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PubMed1988

Effects of succinylacetone on the uptake of sugars and amino acids by brush border vesicles.

Infants with hereditary tyrosinemia excrete succinylacetone (SA) in their urine, and suffer from a reversible renal Fanconi syndrome with glycosuria and hyperaminoaciduria. Thus, we have examined the effects of 4 mM SA on rat renal brush border membrane vesicle uptake of sugars and amino acids. SA, unlike sodium maleate, significantly inhibits Na+-dependent vesicular sugar and amino acid uptake. 22Na-uptake, as well as membrane fluidity of the vesicles, are also affected by SA. Inhibition of glycine uptake by SA is reversible and competitive in nature, while alpha-CH3-D-glucoside uptake is non-competitively affected. We conclude, therefore, that SA has a more complex action on the rat renal tubule than sodium maleate, and is likely a much more physiologic model for study of the human renal Fanconi syndrome.

Amino Acid Metabolism, Inborn Errors↗

PubMed1990

Transport of organic compounds in renal plasma membrane vesicles of cadmium intoxicated rats.

Effects of cadmium intoxication on renal transport systems for various organic compounds were studied. Subcutaneous injections of CdCl2 (2 mg Cd/kg.day) for two to three weeks induced marked polyuria, glycosuria, and proteinuria without altering glomerular filtration rate. In renal cortical brush border membrane vesicles (BBMV) isolated from cadmium treated rats, Na(+)-dependent D-glucose uptake was markedly attenuated, and this was due to reduction in Vmax and not Km. Likewise, Na(+)-driven L-glutamate transport and H(+)-driven tetraethylammonium transport were significantly reduced. In renal cortical basolateral membrane vesicles (BLMV) of cadmium intoxicated rats, Na(+)-dependent succinate transport was drastically reduced. These results indicate that cadmium intoxication impairs various transport systems for organic compounds in the brush border and basolateral membranes of proximal renal tubules.

Cadmium Poisoning↗

PubMed1991

Protective action of glycine in cisplatin nephrotoxicity.

Because glycine is cytoprotective for kidney cells in vitro, we investigated its possible action in vivo to protect rats against cisplatin nephrotoxicity, a well-established experimental model of renal tubular injury. Glycine was infused at a dose of 1 mmol per 100 g body weight per hour for 75 minutes, starting 15 minutes before cisplatin, 5 mg per kg, was injected intravenously. Plasma concentration of glycine rose to 3.5 mmol per liter at the time cisplatin was injected. These rats were compared with cisplatin-treated animals treated with L-alanine or with isotonic saline. After five days plasma creatinine of saline-treated rats given cisplatin had risen threefold to 2.6 +/- 1.5 mg per 100 ml (mean +/- SD), as creatinine clearance fell to 25% of baseline (0.14 +/- 0.05 ml/min/100 g). Morphological evaluation disclosed extensive damage involving all S3 segments in the outer medulla as well as the medullary rays of the cortex. In contrast, in rats treated with glycine, plasma creatinine rose only to 1.2 +/- 0.2 mg/100 ml and creatinine clearance was maintained at 75% of baseline (0.35 +/- 0.05 ml/min/100 g). Glycine also attenuated the weight loss, polyuria, increased fractional excretion of sodium and potassium, decreased urinary osmolality, and renal glycosuria observed in control, saline-treated rats after cisplatin, while substantially decreasing the percentage of S3 tubules with evident morphological injury. Renal platinum content was unaffected by glycine. The administration of L-alanine or the delayed infusion of glycine, starting one hour after cisplatin was given, did not prevent cisplatin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Early increased renal procollagen alpha 1(IV) mRNA levels in streptozotocin induced diabetes.

Changes in renal procollagen mRNA levels were measured shortly after the induction of streptozotocin induced diabetes in the rat. "Medullary" procollagen alpha 1(IV) levels seven days after diabetes induction was significantly higher in untreated diabetic rats (DM, N = 12; 244 +/- 57% of the mean control value), than in diabetic rats receiving small doses of insulin insufficient to achieve euglycemia (NPH, N = 10; 87 +/- 12%) and in diluent injected nondiabetic control rats (C, N = 15; 100 +/- 12%; P less than 0.01, DM vs. C and DM vs. NPH). "Medullary" procollagen alpha 1(I) mRNA levels were numerically increased in DM to a lesser degree (141 +/- 5%, ANOVA not significant) compared to C (100 +/- 13%), and this small increment was further normalized by insulin treatment (NPH, 120 +/- 11%). A trend for increased beta-actin mRNA levels in DM did not reach significance (P greater than 0.05). Increases in "medullary" procollagen mRNA levels did not correlate with kidney weight, glomerular tuft volume, creatinine clearance, food intake, or body weight gain, and occurred when renal morphology was normal by light microscopy. Statistically significant but weak correlations were noted between the serum glucose levels and "medullary" procollagen alpha 1(IV) mRNA levels (r = 0.43, P less than 0.05). In addition, weak correlations were noted between glycosuria and "medullary" procollagen alpha 1(I) levels (r = 0.38, P less than 0.05). In situ hybridization studies localized the increased procollagen alpha 1(IV) mRNA levels predominantly in the DM group primarily in the deep cortex and medullary outer stripe of proximal tubules. Glomerular procollagen alpha 1(IV), alpha 1(I), alpha 1(III) and beta-actin mRNA levels were not increased in untreated diabetic rats 7 or 28 days after diabetes induction. Thus, tubular procollagen alpha 1(IV) mRNA levels increased prior to any measurable change in glomerular levels and were ameliorated by insulin administration.

Animals↗

PubMed1994

Loop diuretics reduce hypoxic damage to proximal tubules of the isolated perfused rat kidney.

The straight portion (S3) of the proximal tubule lies in close proximity to the thick ascending limbs (TALs) at the cortico-medullary junction. Since a delicate balance exists between oxygen demand and the limited oxygen supply in this region, we hypothesized that reduction of thick limb metabolic activity might augment oxygen availability to S3 segments, which depend heavily upon aerobic metabolism, and prevent hypoxic damage. The degree of functional deterioration and morphological damage to S3 was assessed in isolated rat kidneys perfused with an erythrocyte-free medium. Bumetanide (10(-5) M) and furosemide (10(-4) M) reduced S3 fragmentation from 9.8 +/- 3.9% of tubules in controls to 0 and 1.4 +/- 0.9%, respectively (P < 0.0005). Tubular glucose reabsorption was better preserved in kidneys exposed to loop diuretics than in control kidneys (P < 0.01), and urinary alkaline phosphatase (P < 0.05) and the total amount of LDH released into the perfusate and urine (P < 0.01) were lower in the treatment groups. Morphological damage to S3 was closely correlated with medullary TAL necrosis (r = 0.66, P < 0.001), urinary alkaline phosphatase excretion (r = 0.89, P < 0.001) and glycosuria (r = 0.83, P < 0.001). We conclude that under hypoxic conditions TALs and S3 segments may compete with each other for a limited oxygen supply. Reduction of active transport in the mTAL might augment oxygen availability to S3 segments and improve their survival.

Alkaline Phosphatase↗

PubMed1994

Kidney in Galloway-Mowat syndrome: clinical spectrum with description of pathology.

The Galloway-Mowat syndrome, a rare inherited disorder, is characterized by congenital microcephaly with hypotonia and developmental delay, often hiatus hernia, and nephrotic syndrome manifested in infancy or in early childhood. The glomerular lesion has been poorly characterized in the few previous reports of this syndrome. We studied three siblings with microcephaly and nephrotic syndrome occurring during the first two weeks of life. Hematuria, glycosuria and renal failure were also present. Renal biopsy and postmortem specimens of two patients were studied. Glomerular structure was disorganized; capillary lumina were of varying calibers, capillary walls were adherent to one another, and mesangial zones were poorly demarcated. Glomerular basement membrane ultrastructure was markedly altered. The normal trilaminar structure was obscured or replaced by flocculent material; furthermore, 6 to 8 nm fibrils of unknown nature permeated the space between endothelial and epithelial cells. Non-glomerular basement membranes were unaltered in appearance. This syndrome apparently represents, in part, a new disorder of glomerular basement membrane formation and function.

Basement Membrane↗

PubMed1996

Risk of developing end-stage renal disease in a cohort of mass screening.

The prognostic significance of abnormal findings has not been demonstrated in a setting of mass screening. To evaluate the relative risk of end-stage renal disease (ESRD) indicated by various results of community-based mass screening, we utilized the registries of both community mass screening and chronic dialysis programs. In 1983, a total of 107,192 subjects over 18 years of age (51,122 men and 56,070 women) participated in dipstick urinalysis and blood pressure measurement in Okinawa, Japan. During ten years of follow-up, we identified 193 dialysis patients (105 men and 88 women) among them. Logistic regression analysis of clinical predictors of ESRD over 10 years was done and the adjusted odds ratio and 95% confidence interval were calculated in each of the predictors with adjustment to others. In the clinical predictors such as sex, age at screening, proteinuria, hematuria, systolic and diastolic blood pressure, proteinuria was the most potent predictor of ESRD (adjusted odds ratio 14.9, 95% confidence interval 10.9 to 20.2), and the next most potent predictor was hematuria (adjusted odds ratio 2.30, 95% confidence interval 1.62 to 3.28). Being of male gender was a significant risk factor for ESRD (adjusted odds ratio 1.41, 95% confidence interval 1.04 to 1.92). Diastolic blood pressure was also a significant predictor of ESRD (adjusted odds ratio 1.39, 95% confidence interval 1.17 to 1.64), but systolic blood pressure was not. In a mass screening setting, positive urine test, high diastolic blood pressure, and male sex were identified as the significant predictors of ESRD. Effect of glycosuria and other possible predictors of ESRD remained to be determined.

Adolescent↗

PubMed2000

Acquired Pelger-Huët anomaly in association with concomitant tacrolimus and fluconazole therapy following allogeneic bone marrow transplantation.

A 38-year-old Japanese woman with severe aplastic anemia received an allogeneic bone marrow transplant from her serologically HLA-identical father. Cyclosporine and methotrexate were administered to prevent graft-versus-host disease (GVHD). However, grade III acute GVHD developed on day 44, which was successfully treated with methylprednisolone and tacrolimus. Fluconazole therapy was started for oral candidiasis on day 112, but she complained of headache soon after. In addition to glycosuria and increased serum creatinine levels, Pelger-Huët anomaly of granulocytes was found in her blood, which disappeared after discontinuation of tacrolimus. Transient occurrence of Pelger-Huët cells may be associated with tacrolimus toxicity due to drug interaction with fluconazole.

Adult↗

PubMed2004

The Fanconi-Bickel syndrome: a case of neonatal onset.

A male newborn infant was recognized having Fanconi-Bickel syndrome (FBS) in the neonatal period. The presenting clinical findings were hyperglycemia and polyuria detected during an episode of acute enteritis. Physical examination was normal, biochemical analyses were suggestive of FBS: glycosuria, proteinuria, phosphaturia, generalized aminoaciduria, and increased levels of urinary beta 2-microglobulin, serum glucose and serum alkaline phosphatase. The molecular genetic analysis showed homozygosity for mutations within the gene of the glucose transporter 2 (Glut 2), 1213 C>T. The patient demonstrated improved clinical and metabolic status following institution of diet with frequent small meals and galactose-free-milk as well as pharmacological treatment with phosphate and vitamin alpha-OH-D3. In conclusion, infants showing hyperglycemia and polyuria may be considered having FBS also in the neonatal period. Early institution of adequate caloric intake and replacement of electrolytes and vitamin D may avoid or reduce metabolic complications.

Age of Onset↗

PubMed2002

Metabolic trajectory characterisation of xenobiotic-induced hepatotoxic lesions using statistical batch processing of NMR data.

Multivariate statistical batch processing (BP) analysis of 1H NMR urine spectra was employed to establish time-dependent metabolic variations in animals treated with the model hepatotoxin, alpha-naphthylisothiocyanate (ANIT). ANIT (100 mg kg(-1)) was administered orally to rats (n = 5) and urine samples were collected from dosed and matching control rats at time-points up to 168 h post-dose. Urine samples were measured via 1H NMR spectroscopy and partial least squares (PLS) based batch processing analysis was used to interpret the spectral data, treating each rat as an individual batch comprising a series of timed urine samples. A model defining the mean urine profile over the 7 day study period was established, together with model confidence limits (+/-3 standard deviation), for the control group. Samples obtained from ANIT treated animals were evaluated using the control model. Time-dependent deviations from the control model were evident in all ANIT treated animals consisting of glycosuria, bile aciduria, an initial decrease in taurine levels followed by taurinuria and a reduction of tricarboxylic acid cycle intermediate excretion. BP provided an efficient means of visualising the biochemical response to ANIT in terms of both inter-animal variation and net variation in metabolite excretion profiles. BP also allowed multivariate statistical limits for normality to be established and provided a template for defining the sequence of time-dependent metabolic consequences of toxicity in NMR based metabonomic studies.

1-Naphthylisothiocyanate↗

PubMed1977

The effect of chronic diabetes, induced by streptozotocin, on the activities of some enzymes of glycerolipid synthesis in rat liver.

1. Rats were injected with a single dose of 35mg of streptozotocin/kg body wt. They exhibited a diabetes that was characterized by glycosuria, polyuria, polydipsia, hyperphagia, hyperglycaemia, increased concentrations of unesterified fatty acids, glycerol and triacylglycerols in the serum and an increased activity of glucose 6-phosphatase in the liver. 2. After 10 weeks the hepatic activities of the microsomal glycerol phosphate acyltransferase, phosphatidate phosphohydrolase, phosphatidate cytidylyltransferase, diacylglycerol acyltransferase, choline phosphotransferase, CDP-diacylglycerol--inositol phosphatidyltransferase and the soluble phosphatidate phosphohydrolase were measured. 3. The only significant changes were an increase in the activity of the soluble phosphatidate phosphohydrolase and a decrease in that of the CDP-diacylglycerol--inositol phosphatidyltransferase in the diabetic rats. 4. These results are discussed in relation to the control of glycerolipid synthesis.

Acyltransferases↗

PubMed1979

Effect of glucocorticoid administration on the rate of muscle protein breakdown in vivo in rats, as measured by urinary excretion of N tau-methylhistidine.

The role of glucocorticoids in regulating the rate of muscle protein breakdown was evaluated by measuring excretion of N(tau)-methylhistidine during administration of various doses of corticosterone to adrenalectomized rats. Groups of rats received daily subcutaneous injections of 0, 0.2, 0.5, 1.0, 5.0 or 10.0mg of corticosterone/day per 100g body wt. for 7 days, followed by 3 days without hormone treatment, after which they were killed. A group with intact adrenal glands served as an additional control. All animals were pair-fed with the untreated adrenalectomized group. No significant differences were noted in growth rate or N(tau)-methylhistidine excretion between the intact or adrenalectomized control groups, or those given 0.2, 0.5 and 1.0mg of corticosterone, whereas growth ceased and N(tau)-methylhistidine excretion rose markedly in the groups receiving 5 and 10mg of corticosterone. After these two high doses of corticosterone, but not after lower doses, there was a loss of weight of the gastrocnemius muscle per 100g of final body wt., but not of the soleus and extensor digitorum longus muscles. The two highest doses of corticosterone also resulted in an increase in liver weight per 100g of final body wt. Lower doses of corticosterone did not cause these changes. Plasma corticosterone concentrations, measured on the final day of injection and again at the time of killing, were decreased to near zero by adrenalectomy and were little raised by doses of 0.2 and 0.5mg daily, but were increased to within the normal range by the 1mg dose. At 5 and 10mg doses, plasma corticosterone concentrations were sustained at 2-3 times those of intact rats, and thus in the range reported for rats exposed to severe stress. Rats given 5 and 10mg doses of corticosterone had glycosuria, and showed considerably elevated concentrations of insulin in the plasma. It is concluded that plasma concentrations of glucocorticoids within the normal range do not regulate the rate of muscle protein breakdown, whereas excessive plasma concentrations of corticosteroids, equivalent to those observed in severe stress, can accelerate muscle protein breakdown.

Adrenalectomy↗

PubMed1986

Activation of hepatic glycogen phosphorylase b in vivo by sodium sulphate in normal (Wistar) and phosphorylase b kinase-deficient (gsd/gsd) rats.

Sulphate ions have been known for some years to enhance the activity of hepatic glycogen phosphorylase b in vitro. Here we report that intravenous injections of 4.92 mmol of Na2SO4/kg body wt. to rats induced marked hepatic glycogenolysis in vivo, accompanied by polyuria, glycosuria and a mild hyperglycaemia. These effects were observed both in normal (Wistar) rats and in gsd/gsd rats that lacked hepatic phosphorylase kinase. In both rat strains the activity of glycogen phosphorylase in liver extracts was enhanced by pretreatment of the animals with Na2SO4, but in phosphorylase kinase-deficient livers the enhancement was solely in phosphorylase b activity, whereas both the a and b forms of the enzyme were activated in normal livers. Hepatic glycogenolysis was also induced by perfusing rat livers, both normal and gsd/gsd, with 25 mM-Na2SO4. Under these conditions both the rat strains showed only enhanced activities of glycogen phosphorylase b. This suggested that the increased activity of phosphorylase a in the extracts of normal livers after Na2SO4 administration in vivo was due to a hormonally mediated conversion of the b form into the a form. The activation of glycogen phosphorylase b was stable to dilution and appeared to be due to a long-lasting structural change in the enzyme or very tight binding of an activator.

Animals↗

PubMed1988

Lithium clearance measurements as an indication of cyclosporin A nephrotoxicity in the rat.

1. Measurements of the rate of lithium clearance, which provides an estimate of proximal renal tubular iso-osmotic reabsorption (i.e. sodium and H2O), were used to study H2O and electrolyte reabsorption during the development of cyclosporin A (CsA) induced nephrotoxicity. 2. CsA, administered daily by gavage at 50 mg/kg body weight, produced a nephrotoxicity which was characterized by reductions in the clearance rates of creatinine, sodium and potassium, and increased glycosuria, enzymuria and urine flow rate. 3. Decreased lithium clearance rate and increased proximal iso-osmotic reabsorption accompanied significant reductions in creatinine clearance rate. Absolute proximal tubular reabsorption, however, was not affected by CsA administration. 4. Reductions in the absolute distal tubular reabsorption of sodium, potassium and H2O were also observed. 5. Alterations in renal tubular function occur early in the development of CsA nephrotoxicity as a result of both direct proximal tubulotoxicity and an effect on the afferent arteriole. 6. Measurements of the rate of lithium clearance may be a useful adjunct to the diagnosis of CsA nephrotoxicity.

Animals↗

PubMed1996

Diabetes-prone NOD mice are resistant to Mycobacterium avium and the infection prevents autoimmune disease.

It was recently proposed that the diabetes genes of non-obese diabetic (NOD) mice are linked to the Bcg gene that is associated with resistance to infection by mycobacteria; however, it has not been established whether NOD mice are resistant or susceptible to the infection, although there are previous investigations on response of NOD mice to other intracellular parasites (e.g. Kaye et al., Eur. J. Immunol. 22: 357-364). We have investigated here this question, as well as the consequences of mycobacterial infection on the natural history of murine diabetes. Female NOD mice were intraperitoneally infected with 10(8) viable bacilli of Mycobacterium avium at 2 months of age, i.e. before the mice show diabetes; they were studied up to the sixth month of age (when more than half of untreated female NOD mice show glycosuria). To determine whether NOD mice were susceptible or resistant to M. avium infection, we have compared the kinetics of bacterial growths in liver and spleen of the mice with those determined in M. avium-susceptible (BALB/c) and resistant (C3H) strains of mice. NOD mice were able to control the M. avium infection, following a pattern similar to that observed in infected C3H mice. The mycobacterial infection prevented the expression of diabetes in all of the infected NOD mice and it also decreased the incidence of proteinuria in the treated mice. The infected NOD mice showed a marked enhancement in antibodies against the 65,000 mycobacteria antigen (heat-shock protein (hsp) 65) up to the second month of infection and these elevated titres slowly decreased in the following months; anti-hsp 65 antibodies were not detected in age-matched controls. This is the first demonstration that NOD mice are naturally resistant to mycobacterial infection, and we reinforce evidence on the role of immune response triggered by mycobacteria and its hsp 65 antigen in prevention of diabetes in NOD mice.

Animals↗

PubMed1998

Glycated plasma proteins in experimentally induced acute toxic renal failure by dichromate injection: evidence for loss with urine and decreased plasma levels.

In the rat, a single subcutaneous injection of sodium dichromate (20 mg/kg) causes acute renal injury and significant polyuria, proteinuria, and glycosuria (peaking 2-3 days after treatment, and returning to normal by day 5) without any changes in the plasma levels of protein, glucose, and glycated haemoglobin. Surprisingly, the percentage levels of glycated plasma total proteins and albumin (assayed by boronate affinity chromatography) transiently and significantly decrease during recovery from proteinuria (days 4 and 10 after treatment) and were found in the normal range of values by day 18. These changes are concomitant with a significant increase in the percentage level of glycated albumin in urine. Constancy of total plasma protein and the temporal pattern of levels of glycation suggest that changes in the percentage values of glycated proteins are secondary to a transient selective loss of glycated plasma proteins in urine.

Acute Kidney Injury↗

PubMed2001

Effect of metabolic control on nitrite and nitrate metabolism in type 2 diabetic patients.

1. The measurement of nitrite and nitrate levels in plasma and urine is an approach to assess the activity of the endogenous nitric oxide (NO) system. The aim of the present study was to evaluate whether metabolic control may affect plasma levels and urinary excretion of nitrates and nitrites in type 2 diabetic patients. 2. Twenty consecutive type 2 diabetic patients were studied twice: first (study 1), under poor metabolic control; and, second, after improved metabolic conditions. Determinations of the main metabolic parameters and of plasma nitrates and nitrites (NOX) were performed in the fasting state. A 24 h urinary specimen was obtained for glycosuria, NOX and creatinine. Diet compliance and home blood glucose monitoring was evaluated on a weekly basis until study 2 was performed after 32 +/- 7 days: then, an identical protocol was repeated (study 2). 3. Fasting plasma glucose was lower in study 2 (8.27 +/- 2.11 vs 10.77 +/- 3.88 mmol/L, respectively; P < 0.05); similarly glycosylated haemoglobin (HbA1c) improved significantly. Plasma NOX levels were similar between the first and second studies (14.3 +/- 7.8 vs 13.5 +/- 8.1 micromol/L, respectively); nor were any differences observed in urinary NOX excretion rates (726 +/- 607 vs 689 +/- 444 micromol/day, respectively). The urinary excretion fraction of NOX was higher during study 1 than during study 2 (3.22 +/- 2.38 vs 1.88 +/- 1.98%, respectively; P = 0.031). A relationship was observed between fasting plasma glucose levels and the urinary excretion fraction of NOX (r2 = 0.12; P = 0.026). 4. In type 2 diabetic patients, plasma and urinary levels of NOX do not change after improvement of metabolic control. A worse metabolic control is associated with an increased urinary fraction excretion of NOX: thus, changes in plasma NOX concentration may reflect the effect of hyperglycaemia in the renal handling of these compounds rather than the effects on the L-arginine-NO pathway.

Blood Glucose↗

PubMed1998

Renal tract abnormalities detected in Australian preschool children.

OBJECTIVE: To quantify the incidence of abnormalities in urinalysis and blood pressure from preschool children and their predictive value in detecting renal disease within an Australian community. METHODOLOGY: Urine samples, blood pressure and height measurements and parental reports of significant medical problems were collected from a total of 9355 South Australian preschool children. Seven hundred and forty-three children with abnormal results were investigated in a nephrology outpatient clinic. A control group of 357 children with no detectable abnormality were also recalled, examined and, where appropriate, investigated. RESULTS: Nine thousand, three hundred and fifty-five children were tested. Of these, 0.81% were shown to have a clinically significant renal tract abnormality. The findings included children with urinary tract infections, vesico-ureteric reflux, glomerular disease, renal calculi, essential hypertension and a renal neoplasm. While dipstick-based methods were the most specific indicators of renal tract abnormalities, measurement of blood pressure and urinary beta2-microglobulin were also important in detecting abnormalities. Screening for glycosuria did not result in the detection of significant undiagnosed abnormalities. In the control group with no abnormality detected at testing, there was one case each of aortic coarctation, polycystic kidney disease and vesico-ureteric reflux diagnosed. CONCLUSION: Undiagnosed renal tract abnormalities are present in many Australian preschool children. Most are detectable by a thorough history, examination and urinalysis.

Blood Pressure Determination↗