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PubMedDate not supplied

Dose-response relationship between total cadmium intake and prevalence of renal dysfunction using general linear models.

To determine the maximum allowable intake limits for chronic dietary exposure to cadmium (Cd), the dose-response relationship between total Cd intake and prevalence of renal dysfunction was examined using general linear models considering the effect of age as a confounder. The target population comprised 1850 Cd-exposed and 294 non-exposed inhabitants of Ishikawa, Japan. They were divided into 96 subgroups by sex, age (four categories) cadmium concentrations in rice (three categories) and length of residence (four categories). As indicators of the cadmium-induced renal dysfunction, glucose, total protein, amino nitrogen, beta 2-microglobulin and metallothionein in urine were employed. General linear models were fitted statistically to the relationship among prevalence of renal dysfunction, sex, age and total Cd intake. Prevalence of abnormal urinary findings other than glucosuria had significant associations with total Cd intake. When total Cd intake corresponding to the mean prevalence of each abnormal urinary finding in the non-exposed subjects was calculated using general linear models, total Cd intakes corresponding to glucosuria, proteinuria, aminoaciduria (men only) and proteinuria with glucosuria were determined to be ca. 2.2-3.8 g and those corresponding to prevalence of metallothioneinuria were calculated as ca. 1.5-2.6 g. The low-molecular-weight protein in urine was confirmed to be a more sensitive indicator of renal dysfunction, and these total Cd intake values were close to those calculated previously by simple regression analysis, suggesting them to be reasonable values as the maximum allowable intake of Cd.

Age Distribution↗
PubMed1986

Studies on renal adaptation to altered dietary amino acid intake: tissue taurine responses in nursing and adult rats.

This study examines the effect of a low sulfur amino acid diet (LTD) and a high taurine diet (HTD), compared with a normal diet, on the plasma, urine, muscle, brain and renal cortex levels of taurine in immature and adult rats. Milk taurine from lactating dams reflected the taurine content of the diet, being low in LTD-fed and high in HTD-fed animals. Nursing pups (7, 14 and 21 d old) often had plasma, urine and tissue--renal cortex, heart, skeletal muscle--levels of taurine related to dietary exposure, a situation also found in adult animals. These diets did not influence the urinary excretion of the sulfur-containing alpha-amino acids methionine and cystine but a sulfur aminoaciduria of immaturity was evident. By contrast, the content of taurine in brain was constant regardless of dietary intake of sulfur amino acids. An age-related decline in brain taurine content was found--as noted by others--but this too was influenced by diet. This dual finding of brain taurine constancy despite wide differences in sulfur amino acid intake and changes in the renal handling of taurine as influenced by diet suggest that the renal adaptive response serves to maintain the stability of brain taurine content.

Adaptation, Physiological↗
PubMed1983

[Mechanism of beta 2-microglobulinuria in experimental chronic cadmium intoxication].

Natural history of cadmium health effects was studied on monkeys and rabbits given cadmium chloride orally or subcutaneously for a long period: 6 male monkeys were given pelleted food containing 100 micrograms Cd/g over a period of 180 weeks, 15 male rabbits pelleted food containing 300 micrograms Cd/g over a period of 24 weeks, 13 male rabbits daily subcutaneous injections at a dose level of 0.5 mg Cd/kg over a period of 44 weeks, and 23 rabbits subcutaneous injections at a dose level of 0.5 mg Cd/kg 6 times a week over a period of 21 weeks, respectively. Sodium dodecyl polyacrylamide gel electrophoresis and silver staining (detection limit of protein: 80 micrograms/dl) revealed that urinary protein of molecular weight 12,000 (probably beta 2-microglobulin) increased slightly prior to the appearance of proteinuria, glycosuria or aminoaciduria. Remarkable increase in urinary protein of molecular weight 12,000 was observed by Amidoblack 10 B staining (detection limit: 4 mg/dl) around the time when renal dysfunctions appeared. The above result might suggest that the remarkable increase in urinary beta 2-microglobulin is associated with renal dysfunctions, while the slight increase is caused by other mechanisms than renal dysfunctions.

Administration, Oral↗
PubMed1978

Urinary excretion of acid glycosaminoglycans and hydroxyproline in a patient with oculo-cerebro-renal syndrome.

The metabolism of ground substance in connective tissue of an 18-year-old boy with oculo-cerebro-renal syndrome was studied. He had characteristic clinical and laboratory findings described by Lowe et al. such as growth retardation, mental deficiency, glaucoma, cataracta, decreased muscle tone, metabolic acidosis, aminoaciduria and osteomalacia. The urinary excretion of acid glycosaminoglycans and of total hydroxyproline were 27 mg/day (as glucuronic acid) and 280 mg/day respectively on admission. Both values decreased to the upper limits of normal level transiently during treatment with alkali and vitamin D2. At that time, an improvement in bone abnormalities, a decrease of serum alkaline phosphatase, and an elevation of serum inorganic phosphate were observed. The therapy prevented him from progressive osteomalacia and cured him of it, but mucopolysacchariduria and hydroxyprolinuria did not disappear. Analytical electrophoresis on cellulose acetate sheets showed that urinary acid glycosaminoglycans were composed of undersulfated chondroitin 4-/6-sulfate and heparan sulfate with a ratio of 6:4, on admission. After oral administration of alkali, the excretion of heparan sulfate decreased and undersulfated chondroitin 4-/6-sulfate was determined as a main component of urinary acid glycosaminoglycans. The clinical and laboratory data in this case suggested that the increased excretion of acid glycosaminoglycans and total hydroxyproline was caused by abnormal metabolism in connective tissues, especially by the bone abnormalities, in this syndrome.

Adolescent↗
PubMedDate not supplied

Renal tubular function in protein energy malnutrition.

Renal tubular handling of sodium, potassium, calcium, magnesium, phosphate and aminoacids in children suffering from marasmus and kwashiorkor revealed wastage of phosphate and aminoacids. In the malnourished children aminoaciduria could contribute significantly to the negative nitrogen balance. Exact cause of this tubular functional defect is not known.

Amino Acids↗
PubMedDate not supplied

The amino acid transport system b(o,+) and cystinuria.

Amino acid transport in mammalian plasma membranes is mediated by a multiplicity of amino acid transport systems. Some of them (systems L, y+ L, x(c)- and b(o,+)) are the result of the activity of heteromeric amino acid transporters (HAT) (i.e. transport activity is elicited by the coexpression of a heavy and a light subunit). The two heavy subunits known today (HSHAT: rBAT and 4F2hc) were identified in 1992, and light subunits (LSHAT: LAT-1, LAT-2, asc-1, y+ LAT-1, y+ LAT-2, xCT and b(o,+)AT) have been cloned in the last 2 years. Defects in two genes of this family (SLC3A1, encoding rBAT and SLC7A9, encoding b(o,+)AT) are responsible for cystinuria, an inherited aminoaciduria of cystine and dibasic amino acids. This finding and functional studies of rBAT and b(o,+)AT suggested that these two proteins encompassed the high-affinity renal reabsorption system of cystine. In contrast to this view, immunofluorescence studies showed that rBAT is most abundant in the proximal straight tubule, and b(o,+)AT is most abundant in the proximal convoluted tubule of the nephron. The need for a new light subunit for rBAT and a heavy subunit for b(o,+)AT is discussed.

Amino Acid Transport Systems↗
PubMed1987

Early detection of the nephrotoxic effects of industrial chemicals: state of the art and future prospects.

This paper discusses several tests that may permit the early detection of renal changes induced by long-term exposure to nephrotoxic industrial chemicals and may possibly serve as advance warning of pending renal damage. Some tests mainly attempt to assess the integrity of the glomerulus: high molecular weight proteinuria, glomerular basement membrane (GBM) antigens in blood and in urine, circulating anti-GBM antibodies, glomerular filtration rate after an acute oral load of proteins, and estimation of membrane negative charges (ie, glomerular polyanion). Others mainly attempt to identify functional and/or morphological changes at the tubular level: low molecular weight proteinuria, aminoaciduria, glucosuria, hyperphosphaturia, hypercalciuria, enzymuria, tubular antigen excretion, kallikrein, and prostaglandin excretion. Some of these tests are already routinely used, although controversy may still persist with regard to their clinical significance. Recently, new tests have been developed that may open new perspectives for assessing the significance of the early renal changes induced by chemicals.

Autoantibodies↗
PubMed1993

A potential role for endogenous adenosine in control of human glomerular and tubular function.

Adenosine has profound effects on renal function in experimental animals, but little is known about its role in human subjects. The recent advent of specific adenosine agonists and antagonists suitable for human use, however, now makes it possible to evaluate the influence of this potent vasoactive compound in both normal and pathological states. In this study we assessed the effects of FK-453, a nonxanthine, selective adenosine A1-receptor antagonist, on normal renal hemodynamics, tubular function, and plasma renin release. Eight healthy, male subjects each received three single oral doses of FK-453 (50, 100, and 200 mg) in ascending dose order with random allocation of one matched placebo dose, each on a separate study day. Renal hemodynamics, tubular function, and plasma renin concentrations (PRC) were assessed at baseline and postdose on each study day. Glomerular filtration rate (clearance of 51Cr-labeled EDTA) rose by 18.0%, 3 h after the administration of 100 mg of FK-453 and by 18.3% and 23.5%, 2 and 3 h, respectively, after the 200-mg dose, which was significantly different from the changes following placebo. There were no significant changes in mean arterial blood pressure or effective renal plasma flow (clearance of 125I-Hippuran). In contrast there were statistically significant increases in urine flow rate and osmolar clearance, as well as absolute and fractional excretions of sodium, phosphate, bicarbonate, chloride, magnesium, and uric acid in response to FK-453. No glycosuria or aminoaciduria was detected on urinalysis. There was, in addition, a marked increase in PRC in response to FK-453.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1985

[Nitrogen metabolism and renal amino acid excretion during total parenteral feeding of hypermetabolic patients with various carbohydrate regimes].

During an investigative study about the utilization of parenterally administered amino-acids (AA) in severe catabolic states nitrogen balances, urea production rates and catabolic nitrogen as well as urinary losses of amino-acids were determined in six adult polytraumatized patients treated in an intensive care unit. In addition to 19 g nitrogen (0.3 g N/kg/day) 3,000 kcal (12.5 MJ) were given simultaneously as carbohydrates. Either a mixture of laevulose 20%, glucose 10%, xylitol 10% (LGX) or glucose 50% were infused alternatively for four days in a randomized cross-over scheme. Another group of three patients received the LGX-regime alone for six days altogether. Higher urinary N-losses, increased urea production rates corresponding to a rise in the s.c. catabolic nitrogen were obtained on days where the LGX-mixture was infused; there was also an increased excretion of alpha-amino-N due to a distinct aminoaciduria. Not all amino-acids did react in the same manner. When comparing excretion to supply higher losses (greater than 20%) were observed for: THR greater than TRY greater than VAL greater than ILE greater than PHE. Methionine and alanine were also excreted in higher amounts, whereas under glucose an elevated excretion was especially noted with glutamine and alpha-aminobutyric acid. The increased urea production rate associated with a reduced incorporation of amino-acids as well as the accentuated renal AA-losses under LGX may be ascribed to a slight increase in protein catabolism connected with some impairment of AA-utilization due to a temporary metabolic hepatic 'block'. Under glucose an intensified endogenous mobilization as well as the higher exogenous supply of insulin might be responsible for a somewhat better AA-utilization. Amino-acid clearances under the carbohydrate mixture in the second group were - with the exception of lysine and leucine - raised distinctly similar to values seen in aminoaciduria of other origin. This leads to the assumption that the AA-overflow might result from a partial insufficiency or overload of renal transport ('carrier') systems being responsible for amino-acid reabsorption. The question of an adequate supply - concerning essential amino acids in particular - taking into consideration the relatively high losses under one of the nutritional regimes investigated is shortly touched upon. Finally the possibility of adapting AA-mixtures to the respective carbohydrate solutions in order to improve nitrogen balances and utilization is discussed.

Adolescent↗
PubMed1980

Hyperreninemia, lysozymuria, and erythrocytosis in Fanconi syndrome with medullary cystic kidney.

Adult onset Fanconi syndrome with medullary cystic kidney was diagnosed in a 30-year-old male with muscular weakness, hypokalemia, normal BP, hyperreninemia, and secondary aldosteronism. He also had non-specific aminoaciduria, lysozymuria, and beta 2-microglobulinuria. Urinary concentrating and acidifying capacity was impaired, and both sodium and potassium were lost into the urine. I.v. pyelography revealed medullary cystic kidney. Renal biopsy showed juxtaglomerular hyperplasia, heavy subintimal deposits and C3 and IgG in preglomerular arteriolar walls, and degenerative changes in the tubules, including loss of brush border and "macula densa-like" lesions. Polycythemia with elevated serum erythropoietin levels, and raised blood ACTH values with features of cortisolism were also present. Indomethacin therapy decreased plasma renin activity (PRA), plasma aldosterone, and urinary loss of potassium and sodium, while serum potassium approached normal levels. Metoprolol, a beta-adrenergic blocking agent, caused similar effects. Insensitivity to the pressor effect of angiotensin II was reversed by indomethacin treatment. Somatostatin infusion lowered PRA and aldosterone without affecting BP. Several biochemical aberrations of this patient resemble Bartter's syndrome, including the effect of indomethacin.

Adult↗
PubMed1980

Fatal infantile mitochondrial myopathy and renal dysfunction due to cytochrome-c-oxidase deficiency.

A 1-month-old boy was admitted because of failure to thrive. He was floppy and had bilateral ptosis, diminished reflexes, and poor suck. He had aspiration pneumonia, developed seizures, and died at age 3 1/2 months. Laboratory data showed lactic acidosis, proteinuria, glycosuria and generalized aminoaciduria. He was an only child, and family history was negative. Muscle biopsy showed large clumps of granules positive with oxidative enzyme stains and increased lipid droplets. Ultrastructural studies showed large aggregates of mitochondria, many of which were greatly enlarged and contained disoriented or concentric whorls of cristae and paracrystalline inclusions. Cytochrome c oxidase was absent in fresh frozen sections by histochemical staining. By biochemical assay, cytochrome c oxidase (cytochrome aa3) was 6% of normal in muscle biopsy and undetectable in autopsy muscle; spectra and content of cytochromes showed lack of cytochrome aa3, decreased cytochrome b and normal cytochrome cc1. In kidney, cytochrome-c-oxidase activity was 38% of normal and spectra showed decreased cytochromes aa3 and b. The association of fatal infantile mitochondrial myopathy, lactic acidosis and renal dysfunction was previously reported by Van Biervliet et al and appears to be a distinct nosologic entity, one of the few biochemically defined mitochondrial myopathies.

Carnitine O-Palmitoyltransferase↗
PubMed1989

Investigations into the biochemical effects of region-specific nephrotoxins.

1H NMR spectroscopy provides a useful initial biochemical screen with which to detect abnormal patterns of metabolites in urine collected from animals with different sites of nephrotoxic lesions. Male Fischer 344 rats were treated with nephrotoxic doses of sodium chromate (pars convoluta of proximal tubule), cisplatin, hexachlorobutadiene, mercury II chloride (pars recta of proximal tubule), propylene imine, and bromoethanamine (renal papilla) in order to induce damage in specific regions of the kidney. Urine was collected for up to 48 hr after dosing and was analyzed by 1H NMR spectroscopy (400 MHz) and conventional biochemical methods to provide biochemical fingerprints of urine in various site-specific nephrotoxic states. Hexachlorobutadiene and HgCl2 produced severe glycosuria and transient enzymuria. 1H NMR urinalysis revealed aminoaciduria, glycosuria, and lactic aciduria after exposure to all proximal tubular toxins except cisplatin, whereas papillary insult resulted in early elevations in urinary trimethylamine N-oxide and dimethylamine, together with later elevations in urinary acetate, succinate, and N,N-dimethylglycine (after propylene imine). Trimethylamine N-oxide and dimethylamine are suggested as novel markers of site-specific renal papillary injury in the rat.

Acetylglucosaminidase↗
PubMed1986

Renal tubular acidosis.

The clinical features and biochemical profile of 10 patients with Renal Tubular Acidosis (RTA) were described. The commonest mode of presentation was muscular weakness due to severe hypokalaemia in 5 patients while the other 5 presented with renal colic, haematuria or passage of gravel. Nine patients had nephrocalcinosis on X-rays and one had rickets. All the patients had Type I RTA, 2 of whom presenting initially with Incomplete Type I RTA which progressed to Complete Type I RTA. Two other patients had associated features of proximal tubular involvement evidenced by hypophosphatemia, hypouricemia, hyperphosphaturia, aminoaciduria and glycosuria. Six of the 10 patients had secondary RTA: 2 associated with medullary sponge kidneys, 2 with gout, 1 with idiopathic hypercalciuria and hyperuricosuria and the remaining patient with systemic lupus erythematosus.

Acidosis, Renal Tubular↗
PubMed1985

Acute renal failure and glucosuria induced by ferric nitrilotriacetate in rats.

Nitrilotriacetate (NTA), an effective metal-chelating agent, has been used as a substitute for polyphosphates in household laundry detergents. Nephrotoxicity and renal tumorigenicity have been reported in experimental animals that received high doses of NTA po for 4 weeks to 2 years. Since NTA exists in water as a variety of NTA-metal complexes, it was important to investigate the biological effects of NTA in a complexed form. In this study, acute and subchronic toxicity of a ferric iron chelate of NTA (Fe-NTA) was investigated in rats. When Fe-NTA was given ip, acute tubular necrosis and renal failure occurred following a single injection of 15 mg iron/kg. Repeated injections of sublethal doses produced degeneration and necrosis of the proximal tubular epithelium and was associated with polyuria, glucosuria, aminoaciduria, and azotemia. After 9 days of treatment, regeneration of the tubular epithelium with atypical cells was observed. Except for a parenchymal iron deposit, no marked changes were observed in other organs. None of these effects were observed in animals given noncomplexed NTA. In conclusion, the toxicity observed following high doses of NTA given po may be the result of an absorbed metal-NTA chelate.

Acute Kidney Injury↗
PubMed2002

Balkan nephropathy: a disorder of renal embryogenesis?

There is evidence to suggest that a renal embryogenesis disorder, with an associated deficit of nephrons, may be the cause of nephropathy later in the lives of patients with Balkan endemic nephropathy (BEN). This evidence includes the renal dysplasia or hypoplasia observed in BEN patients, the high incidence of renal pelvic and renal artery aberrations, primitive glomeruli and obstructed tubules on kidney biopsy, and an adult Fanconi-type syndrome of generalized proximal tubular dysfunction with hyperchloremic acidosis, potassium wasting, preserved urinary acidification, tubular proteinuria, aminoaciduria, uricosuria, hypomagnesemia, sodium wasting and normotension, as well as evidence from epidemiological data. The disease has affected no more than 2 generations, most of whom were in their 50s during 1965-1970, when maximal numbers of patients were seen. We are now observing a decreasing prevalence of BEN in Bulgaria and, even though this may have resulted from some prophylactic measures, the disease disappears much as it had appeared, as an epidemic. We speculate that some environmental factor may have had an impact on embryogenesis and resulted in nephropathy in patients with BEN. This could have been famine during the devastating Balkan wars in the beginning of 20th century, but may also have been an infectious or environmental factor, limited to the affected areas around the Danube river, which acted only during a limited period of time.

Adult↗
PubMed1998

Renal tubular function in beta-thalassemia.

Studies of the renal involvement in thalassemic syndromes have been varied and few. This study was designed to define the renal abnormalities associated with beta-thalassemia and to correlate the renal findings with clinical parameters. One hundred and four beta-thalassemic children with various disease severity were studied. The patients were divided into three groups: 48 with severe anemia [hematocrit (Hct) < 25%], 31 on a hypertransfusion program and desferrioxamine treatment, and 25 with moderate anemia (Hct > 25%). The results were compared with 15 normal children. Significantly higher levels of proteinuria and low molecular weight proteinuria were found in all patients compared with normal children. Aminoaciduria was detected in one-third of patients. Thalassemic patients had significantly lower morning urine osmolarity, higher urine N-acetyl-beta-D-glucoseminidase and malondialdehyde (MDA, an indicator of lipid peroxidation). Patients with severe anemia had significantly higher low-molecular weight proteinuria and MDA, and lower urine osmolarity than those with moderate anemia. Our data confirmed the high frequency of renal abnormalities in beta-thalassemia patients and indicated some degree of proximal tubular dysfunction. Severity of the abnormalities correlated with the degree of anemia and were least severe in patients on hypertransfusion and desferrioxamine therapy. This suggested that the damage might be caused by anemia and increased oxidation induced by excess iron deposits.

Adolescent↗
PubMed1999

Renal function following combination chemotherapy with ifosfamide and cisplatin in patients with osteogenic sarcoma.

BACKGROUND: Ifosfamide and cisplatin are active agents that are currently used in the treatment of osteosarcoma. Nephrotoxicity has been reported following their use in combination and alone. This study evaluates renal function in children and adolescents (median age 16 years) at least 3 months following completion of a chemotherapy regimen which included 54 g/m2 ifosfamide, 360 mg/m2 cisplatin, doxorubicin, and high-dose methotrexate. PROCEDURE: Mean glomerular filtration rate (GFR) was determined by inulin or iothalamate clearance; proximal tubular function was evaluated by measuring fractional excretion of glucose (FEglu), tubular maximum phosphate reabsorption per GFR (TMP/GFR), FE of urate, and 24-hour amino acid excretion. Distal tubular function was evaluated by 24-hour urinary calcium, FE of magnesium, and urinary osmolality after water deprivation. Twenty-four-hour urinary protein excretion was measured. RESULTS: The mean GFR was 97 ml/min/1.73 m2. Although 10 of 24 patients had GFRs lower than normal, the lowest value was only 22% below the lower limit of normal and would not account for any clinical compromise. Proximal tubular function evaluation revealed normal FEglu, normal mean TMP/GFR values, and high FE of urate (1 5.7%). Two of twenty-four patients were shown to have mild generalized aminoaciduria. Distal tubular function evaluation showed normal 24-hour urinary calcium levels (mean 3.4 mg/kg) and FE of magnesium as well as normal urinary osmolality. Twenty-four-hour urinary protein excretion was normal in all patients. CONCLUSIONS: The lack of clinically significant renal abnormalities observed in patients who received combination chemotherapy with ifosfamide and cisplatin for osteosarcoma is encouraging for future osteosarcoma protocol development.

Adolescent↗
PubMed1974

Stimulation of the hydrolytic activity and decrease of the transpeptidase activity of gamma-glutamyl transpeptidase by maleate; identity of a rat kidney maleate-stimulated glutaminase and gamma-glutamyl transpeptidase.

gamma-Glutamyl transpeptidase catalyzes transfer of the gamma-glutamyl moiety of glutathione (and other gamma-glutamyl compounds) to amino acid and peptide acceptors; this reaction probably involves (a) formation of a gamma-glutamyl enzyme and (b) reaction of the gamma-glutamyl-enzyme with an acceptor. Maleate decreases the latter reaction and markedly increases hydrolysis of the gamma-glutamyl donor, apparently by affecting the enzyme so as to facilitate reaction of the gammaglutamyl enzyme with water. Transpeptidase catalyzes gamma-glutamyl hydroxamate formation from many gamma-glutamyl compounds and hydroxylamine; this reaction is stimulated 4- to 5-fold by maleate. Glutamine, a poor substrate for transpeptidation as compared to glutathione, is slowly hydrolyzed and converted to gamma-glutamyl-glutamine by the transpeptidase; in the presence of maleate, hydrolysis of glutamine is markedly (>10-fold) increased, as is also its conversion to gamma-glutamyl hydroxamate in the presence of hydroxylamine. The findings suggest that the previously described "maleate-stimulated phosphate-independent glutaminase" is a catalytic function of gamma-glutamyl transpeptidase. Transpeptidase-catalyzed glutaminase activity may play a role in renal ammoniagenesis. The ability of maleate to decrease transpeptidation of gamma-glutamyl compounds (and to increase their hydrolysis to glutamate), when considered in the light of earlier findings that treatment of animals with maleate produces aminoaciduria, is consistent with function of transpeptidase and the gamma-glutamyl cycle in amino-acid transport.

Ammonia↗