摘要:

Aluminum-containing phosphate binders have been widely employed in the past in the management of uremic hyperphosphatemia. However, an increasing number of reports on aluminum toxicity has stimulated efforts to replace this therapy by safer methods. The aim of the present review is to critically evaluate other treatment strategies. It appears that aluminum-containing phosphate binders should no longer be considered the treatment of choice for controlling uremic hyperphosphatemia. Calcium carbonate, calcium citrate, magnesium carbonate and a mixture of ketoanalogues and amino acids present important therapeutical alternatives which could replace aluminum-containing phosphate binders in the majority of patients. However, it is mandatory, as these therapies also carry some risks, that side effects are detected early.

ISSN:0250-8095    

DOI:10.1159/000167578

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Investigations of biopsy material from human kidneys with different forms of glomerulonephritis (n = 1,240) and with diabetic glomerulosclerosis (n = 406) performed in order to find changes caused by hyperperfusion of the kidney tissue gave the following results: (1) Hyperperfusion injury occurs in the different forms of glomerulonephritis with varying frequency. It was rarely found in immunologically negative mesangioproliferative glomerulonephritis. The highest incidence was found in patients with membranoproliferative glomerulonephritis type I. (2) Hyperperfusion injury was also found in kidneys with diabetic glomerulosclerosis. The frequency of this finding increased with the degree of the diabetic changes. (3) The hyperperfusion injury was seen as a complication of glomerulonephritis or diabetic glomerulosclerosis only when the patient clinically had developed malignant hypertension and when the serum creatinine level was elevated, a sign of compensated retention. (4) In patients with glomerulonephritis, the hyperperfusion changes occurred more frequently in males than in females. Diabetic glomerulosclerosis was complicated by hyperperfusion injury with the same frequency in both sexes. (5) Patients with hyperperfusion changes of the kidneys always excrete large amounts of protein in the urine. (6) Hyperperfusion changes occur first in the juxtamedullary glomeruli. The intermediate glomeruli are affected later and the subcapsular glomeruli last.

ISSN:0250-8095    

DOI:10.1159/000167579

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The incidence of elevated tumor markers without clinical signs of malignant disease was examined in 93 patients between the age of 29 and 79 years and on chronic dialysis for 3–240 months. Tissue polypeptide antigen was found to be elevated in 92.5%, carcinoembryonic antigen in 29.8, and α-fetoprotein in 6.5%. High levels of tissue polypeptide antigen were accompanied by high levels of β2-microglobulin (p < 0.005). This indicates that tumor markers, and tissue polypeptide antigen in particular, may be unreliable for monitoring malignant disease in patients on hemodialy

ISSN:0250-8095    

DOI:10.1159/000167580

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

To simulate hematuria, blood from healthy volunteers was added to urine samples of varying osmolalities to produce urocrits ranging from 0.01 to 3.0%. Specimens were then analyzed for protein concentration by a method using a combination of 3 % sulfosalicylic and trichloroacetic acids. Microscopic hematuria (urocrit of less than 0.05%) was not associated with proteinuria, but gross hematuria often resulted in substantial amounts of protein being detected. In iso- and hypertonic urines, modest elevations in protein concentration (69–97 mg/dl) were detected. Hypotonic urines produced marked proteinuria (1,302–1,863 mg/dl). Urine protein electrophoreses identified hemoglobin as the responsible protein. Isolated hematuria can cause false-positive proteinuria on the basis of RBC lysis and release of hemoglobin into the urine. The diagnostic and prognostic implications of clinical proteinuria in the hematuric patient can be significant. Thus, in a patient with gross hematuria, a urine protein electrophoresis should be accomplished to assess the contribution of hemoglobin to the total protein determinat

ISSN:0250-8095    

DOI:10.1159/000167581

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

We report on 2 siblings with autosomal-recessive polycystic kidney disease, diagnosed at the ages of 14 and 18 years, respectively. Clinical findings and differential diagnosis, especially for autosomal-dominant polycystic kidney disease, are given. The consequences for genetic counselling are discussed.

ISSN:0250-8095    

DOI:10.1159/000167582

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The protein-creatinine ratio was measured in urine samples obtained at three different times of the day and compared to the 24-hour protein excretion in 51 patients with a wide spectrum of renal function and proteinuria. A linear correlation, which was highly significant, was found between the two variables. The higher correlation was found in urine samples obtained at 08.00 and at 12.00 h and the lowest in samples obtained at 16.00 h. This correlation did not depend on the degree of proteinuria or on the sex of the patients, but was slightly dependent on the glomerular filtration rate. The protein-creatinine ratio was essentially identical with the 24-hour protein excretion. Thus, the normal range of proteinuria was represented by a ratio of less than 0.2, while nephrotic patients had a ratio above 3.5. We suggest that the protein-creatinine ratio in random urine samples could replace the timed collection methods at least for follow-up and screening.

ISSN:0250-8095    

DOI:10.1159/000167583

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

A retrospective study was done on 109 diabetic patients who had renal biopsies during 1974–1984 to determine factors identifying nondiabetic renal disease in patients with diabetes mellitus presenting with renal dysfunction. Six of 49 (12%) patients with type I and 17 of 60 (28%) with type II diabetes mellitus had other renal diseases, with or without diabetic glomerulosclerosis. Multivariate predictors of other renal disease in type I diabetes mellitus were duration < 5 years (p < 0.001), absence of proteinuria (p < 0.001), and absence of neuropathy (p < 0.05). In type II diabetes mellitus these were late age of onset (p < 0.001), absence of neuropathy (p < 0.05), and Caucasian race (p < 0.005). Some patients with other diseases appeared to respond to therapy directed at their nondiabetic glomerulosclerosis disease. We emphasize the need to distinguish between the subgroup of diabetic patients with nondiabetic renal disease from the majority who have diabetic glomerulosclerosis alone. The latter group should be spared the discomforts, risks, and costs of a renal biops

ISSN:0250-8095    

DOI:10.1159/000167584

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1–84 PTH but not its amino-terminal (1–34 PTH) or its carboxy-terminal (53–84 PTH) fragments produced marked and significant (p < 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1–84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p < 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16–20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p < 0.01) reduced and there was a significant (p < 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure. The data show that (1) PMNL are target cells for intact 1–84 PTH; (2) the effect of PTH on PMNL migration is specific to the hormone and is related to its biological activity; (3) this action of the hormone is not mediated by calcium influx into PMNL nor by stimulation of cAMP or cGMP production in these cells but may be due to redistribution of cytosolic calcium between various cell organelles; (4) prolonged exposure to intact PTH may adversely affect random migration of PMNL, and (5) the migration of PMNL is impaired in most patients with chronic renal failure and it is inversely related to serum levels of PTH. The data are consistent with the notion that the state of secondary hyperparathyroidism of chronic renal failure is responsible for altered PMNL migration and assign a new dimension for PTH toxicity in the

ISSN:0250-8095    

DOI:10.1159/000167585

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Elevated creatine kinase (CK) has frequently been described in patients on chronic dialysis, but little is known about its cause and distribution. We, therefore, measured CK in 105 patients on hemodialysis and continuous ambulatory peritoneal dialysis and compared it with biochemical, nutritional, and anthropometric data obtained at the same time. In the entire group, CK was 130.3 ± (SEM) 15.0 IU/1. Thirty patients had elevated levels of enzyme ( > 130 IU/1). Isoenzymes determined in patients with elevated CK levels were all more than 97% MM fraction. Men had significantly higher (p < 0.001) CK values (166.0 ± 25.8 IU/1) than women (82.4 ± 9.0 IU/1). Blacks had higher CK values (158.8 ± 21.7 IU/1; p < 0.001) than whites (92.6 ± 12.5 IU/1). Men and blacks had significantly higher weight and midarm muscle circumference than women and whites, respectively. A positive correlation was found between CK and lactic dehydrogenase (p < 0.001) and between CK and midarm muscle circumference (p < 0.05), and a negative correlation (p < 0.01) was found with age. Predialysis and postdialysis CK was measured in 10 patients and did not rise. Three of the patients with elevated CK who have undergone successful renal transplantation showed normalization of CK levels. We conclude that CK is elevated in both hemodialysis and continuous ambulatory peritoneal dialysis patients, particularly in men and blacks, that CK levels are probably related to muscle mass, and that CK declines with advancing age. Although blacks have higher CK values as a whole, normalization of CK values after renal transplantation suggests a contributory role of renal dysfunc

ISSN:0250-8095    

DOI:10.1159/000167586

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0250-8095    

DOI:10.1159/000167587

出版商:S. Karger AG    

年代:1988

数据来源: Karger