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M Zeier

Publications and source records attributed to M Zeier.

At least 73 records · Page 4Linked to original sources
PubMed1995

Seroprevalence of hantavirus antibodies in Germany as determined by a new recombinant enzyme immunoassay.

In order to elucidate the epidemiological importance of hemorrhagic fever with renal syndrome in Germany, the prevalence of antibodies against hantaviruses was determined in 13,358 sera from residents of various geographic regions, 1,284 sera from occupational risk groups and 287 sera from chronic hemodialysis patients. Serological investigations were performed using a highly specific transferable solid phase enzyme immunoassay based on the recombinant nucleocapsid proteins of a Hantaan and a Puumala serotype strain. The overall antibody prevalence was found to be 1.68%. In the serum panels from western and southern Germany, it was determined to be 1.83% on average in contrast to only 0.8% in the panel from eastern Germany. An endemic focus revealing an antibody prevalence of 3.12% was detected in a low-mountain area called Suebian Alb, which is located in the federal state of Baden-Württemberg. Occupational risk groups and a group of chronic hemodialysis patients showed a significantly elevated antibody prevalence ranging from 3.3% to 10%. The Puumala serotype was found to be the prevailing virus, but the percentage of sera predominantly recognizing the Hantaan nucleocapsid protein increased towards the south and the east and was significantly elevated in dialysis patients.

Antibodies, Viral↗
PubMed1995

More adverse renal prognosis of autosomal dominant polycystic kidney disease in families with primary hypertension.

Marked variability of age at renal death is noted in autosomal dominant polycystic kidney disease (ADPKD). The hypothesis that the coexistence of primary hypertension and ADPKD within families is associated with earlier renal death was tested. Of a total of 162 ADPKD patients treated in one Austrian and three German centers, 57 propositi were identified whose families provided (1) information concerning blood pressure; (2) documented presence of ADPKD (by sonography or autopsy) in one parent; and (3) age at renal death in the propositus. Hypertension of the unaffected parent was defined as blood pressure above 140/90 mm Hg or antihypertensive treatment before age 60 yr. Age at renal death in the propositus was defined as the start of renal replacement therapy. Median age at renal death of 23 offspring (11 male, 12 female) from families with a history of primary hypertension of the nonaffected parent was lower than that of 34 offspring (16 male, 18 female) from families without a known history of primary hypertension of the nonaffected parent, i.e., 49 yr (26 to 64) versus 54 yr (28 to 82) (P < 0.03). The data are consistent with the notion that genetic predisposition to primary hypertension is associated with an earlier onset of terminal renal failure in families with ADPKD.

Adult↗
PubMed1995

Anticipation of age at renal death in autosomal dominant polycystic kidney disease (ADPKD)?

It has been claimed that anticipation occurs in ADPKD, i.e. endstage renal failure at progressively earlier age in successive generations. This observation might possibly point to unstable DNA as the molecular basis of ADPKD. We analysed 74 parent-offspring pairs of 148 families in Germany and Austria in whom (i) ADPKD was verified by appropriate imaging procedures and (ii) age at renal death was accurately known. The median difference for age at renal death between parent and offspring was 0 years, range -26.3 to +27.2 years. There was no deviation from normal (Gaussian) distribution according to the Shapiro-Wilk test (P = 0.75). We conclude that systematic anticipation cannot be demonstrated with this sample which had sufficient size for meaningful biostatistical analysis.

Adult↗
PubMed1994

Clinical nephrology in 19th century Germany.

Bright's work led to the recognition that coagulable protein in the urine indicated macroscopic kidney disease. After light microscopy was introduced, Simon, Nasse, Henle and Frerichs identified the major constituents of urinary sediment. By 1896, Senator had deduced that hyalin cylinders arise in the kidney tubules, and only the discovery of the Tamm-Horsfall protein in the next century separated him from the modern concept. Chemical analysis of urine also advanced greatly. Recognition of the pressure-volume relationship by Traube was probably the most brilliant achievement related to renal disease, and became the basis of the later pressure-natriuresis relationship. Traube also linked left ventricular hypertrophy with renal disease, recognizing that it maintained circulatory homeostasis at a higher level of pressure. The concept of nephritis changed considerably with technical progress, and Gluge was the first to see inflamed Malpighian bodies or glomeruli. The primary site of damage was disputed by many, including Henle, Pfeufer, Virchow, Reinhardt and Frerichs, but all these workers had to reconstruct the sequence of events leading to the autopsy findings. The term glomerulonephritis was first coined by Klebs, and the classification of nephritis adopted by Senator in 1896 led directly to the classic monograph of Volhard and Fahr (1914) on Bright's disease.

Germany↗
PubMed1994

Progression of renal failure in the Han: SPRD polycystic kidney rat.

The Han: SPRD Pkd rat mutant is an autosomal dominant rat model with incomplete penetration of polycystic renal transformation. Progressive renal failure occurs in heterozygous male animals. The mechanisms of progression have not been elucidated. To identify some pathogenetic factors involved we subjected male SPRD Pkd rats (and their non-affected littermates as controls) to uninephrectomy (UNX), castration or enalapril treatment. To assess progression S-urea at age 150 days was chosen as endpoint. (i) In uninephrectomized male Han: SPRD Pkd (n = 12 animals per group) S-urea at age 150 days was consistently above 300 mg/dl, while it was 245 mg/dl (191-290) in control Han: SPRD Pkd. (ii) In castrated male Han: SPRD median S urea at 150 days was 100 mg/dl (69-211) compared to sham-operated male Han: SPRD controls (245; 191-290). Castration did not, however, prevent accelerated progression after uninephrectomy. (iii) Enalapril (50 mg/l) in the drinking fluid did not significantly lower median systolic blood pressure (by plethysmography) in animals on 0.2% sodium diet (at 185 days 160 mmHg; 140-170 versus 170; 140-195 in non-enalapril controls), although circulating ACE was significantly inhibited (17 U; 11-33 versus 89; 52-108 in controls). S-urea at age 185 days was not significantly different in the 2 groups. In conclusion, the Han: SPRD Pkd model differs from human ADPKD to some extent. Uninephrectomy accelerates renal failure in the rat, but not in humans. On the other hand, in contrast to human ADPKD the renin system is suppressed in the rat model and ACE inhibition does not affect the course of renal failure.

Animals↗
PubMed1994

[Cystic kidneys (autosomal dominant polycystic kidney disease)].

Polycystic kidney disease is a rather common genetic disorder, with an estimated amount of 8 to 10% of patients in the dialysis population. Meanwhile the defective gene of autosomal dominant polycystic kidney disease [ADPKD], another common terminus for this disorder, has been localized on the short arm of chromosome 16. The genetic disorder is not strictly localized on the kidney, whereas other organ systems like cardiac valves, brain arteries, liver, colon, etc. may be involved in the disease process. Hypertension is an early and common feature of the disease and its probably an important factor for progression of renal failure in ADPKD. Not all carriers of the ADPKD-trait progress to endstage renal failure, about 50% at the age of 50 years. Patients with ADPKD have a good prognosis in renal replacement therapy programs such as dialysis or renal transplantation.

Adolescent↗
PubMed1994

Role of infection in the genesis of acute renal failure.

While most experimental models of acute renal failure (ARF) involve ischaemic or toxic damage to the kidney in non-infected animals, a surprisingly large proportion of patients with ARF exhibit signs of septicaemia or systemic reaction to local infections. This clinical observation suggests an important role of infection-related mediator mechanisms in the genesis of ARF. Another important aspect is the occurrence of ARF in the context of infections with nephrotropic viruses (e.g. hantavirus accounting for approximately 5% of non-surgical ARF in Germany) and nephrotropic bacteria (e.g. leptospirosis).

Acute Kidney Injury↗
PubMed1993

[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.

Chronic Disease↗
PubMed1993

Autosomal dominant polycystic kidney disease (ADPKD)--mechanisms of cyst formation and renal failure.

None of the hypotheses proposed so far to explain cyst formation in autosomal dominant polycystic kidney disease (ADPKD) is entirely satisfactory, e.g. the theory of tubular obstruction by intraluminal polyps or dilatation of nephron segments as a consequence of abnormal compliance of the basement membrane. Recent in vitro studies show that (i) synthesis of basement membrane material is abnormal and that (ii) the direction of transepithelial resorptive flux into a secretory mode is reversed as a consequence of faulty insertion of Na, K-ATP'ase into the luminal membrane. It remains unclear why cystic transformation of a few percent of nephrons should cause endstage renal failure. Our clinical and experimental studies do not provide evidence to support some hypotheses proposed in the past, i.e. that renal parenchyma is compressed by expanding cysts and that glomeruli are overperfused. Our histological studies show that progression to endstage renal failure is associated with (i) progressive arteriolar lesions (out of proportion to the vascular lesions seen in extrarenal vascular beds; and (ii) progressive interstitial fibrosis. It appears that fibroblasts in ADPKD are particularly sensitive to platelet derived growth factor (PDGF) which is secreted by epithelial cells of the cyst wall in a paracrine fashion. In contrast to previous opinion, which was presumably skewed by ascertainment bias, it appears that not all, and perhaps not even a majority, of ADPKD patients progress to endstage renal failure. Factors related to progression are gender, family history and hypertension. Both abnormal sodium excretion and inappropriate renin secretion play a role in the genesis of hypertension. Elevated blood pressure, albeit within the normotensive range, is demonstrable even in prepubertal children. The involvement of renin in renal vasoconstriction of normotensive ADPKD patients suggests a particular role of ACE inhibitors in the management of these patients.

Dilatation, Pathologic↗
PubMed1993

Renal functional reserve in healthy elderly subjects.

The increase in GFR after an amino acid (AA) load, the so-called renal functional reserve, is impaired in the aged rat. Whether the renal functional reserve predicts the progression of renal disease in humans is controversial, but it is possible that age-related alterations of renal hemodynamics are relevant for the evolution of renal disease in the elderly. We compared renal hemodynamics before and after an AA infusion in 15 healthy normotensive subjects of young age (seven women, eight men; median age, 26 yr; range, 23 to 32) and in 10 subjects of old age (six women, four men; median age, 70 yr; range, 61 to 82) on normal dietary protein intake. Baseline GFR and effective RPF were measured after 12 h of fasting by the inulin (Cin) and para-aminohippurate (Cpah) steady-state infusion techniques. The renal functional reserve was examined after an overnight AA infusion (7% solution; 83 mL/h). Median basal Cin and Cpah were significantly lower (P < 0.01) in the elderly (102 and 339 mL/min per 1.73 m2) than in the young subjects (122 and 647 mL/min per 1.73 m2), but virtually all GFR values of the elderly were still within the normal range. Median Cin upon infusion of AA was 118 mL/min per 1.73 m2 (range, 98 to 137) in the elderly and 146 (range, 120 to 171) in the young, respectively. Corresponding values of Cpah were 349 mL/min per 1.73 m2 in the elderly versus 689 mL/min per 1.73 m2 in the young. Cin increased significantly (P < 0.01) after the AA load in both young and elderly subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗