions can be drawn from the results: (1) all agents normalize aortic wall thickness, but only calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors prevent intramyocardial arteriolar wall thickening: (2) intramyocardial arteriolar wall thickening, capillary rarefaction, and expansion of the cardiac interstitium are seen in SNX even after lowering the blood pressure to subnormal levels; i.e., changes in systemic blood pressure cannot completely explain the altered vascular structure in renal failure; (3) the effects of Ramipril, Nifedipine, and Moxonidine on cardiovascular structures in experimental renal failure are not completely accounted for by their hemodynamic actions.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Effect of ramipril, nifedipine, and moxonidine on glomerular morphology and podocyte structure in experimental renal failure.

BACKGROUND: Experimental renal failure causes structural alterations of the kidney. It is still unresolved how these changes are modified by antihypertensive treatment. Purpose of the study. To examine the effects of different antihypertensive agents (ramipril, nifedipine, moxonidine) mainly on glomerular geometry, cell number, cell morphology, and capillarization, in a subtotal nephrectomy model of renal failure. MATERIAL AND METHODS: Sham-operated male SD rats and subtotally nephrectomized (SNX) ad libitum-fed rats were examined. Groups of 8-10 SNX rats were left untreated or were treated with ramipril (0.5 mg/kg b.w. per day), nifedipine (20 mg/kg b.w. per day) or moxonidine (10 mg/kg b.w.per day) respectively. After perfusion fixation the kidneys were examined using stereological techniques. RESULTS: Systolic blood pressure (by tail plethysmography) was 110+/-13 mm Hg in sham-op and 119+/-9 in SNX. It was effectively and comparably reduced below normal values by ramipril (89+/-11 mmHg), nifedipine (98+/-23 mmHg) and moxonidine (92+/-11 mmHg). The glomerulosclerosis index (SI) was significantly increased in SNX versus sham-op; it was similarly decreased by ramipril and moxonidine but less so by nifedipine. Vascular damage (preglomerular vessels) was reduced by all treatments whereas tubulointerstitial damage was signficantly reduced only by ramipril and moxonidine. Mean glomerular tuft volume was increased in SNX compared to sham-op. controls and was normalized only by ramipril treatment. Glomerular cells were differentially affected the three antihypertensive agents. After subtotal nephrectomy an increase in podocyte volume and mesangial cell number per glomerulus was noted. Nifedipine, and to a lesser extent ramipril, prevented mesangial cell hyperplasia. In contrast, only the ACE inhibitor ramipril, but not nifedipine or moxonidine prevented podocyte abnormalities, particularly podocyte hypertrophy. CONCLUSIONS: (i) Despite comparable reduction in systolic blood pressure, different classes of antihypertensive agents had diverse effects on renal damage in subtotally nephrectomized rat. This observation is consistent with specific, non-hemodynamic actions of anti-hypertensives. (ii) Glomerular and tubulointerstitial damage are prevented by treatment with ACE inhibitors and antisympathotonic agents, but not with the calcium antagonist nifedipine. In contrast, renal vascular changes were also prevented by nifedipine. (iii) Only ACE inhibitors effectively inhibited podocyte hypertrophy and mesangial cell hyperplasia. Whether the superior effect of ACE inhibitors on glomerulosclerosis is related to inhibition of glomerular growth and podocyte hypertrophy as well as preservation of podocyte structure, or whether these findings are merely a passive reflection of greater efficacy, remains unresolved.

Animals↗
PubMed1996

Prescription of calcium concentration and PTH control.

The use of calcium-containing oral phosphate binders, introduced in an effort to avoid aluminum-containing compounds, had led to more frequent episodes of hypercalcemia. This prompted the introduction of continuous ambulatory peritoneal dialysis (CAPD) solutions with diminished calcium content. The problems raised by such solutions included stimulation of parathyroid hormone (PTH) secretion and long-term maintenance of calcium balance. Some of these issues can today be answered on the basis of controlled prospective trials. Variability of the rate of intestinal calcium uptake of bone turnover, of baseline parathyroid activity, and other factors make it necessary to individualize the indication for the use of CAPD solutions with low calcium content.

Calcium↗