SEARCH · PubMed Health

Results for “GLYCOSURIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources

PubMed1991

Adaptive regulation of hepatic bile salt transport: effects of alloxan diabetes in the rat.

The hepatic transport of bile salts appears to be adaptively regulated by changes in the bile salt pool size and in the flux of bile salt through the liver. The maximum secretory rate of taurocholate increases or decreases when the bile salt pool size is modified by either oral feeding of cholate or taurocholate (up-regulation) or prolonged bile salt depletion through a biliary fistula (down-regulation), respectively. It is not known whether adaptive regulation of hepatic bile salt transport operates under conditions in which the bile salt pool size is modified by endogenous changes in bile acid metabolism. Because experimental diabetes mellitus is associated with alterations in the synthesis of bile acids and total bile salt pool size and composition in the rat, we examined the effects of diabetes mellitus induced by alloxan (5 mg/100 gm body weight, intravenously) and insulin treatment on hepatic bile salt transport and relate the changes to bile salt pool size variations. At 3 days after alloxan injection (DIAB-3 group) both taurocholate maximum secretory rate and pool size were significantly decreased, whereas they were restored to normal values after 6 days of diabetes (DIAB-6 group). Insulinopenic diabetes for 14 days (DIAB-14 group) and for 24 days (DIAB-24 group) resulted in a marked increase of basal bile salt secretory rate (secondary to an increased contribution of cholate conjugates) and an enhanced taurocholate maximum secretory rate compared with control rats (147% and 188% increase, respectively) and with a group (PHARM-control) that received alloxan but did not develop detectable glycosuria (224% and 286% increase, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1994

Prognostic significance of diabetes in patients with cirrhosis.

Alterations in carbohydrate metabolism are frequently observed in cirrhosis, and approximately 15% to 30% of patients have overt diabetes. In a retrospective and prospective study in cirrhosis, we analyzed the prognostic significance of diabetes, which was defined as the presence of hyperglycemia and overt glycosuria that in most cases required dietary restrictions or active treatment. The clinical records of all patients with cirrhosis admitted to our department for the period 1980 to 1985 were reviewed in 1985 and 1986, and surviving patients were prospectively followed up until December 1991. Final status could be obtained in 354 (98 with diabetes) of 382 eligible patients; 110 were alive at the end of follow-up. Prognostic factors were identified by Kaplan-Meier analysis, followed by Cox's stepwise regression. The model identified, in sequence, albumin, ascites, age, encephalopathy, bilirubin, diabetes, and platelets as prognostic factors. The larger mortality rate in patients with diabetes was not due to complications of diabetes but to an increased risk of hepatocellular failure. Diabetes was no longer a risk factor as a covariate in a subgroup of 271 patients when varices were added but was again significant when patients who died of gastrointestinal bleeding were excluded. The presence of diabetes, clinically detectable and often requiring adequate treatment, is a risk factor for long-term survival in cirrhosis.

Adolescent↗

PubMed1995

Nonacidotic kidney proximal tubulopathy with absorptive hypercalciuria.

We studied three patients with proximal tubulopathy characterized by defective reabsorption of phosphate, glucose, amino acids, urate, and low molecular weight proteins. This tubulopathy differs from Fanconi syndrome in that the patients had normal plasma bicarbonate and absorptive hypercalciuria associated with increased 1,25-dihydroxyvitamin D levels. The youngest patient was rachitic and may be classified with previously described patients, whereas the other two patients presented with nonrachitic osteopenic bone disease and their tubulopathy started during adult life. Kidney defects appeared sequentially in one of the nonrachitic patients. The two brothers of the youngest patient had similar kidney and bone disturbances. One of the other two patients had a brother with similar kidney reabsorption defects; an additional brother was probably affected and a sister presented with glycosuria, but no other reabsorption defects. The findings in these two families suggest a genetic transmission of proximal tubulopathy. The third case was sporadic. Renal histology of the three patients showed a great number of giant cells in the tubular lumen. We conclude that, at least in our adult patients, tubulopathy may represent a new entity among the proximal tubular dysfunction cases described to date. The features of this proximal defect suggest that it may be caused by a selective alteration of luminal cell membrane transport of phosphate, glucose, amino acids, urate, and proteins in the presence of a normal sodium gradient across the tubular cell membrane.

Amino Acids↗

PubMed1991

Effects of reserpine and L-cysteine and glutathione depletion on 2-bromoethylamine hydrobromide-induced tubular necrosis in Swiss ICR mice.

Female Swiss ICR mice were injected ip with 100 or 300 mg 2-bromoethylamine hydrobromide (BEA)/kg body weight. Male Swiss ICR mice were subjected to water deprivation, or treated with 5% dextrose in water, dimethylsulphoxide, piperonyl butoxide, SKF-525A, sodium phenobarbital, beta-naphthoflavone, probenecid, reserpine, diethyl maleate, buthionine sulphoximine or L-cysteine. Urine collected sequentially from male Swiss ICR mice given 300 mg BEA/kg body weight was analysed for glucose, protein, pH and specific gravity. Female mice were less sensitive to BEA than were male mice. Diuresis, antidiuresis, treatment with cytochrome P-450 inducers and inhibitors, and the antioxidant dimethyl-sulphoxide had no effect on the incidence or severity of tubular necrosis (TN) induced by BEA. Probenecid and L-cysteine decreased the severity, but they had no effect on the incidence of TN. Glutathione depletion by diethyl maleate and inhibition of glutathione synthesis by buthionine sulphoximine decreased the dose of BEA necessary to cause TN; buthionine sulphoximine was more effective than diethyl maleate. Reserpine decreased both the incidence and severity of TN. Glycosuria, aciduria and decreased urinary specific gravity occurred before morphological changes were seen under the microscope, indicating that the functional changes precede the morphological changes. These data indicate that glutathione is important in protecting against BEA-induced TN, that BEA or a metabolite is concentrated in the tubule epithelium by way of anion transport, and that vasoconstriction contributes to the development of BEA-induced TN.

Animals↗

PubMed1980

Some hematological and histopathological effects of the alkaloids gramine and hordenine on meadow voles (Microtus pennsylvanicus).

Meadow voles (Microtus pennsylvanicus) were used to evaluate the relative toxicity of the alkaloids, gramine and hordenine, which are present in reed canarygrass (Phalaris arundinacea) and to assess their effects on the quality of this grass as a forage. One hundred and twenty meadow voles, 31 days of age, were fed gramine (0, 0.125, 0.25, or 0.5% of a nutritionally complete diet) or hordenine sulfate (0, 0.15, 0.31, or 0.62% of the diet) for 21 days. The effects of treatment on growth, mortality, hematology, blood chemistry, and histology of body organs were examined. Approximately one-third of the voles died when fed either 0.25 or 0.50% gramine. Voles that survived on gramine diets had kidney lesions, glycosuria, higher intakes (P less than 0.05), and lower weight gains (P less than 0.01) than control animals. Voles fed 0.25 and 0.50% gramine had increased circulating reticulocyte levels (P less than 0.01) and those fed 0.125% gramine had higher alkaline phosphatase activity (P less than 0.05) than the control voles. Hordenine did not affect vole diet intake, weight gain, or rate of mortality. Voles fed hordenine developed kidney lesions and glucose was detected in the urine of 62% of these animals. Gramine was more toxic than hordenine on a molar equivalent basis.

Alkaloids↗

PubMed1989

Renal kallikrein excretion as a distal nephrotoxicity marker during cadmium exposure in rats.

Cadmium exposure is known to induce hypertension, but development of hypertension is not universal in exposed animals. However, the cellular uptake of cadmium could also exert renal cytotoxic effects which have been, until now, essentially only studied at the proximal tubule level. Kallikrein is an enzyme synthetized in renal cortex and excreted in the urine in the distal tubule. Therefore, to evaluate the distal renal effect of cadmium, we studied the daily urinary kallikrein excretion (UKE) in conscious unrestrained female Brown Norway rats during long-term chronic exposure to 2 dosages of cadmium given subcutaneously 3 times a week, a low dose (LD): 0.25 mg/kg and a high dose (HD): 1 mg/kg. Neither dose of cadmium was able to induce significant hypertension in the treated animals. HD administration for 24 weeks resulted in a decreased UKE associated with an increase in plasma renin activity and sodium and potassium excretions. LD administration had no significant effect on UKE. Twenty weeks after stopping cadmium administration, a persistent reduction in UKE was still observed; furthermore, the group which had been previously administered a LD of cadmium, now also exhibited a reduced UKE. During this re-examination period in both groups, the UKE reductions were associated with normal systolic blood pressure, glycosuria, natriuresis. Our data show that cadmium administration can influence UKE, plasma renin activity, plasma aldosterone concentration and electrolyte excretion without inducing any variation of blood pressure. This may reflect a nephrotoxic, non-hypertensive effect. Since this effect persisted after stopping cadmium administration, it may indicate a prolonged irreversible nephrotoxic effect at the distal nephron level. Thus, UKE may be a useful non-invasive index to evaluate distal nephrotoxicity.

Aldosterone↗

PubMed1992

Effect of genetic dilution on development of diabetes, impaired glucose tolerance and in vitro glucose oxidation in LA/N-cp x SHR/N-cp F1 hybrid rats.

1. To determine the effects of gene dilution on development of IGT, NIDDM and in vitro glucose oxidation, heterozygous lean LA/N-cp female and SHR/N-cp male rats were mated, and F1 offspring studied at periodic intervals to determine the prevalence of obese and diabetic traits. 2. Obesity occurred in 25% of offspring by 5 weeks of age, consistent with inheritance of the autosomal recessive cp trait. 3. IGT occurred in all obese male F1, 67% of obese female F1, and 18% of the lean male F1 rats by 5 months of age, and diabetes occurred in 80% of male obese and 17% of female obese rats from 6 months of age. Glycosuria occurred with glucose intolerance, and was more severe in rats with NIDDM than IGT. 4. Rates of in vitro glucose oxidation were greater in diaphragm and adipose tissue, and were greater in the presence of insulin (100 mu Units/ml) in obese female but not obese male F1 rats. 5. These results indicate that the development of glucose intolerance is more prominent in male than in female F1 rats, that the progression of IGT to NIDDM occurs later in life in the F1 hybrid than in the SHR/N-cp strain from which the diabetic trait was transmitted, and that genetic dilution of the diabetic trait via hybrid breeding results in a delay in the expression of NIDDM which is chronologically more similar to that which occurs in man.

Animals↗

PubMed1990

Mild renal failure induced by subchronic exposure to molybdenum: urinary kallikrein excretion as a marker of distal tubular effect.

In this study we investigated the effect of two molybdenum (Mo) doses (40 and 80 mg/kg/d) on renal function. Neither dose of Mo was able to induce significant hypertension in treated animals. Subchronic exposure to high doses of Mo resulted in a delay in body weight gain associated with mild renal failure marked by a decrease in glomerular filtration. An increase in diuresis and urinary kallikrein excretion associated with unchanged glycosuria and proximal tubular enzymuria (alanine aminopeptidase and gamma-glutamyl transpeptidase) evoked a preferential mild effect at the distal tubule.

Acute Kidney Injury↗

PubMed1987

Regulation of hepatic gluconeogenesis and glycogenolysis by phosphorylated glycerol and glycolytic intermediates in diabetic and control Chinese hamsters.

Metabolic regulation of gluconeogenesis and glycogenolysis by two phosphorylated derivatives of glycerol, G3P, and DHAP, and by F2,6BP, was assessed in vitro in liver homogenates obtained from Chinese hamsters (C. griseus) of two types: diabetic animals from sublines with consistent glycosuria and hyperglycemia, and normoglycemic controls. Only FBPase was sensitive to inhibition by the phosphorylated metabolites. G3P was weakly inhibitory of FBPase. Addition of 7 X 10(-3) M DHAP halved FBPase activity in the diabetic hamsters and 4 X 10(-3) M DHAP produced the same effect in the controls. The other gluconeogenic enzymes and phosphorylase a were only negligibly inhibited. In contrast, F2,6BP inhibited FBPase at concentrations in the micromolar range. Liver homogenates from diabetic hamsters appeared significantly more sensitive to F2,6BP inhibition of FBPase than those from controls at concentrations 0.6 X 10(-6) M and higher. These data indicate that in well-fed hamsters phosphorylated glycerol derivatives are unlikely to regulate hepatic gluconeogenesis at physiologic concentrations. However, the effects of F2,6BP on gluconeogenesis and glycolysis may be linked to those mediated by insulin. Thus, the deficiency of insulin, elevated end-organ insulin resistance, the alteration in the glucagon-insulin interaction, or a combination of these possible causes can be involved in an abnormal regulation of glycolysis and gluconeogenesis at the FBPase step, associated with changes in F2,6BP concentration.

Animals↗

PubMed2005

alpha-Lipoic acid prevents diabetes mellitus in diabetes-prone obese rats.

Several lines of evidence have suggested that triglyceride accumulation in skeletal muscle and pancreatic islets is causally related to type 2 diabetes mellitus. We recently showed that alpha-lipoic acid (ALA), a potent antioxidant and cofactor of mitochondrial respiratory enzymes, reduces body weight of rodents by suppressing food intake and increasing energy expenditure. We sought to determine if ALA can prevent the development of diabetes mellitus in obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Most (78%) untreated OLETF rats showed glycosuria at 40 weeks of age, but this was completely prevented by ALA. Compared with untreated OLETF rats, ALA reduced body weight and protected pancreatic beta-cells from destruction. ALA also reduced triglyceride accumulation in skeletal muscle and pancreatic islets. These results indicate that ALA prevents diabetes mellitus in obese diabetes-prone rats by reducing lipid accumulation in non-adipose tissue as well as in adipose tissue.

Animals↗

PubMed2006

Gatifloxacin-induced hyperglycemia: a case report and summary of the current literature.

BACKGROUND: Gatifloxacin is a fluoroquinolone antibiotic that has been associated with severe hypoglycemic and hyperglycemic events. OBJECTIVE: The purpose of this report was to describe a new case of gatifloxacin-associated hyperglycemia in an elderly patient and to provide a summary of case reports. CASE SUMMARY: A male patient, aged 86 years, was hospitalized with small bowel obstruction due to adhesions from a previous appendectomy. At the time of admission, the patient weighed 78.5 kg (ideal body weight, 73 kg), had a body mass index of 24.8 kg/m2, and had a calculated creatinine clearance of 45.6 mL/min. The patient's hospital medications were metoprolol, diltiazem, subcutaneous heparin, ranitidine, vancomycin, piperacillin/tazobactam, and aspirin. He also was treated with gatifloxacin 400 mg QD for suspected pneumonia during the hospital stay. After 4 days of the gatifloxacin regimen, the patient's mean blood glucose concentration increased from 133 mg/dL at the time of admission to 537 mg/dL. Although the patient exhibited signs of glycosuria (ie, urine glucose concentration >1000 mg/dL), he did not complain of symptoms of hyperglycemia, such as polyuria, polyphagia, or polydipsia. The hyperglycemia resolved after administration of gatifloxacin was discontinued and the patient had received regular insulin 15 U SC over 5 hours. DISCUSSION: The exact mechanism by which gatifloxacin induces hyperglycemia is unknown, but it may be related to vacuolation of pancreatic beta-cells, leading to a decrease in insulin secretion. This case, along with the 15 other summarized cases, adds to the evidence for an association between gatifloxacin and hyperglycemia. These patients had other risk factors that may have contributed to the development of hyperglycemia, including age >65 years and renal impairment. CONCLUSION: An elderly patient with no history of diabetes developed severe hyperglycemia after receiving doses of gatifloxacin 400 mg that had not been adjusted for age-related renal impairment. The hyperglycemia resolved after discontinuation of gatifloxacin.

Age Factors↗

PubMed2004

Weight gain during insulin therapy in patients with type 2 diabetes mellitus.

In patients with diabetes, the benefits of tight glycemic control are unequivocal--delayed onset and progression of complications such as retinopathy, nephropathy, and neuropathy. However, intensive therapy with insulin and some oral antidiabetic agents come at the price of weight gain, a condition that can prevent attainment of tight glycemic goals and probably limits success of treatment. Insulin-related weight gain has been attributed to anabolic effects of insulin, appetite increases, and reduction of glycosuria. Use of metformin in combination with insulin is commonly recommended as a way to limit weight gain in patients with type 2 diabetes, and other new oral therapies and insulin analogs may also provide weight-control advantages. Lifestyle interventions (patient education about diet and exercise) promote weight loss in the short-term, but have not sustained weight control over long-term intervals. For lasting weight control, such interventions may need to continue throughout the course of treatment. Likewise, weight-loss agents, such as sibutramine and orlistat promote short-term weight loss, but no follow-up studies have yet demonstrated that this loss can be maintained for 5 years or longer. Bariatric surgery is the only treatment recognized to have lasting effects on weight control, but its use is limited at present to those who are morbidly obese.

Blood Glucose↗

PubMed2005

Gestational diabetes in Iran: incidence, risk factors and pregnancy outcomes.

The objective of this study was to determine the incidence of gestational diabetes mellitus (GDM) and compare fetal, maternal and neonatal complications amongst women with GDM and pregnant women with normal glucose tolerance in an urban Iranian population. In a prospective cohort study, universal screening for gestational diabetes mellitus was performed for 1310 pregnant women who were referred from private clinics and community health care centers to Fatemiyeh Hospital in Shahrood City. Screening was performed with a 50 g oral Glucose Challenge Test (GCT) with 130 mg/dl cut-off point, then a diagnostic 100 g Oral Glucose Tolerance Test (OGTT) was done according to Carpenter and Coustan criteria. The incidence of GDM was 4.8%. There were differences in risk factors: age >30 years, family history of diabetes, obesity, previous macrosomia, glycosuria between the two groups (P<0.001). Women with GDM had a higher rate of stillbirth (P<0.001; odds ratio 17.1, 95% CI=4.5-65.5), hydramnios (P<0.001; odds ratio 15.5, 95% CI=4.8-50.5), gestational hypertension (P<0.001; odds ratio 6, 95% CI=2.3-15.3), macrosomia (P<0.05; odds ratio 3.2, 95% CI=1.2-8.6) and caesarean section (P<0.001). We have found that the incidence of GDM in an urban Iranian population is similar to developed countries. Complications were more common in the GDM group than in the normal group and outcomes for women with persistent diabetes post-partum were particularly poor. We recommend screening for GDM in Iran, but further evaluation of selective screening and cost effectiveness will need to be performed. Measures to improve the outcome of GDM pregnancy will also need to be addressed in the future.

Adult↗

PubMed2006

Undiagnosed phaeochromocytoma mimicking severe preeclampsia in a pregnant woman at term.

We report an unusual case of phaeochromocytoma in pregnancy. The patient presented with severe hypertension, visual disturbances, proteinuria, glycosuria and pulmonary oedema at 38 weeks' gestation. The initial diagnosis was severe preeclampsia, but rapid deterioration of the fetus necessitated an emergency caesarean section under general anaesthesia, following which the maternal condition deteriorated rapidly. Differential diagnoses included pulmonary embolus, cardiomyopathy, amniotic fluid embolus and ischaemic/embolic cerebrovascular accident. Despite aggressive maximal treatment, mother and baby died 36 h later. Post mortem examination of the mother revealed a 5.5-cm tumour of the right adrenal gland confirmed histologically as a phaeochromocytoma. We examine the diagnostic dilemmas of this case and consider the treatment and management options when faced with a critically ill mother and the need to deliver her fetus by emergency caesarean section. We also question the clinical priorities during management of a sudden deterioration in both maternal and fetal health.

Adrenal Gland Neoplasms↗

PubMed2005

G-CSF treatment prevents cyclophosphamide acceleration of autoimmune diabetes in the NOD mouse.

Cyclophosphamide (CY) accelerates autoimmune diabetes in the NOD mouse at different levels, including critical targeting of a regulatory T cell subset, exacerbation of pro-Th1 IFN-gamma production and promotion of inflammation in pancreatic islets. Here we evaluated the ability of G-CSF to antagonize the acceleration of the disease induced by CY. Human recombinant G-CSF, administered daily at 200 microg/kg by s.c. injection, protected NOD mice from CY-accelerated onset of glycosuria and insulitis. G-CSF accelerated the recovery of the T cell compartment after the depletion of the lymphoid compartment triggered by CY injection. It selectively prevented the loss of the immunoregulatory T cells expressing the CD4(+)CD25+ phenotype that also stained CD62L+ in peripancreatic lymph nodes and promoted their expansion in the spleen. In addition to this, it abrogated the robust cytokine--particularly IFN-gamma- and chemokine burst triggered in immune cells by CY. G-CSF promoted only slight changes in the inflammatory effects of CY at the target tissue site, assessed by chemokine induction within the pancreas. Thus the immunoregulatory properties of G-CSF were critical in the early control of the accelerating effects of CY on autoimmune diabetes in the NOD mouse.

Animals↗

PubMed2005

Hyperglycaemia and the very preterm baby.

Neonatal hyperglycaemia, as usually defined (a whole blood glucose of >7 mmol/L), is common in the first week of life in babies born more than 12 weeks early. However, a review of a cohort of all such births in the north of England suggests that significant glycosuria is uncommon, and that there is no threat of an osmotic diuresis until the urine contains 2% glucose (by which time the blood glucose level almost always exceeds 15 mmol/L). The current statistical or epidemiological definition of hyperglycaemia (derived from data on term babies) needs to be replaced, for clinical purposes, by a more operationally relevant definition.

Blood Glucose↗

PubMed2006

Colchicine antimitosis causes progression of S-(1,2-dichlorovinyl)-L-cysteine-induced injury leading to acute renal failure and death in mice.

Objective of the present study was to test the importance of tissue repair in the final outcome of S-(1,2-dichlorovinyl)-L-cysteine (DCVC)-induced nephrotoxicity using colchicine (CLC) intervention. Male Swiss Webster (SW) mice were administered a normally nonlethal dose of DCVC (30 mg/kg, i.p.) on day 0 and CLC (2 mg/kg, i.p.) at 42 and 66 h after administration of DCVC. The mice were observed for mortality and various renal injury and repair parameters were studied during a time course of 0-14 days. Administration of 30 mg DCVC/kg led to loss of renal architecture by day 1, which sustained until day 5, and regressed thereafter to reach normal architecture by day 10 resulting in 100% survival. Renal dysfunction as assessed by increases in plasma BUN and creatinine levels was concordant during this time course. Urinary volume increased significantly between days 10 and 14 with significant increases in urinary glucose concentrations on days 1-4. Calpain leakage increased from day 1 and remained so until day 5 before declining at later time points. In contrast, CLC intervention led to marked inhibition of S-phase DNA synthesis and 100% mortality by 120 h. H&E sections of kidneys revealed loss of renal architecture on day 1 which progressively worsened from day 2 to 4. Polyuria and glycosuria were evident during the first 2 and 3 days, respectively. Calpain immunohistochemistry revealed progressive leakage of calpain in the extracellular space during 2-4 days which lead to increased renal injury as evident from significant increases in calpain specific breakdown products (CSBPs) of alpha-fodrin during the same period of time. The group of mice receiving 2 mg CLC/kg alone showed a significant increase in urinary creatinine concentration on day 5. Neither the expression nor localization of aquaporin 1 was altered in any of the treatment groups. These results show that antimitotic intervention after DCVC-initiated renal injury leads to expansion and progression of that injury, which appears to be due to proteolytic destruction of neighboring cells mediated by calpain leaking out of necrosed renal tubular epithelial cells.

Acute Kidney Injury↗

PubMed2006

Outcome of pregnancy in renal allograft recipients: SIUT experience.

The course of pregnancy and its outcome was studied in renal allograft recipients. Between November 1985 and November 2005, a total of 1481 renal transplants were carried out at the Sindh Institute of Urology and Transplantation (SIUT); among them were 348 females, with 73 potential females for pregnancy. All patients received cyclosporine and prednisolone, with 82% also receiving azathioprine and 4 patients mycophenolate mofetil as a third immunosuppressant drug. We evaluated incidence of hypertension, diabetes, pre-eclampsia, urinary tract infection (UTI), rejection during pregnancy and during 3 months' postdelivery as well as outcomes of pregnancy. Among 73 potential candidates, 31 had 47 pregnancies, after an average of 31 months (8-86 months). Of 31 subjects, 21 subjects were hypertensive on one or two drugs prior to conception. A rise in blood pressure during pregnancy was noticed in 7 patients. Albuminuria from trace to 3+ appeared in 13 patients and glycosuria in one other. Blood sugar levels remained within normal range in all subjects. UTIs occurred during pregnancy in 7 patients. Among 47 pregnancies, 9 had abortions (7 spontaneous, 2 therapeutic) and 6 had preterm deliveries. The others were full-term deliveries: 12 via a lower segment caesarean section and 20 were normal vaginal deliveries. Average birth weight was 4.8 lbs. At an average follow-up of 38 months the serum creatinine values ranged from 0.94 to 2.3 mg %. One patient developed acute irreversible graft dysfunction soon after delivery. Our study demonstrated that pregnancy did not reduce renal graft survival, but newborns are at greater risk of premature birth and low birth weight.

Albuminuria↗