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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 577 records · Page 32Linked to original sources
PubMed1990

Natriuresis-pressure relationship in polycystic kidney disease.

We studied, under outpatient conditions, nine patients with autosomal dominant polycystic kidney disease who were hypertensive on their usual diet, and nine normotensive healthy probands. The subjects were examined in random order on the 7th day after equilibration on a low-sodium diet (20 mmol/day) and again on the 7th day after equilibration on the same diet but with added sodium to yield a final intake of 200 mmol/day (or vice versa). Blood pressure was monitored non-invasively for 2 h at 4-min intervals using an automatic system. In healthy probands, mean arterial pressure (MAP) was similar on the low- and the high-sodium diets (92.7 versus 91.9 mmHg). In hypertensive patients, a significant (P less than 0.02) increase in mean MAP (107.2 versus 111.2 mmHg) and in systolic blood pressure (140.6 versus 148.7 mmHg) was observed irrespective of whether the glomerular filtration rate (GFR) was normal or reduced. The natriuresis pressure curve showed an upward shift (resetting) and a positive slope (sodium sensitivity). Patients with a reduced GFR as shown by inulin clearance differed from probands and patients with a normal GFR, by showing greater proportional changes in GFR and body weight. In hypertensive patients, atrial natriuretic factor (ANF) levels were higher at baseline and showed an exaggerated response to sodium loading. Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. These data show a resetting of the natriuresis-blood pressure relationship and an increased blood pressure sensitivity to sodium in hypertensive patients with adult, dominant, polycystic kidney disease.

Adult↗
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

Pharmacokinetics of ramipril in hypertensive patients with renal insufficiency.

In an open trial, the pharmacokinetics of ramipril and its active metabolite ramiprilat were studied in 25 hypertensive patients with various degrees of renal insufficiency given 5 mg ramipril p.o. for 14 days. Ramipril was rapidly absorbed and reached a peak concentration after 1-2 h. Cmax was greater in patients with severe renal insufficiency, which might indicate a reduced renal elimination rate, although, the rapid decline of the concentration-time curve for ramipril was almost independent of renal function. The mean initial apparent half-lives on Days 1 and 12, respectively, were 2.8 and 3.4 h (Group I: creatinine clearance 5-15 ml/min), 1.8 and 2.3 h (Group II: creatinine clearance 15-40 ml/min), and 1.9 and 1.9 h (Group III: creatinine clearance 40-80 ml/min). No accumulation was observed after multiple dosing. In contrast, the kinetics of its active acid metabolite ramiprilat was significantly influenced by renal function. The mean times to the peak plasma concentration were 5.7 h in Group I, 4.4 h in Group II and 3.8 h in Group III. The initial decline in plasma ramiprilat was dependent upon renal function; the mean initial apparent half-lives (Days 1 and 12, respectively) were 16.0 and 14.8 h (Group I), 10.1 and 9.5 h (Group II) and 10.6 and 8.0 h (Group III). Mean trough concentrations and absolute accumulation also increased with worsening renal function, and the renal clearance of ramiprilat was significantly correlated with the creatinine clearance. The subsequent long terminal phase at low plasma ramiprilat concentrations represented slow dissociation of the ACE-inhibitor complex.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Evidence for in vivo upregulation of 1,25(OH)2 vitamin D3 receptor in human monocytes.

Mammalian cells increase net expression of 1,25(OH) 2D3 receptors after exposure to physiological concentrations of 1,25(OH) 2D3 in vitro. We examined specific binding of 1,25(OH) 2D3 by human monocytes before and after daily administration of 1.5-2 micrograms 1,25(OH) 2D3 p.o. for 3 days in 5 healthy normal D-replete probands. Median specific binding (Nmax) at baseline was 793 molecules/cell and 2052 or 2828 at 24h and 72h of 1,25(OH) 2D3 treatment respectively. The results suggest (a) upregulation of 1,25(OH) 2D3 receptors occurs in man and (b) monocyte preparations can be used to assess receptor regulation in vivo.

Adult↗
PubMed1989

Is gender a determinant for evolution of renal failure? A study in autosomal dominant polycystic kidney disease.

More males than females enter renal replacement therapy programs. This may reflect greater propensity of men to acquire renal disease, faster progression of renal disease, or a combination of both. In order to address this problem, autosomal dominant polycystic kidney disease (ADPKD), a well-defined genetically homogenous hereditary disorder, was studied. One hundred fifty-eight cases of the disease in adults were diagnosed by sonography and studied (73 men, 85 women); 58 of the patients had reached end-stage renal failure. Survival analysis of age at renal death revealed a significant gender difference (log-rank test, P = 0.0072): median age at renal death was 52.5 years in men and 58.0 years in women. In 64 patients with adequate sequential measurements of serum creatinine, progression of renal failure was followed retrospectively. When serum creatinine was greater than 3 mg/dL, the average rate of progression was similar in both sexes. In contrast to ADPKD, a sex difference for the age at renal death was not found in prepubertal individuals with hereditary renal diseases, ie, cystinosis or nephronophthisis. The data suggest that sex (hormones) influences evolution of renal failure.

Creatinine↗
PubMed1989

Acrorenal syndrome in an adult--presentation with proteinuria, hypertension, and glomerular lesions.

Acrorenal syndrome is characterized by central longitudinal axis defects of the limbs, ie, split hand and/or foot. Associated renal lesions described so far comprise agenesis, bilateral hypoplasia (originally diagnosed as oligomeganephronia), and duplication abnormalities. The case of a 29-year-old patient with split hand resulting from bilateral aplasia of the third phalanges associated with dysplasia of the third and fourth metacarpals is reported. In addition, the following lesions were noted: hypoplasia of the middle phalanx of the fifth toe, arched palate, pectus excavatum, hypoplastic mammilae, scoliosis, and congenital hip dislocation. The patient presented with hypertension, modest reduction of glomerular filtration, proteinuria, microhematuria, cylindruria, and moderate harmonic hypoplasia of the right kidney on angiography. Glomeruli had no immune deposits on immunohistology. Light microscopy showed widening of the mesangial axis, focal segmental glomerular sclerosis, and renal interstitial fibrosis with occasional foam cells. This case shows that the spectrum of renal abnormalities in the acrorenal syndrome is wider than previously noted.

Abnormalities, Multiple↗
PubMed1989

Lysine-specific cleavage of beta 2-microglobulin in amyloid deposits associated with hemodialysis.

Amyloid fibrils isolated from bone and carpal synovia of seven patients on long-term hemodialysis were further characterized biochemically. In addition, renal amyloid stones of three dialyzed patients were examined. All deposits and stones were of beta 2-microglobulin-origin (AB-amyloid) by immunohistochemical and immunochemical evaluation. Amyloid fibril extracts were dissolved in 80% formic acid and separated by high performance liquid chromatography in 60% formic acid and 20% 2-propanol. Three major retarded fractions with molecular weights of approximately 24, 12 and 7 to 10 kD were recovered. N-terminal amino acid sequence analysis documented beta 2-microglobulin (beta 2m) as the principal polypeptide in all investigated cases. In addition to proteins with intact N-termini, one fragment commencing with isoleucine in position 7 was found in osseous or synovial amyloid. In renal amyloid stones, one additional fragment was found beginning with serine in position 20. Generally, these data point to proteolytic cleavage carboxyterminal to a lysine residue and establish that not only intact beta 2m but also at least one beta 2m fragment is present in beta 2m-derived amyloid deposits of patients with long-term hemodialysis. The fragmentation pattern is consistent with the action of lysine-specific protease(s) and underscores a potentially important role of limited proteolysis in the pathogenesis of AB-amyloid deposits.

Adult↗
PubMed1989

1,25(OH)2 vitamin D3 inhibits parathyroid cell proliferation in experimental uremia.

Parathyroid cell proliferation and parathyroid hyperplasia are features of renal secondary hyperparathyroidism. Since parathyroids have recently been recognized as an important target for 1,25(OH)2D3, the effects of administration of variable doses of 1,25(OH)2D3 on ex vivo radiothymidine incorporation in the parathyroid glands, on parathyroid cell mitoses, on parathyroid weight, morphometric indices and on parathyroid protein/DNA ratio were examined in rats with uremia (subtotal nephrectomy; NX) or with calcium deficiency. 3H-thymidine incorporation (3 hr; 37 degrees C; PBS with 10 mmol glucose) was elevated in NX animals, that is, 204 +/- 51 dpm/micrograms DNA versus 96 +/- 28 in controls. In vivo pretreatment with 1,25(OH)2D3, either by intermittent i.p. injection or by osmotic minipump, dose-dependently decreased 3H-thymidine incorporation and parathyroid cell mitoses without affecting morphometric indices of parathyroid cells. Prophylactic administration (i.p.) of 1,25(OH)2D3, starting on the day of nephrectomy, prevented parathyroid hyperplasia (NX + 1,25(OH)2D3 0.84 micrograms tissue/g body wt vs. 1.25 micrograms in untreated NX and 0.54 in ad libitum fed controls), but 10 days of treatment beginning on the 21st day of uremia did not reverse existing hyperplasia (NX + 1,25(OH)2D3 1.5 micrograms/g body wt vs. 1.37 micrograms in untreated NX and 0.56 micrograms in ad libitum fed controls). The inhibitory effect was specific for 1,25(OH)2D3 and not imitated by Dexamethason. However, the effect was not specific for parathyroid hyperplasia of uremia, since similar inhibition of 3H-thymidine incorporation by 1,25(OH)2D3 was also observed in rats on low calcium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

Frequency of mesangial IgA deposits in a non-selected autopsy series.

The frequency of mesangial IgA deposition was examined in 250 consecutive autopsy cases without known renal disease. Diffuse granular mesangial deposits of IgA were detected in 12 of 250 cases (4.8%). In six patients IgA deposits were associated with liver cirrhosis. Six patients (2.4%) suffered from various other conditions including endocarditis, bronchial asthma, cardiovascular disease, and neoplasia. Two of these patients had completely negative urine analysis on repeated investigations, whereas three patients exhibited microscopic haematuria and/or mild proteinuria. IgA1 was the major constituent in all specimens. C3c deposits in glomeruli were detected in one kidney. Our findings indicate that clinically overt renal disease is present in only a limited proportion of individuals with mesangial IgA deposits. Apparently, it represents the tip of an iceberg.

Antibodies, Monoclonal↗