Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GLYCOSURIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 721 records · Page 40Linked to original sources
PubMed1993

An insulin-like growth factor I-resistant state in cartilage of diabetic rats is ameliorated by hypophysectomy. Possible role of metabolism.

This study investigated the effect of IDDM on cartilage anabolic activity in rats. Rats were injected with STZ to induce IDDM, were hypophysectomized, or were injected with STZ and hypophysectomized. After 14 days, control (intact and sham-Hx) and Hx rats were normoglycemic, whereas the rats with IDDM exhibited hyperglycemia and glycosuria. The HxDb rats, however, had normal blood glucose levels and no glycosuria. Both growth, serum levels of IGF-I, and basal cartilage 35SO4 incorporation measured in vitro were decreased in the Hx, IDDM, and HxDb groups. IGF-I added in vitro significantly stimulated 35SO4 incorporation by cartilage explants from control and Hx animals, whereas explants from the animals with IDDM were unresponsive. Explants from the HxDb rats, however, were stimulated by IGF-I in a dose-related manner. Because Hx corrected the glycemic status of the IDDM rats and restored cartilage responsiveness to IGF-I, a second set of experiments was undertaken to further investigate the relationship between cellular metabolism and anabolic activity in cartilage. Cartilage explants from rats fasted for 48 h showed significantly decreased basal 35SO4 incorporation, which was as low as that in explants from rats with severe IDDM. Whereas explants from the IDDM rats were completely unresponsive, those from the fasted rats (and fed rats) were significantly stimulated by the added IGF-I. However, incubation in the presence of 2-D-G, which causes intracellular glucopenia, or in the absence of glucose, completely blocked the anabolic response to IGF-I in otherwise responsive tissues. In conclusion, an important component of diabetic growth inhibition appears to be tissue resistance to the anabolic action of IGF-I, a condition that is correctable by Hx and that may be a result of metabolic impairment at the tissue level.

Analysis of Variance↗
PubMed1993

Symptoms of sensory neuropathy in adults with NIDDM in the U.S. population.

OBJECTIVE: To ascertain the prevalence and determinants of sensory neuropathy symptoms through structured interview of a representative sample of people with diabetes in the U.S. population. RESEARCH DESIGN AND METHODS: The 1989 National Health Interview Survey consisted of a representative sample of 84,572 persons in the U.S. > or = 18 yr of age. A household respondent identified all people in the household believed to have diabetes (n = 2829). Subjects who could not be personally interviewed (n = 129) and individuals who stated they did not have diabetes (n = 295) were excluded. A detailed questionnaire was administered to 99.3% of the remaining 2405 subjects. Questions on symptoms of sensory neuropathy included whether during the past 3 mo the subjects had experienced numbness or loss of feeling, pain or tingling, or decreased ability to feel hot or cold. The neuropathy questions were also administered to a representative sample of 20,037 subjects who were not known to have diabetes. RESULTS: Prevalence of symptoms of sensory neuropathy was 30.2% among people with IDDM. This prevalence was 36.0% for men with NIDDM and 39.8% for women with NIDDM, compared with 9.8 and 11.8% for nondiabetic men and women, respectively. In logistic regression, factors independently related to symptoms of sensory neuropathy in people with NIDDM included duration of diabetes, hypertension, hyperglycemia, and glycosuria. Long duration of NIDDM (> or = 20 yr) was associated with a twofold increased risk of symptoms of sensory neuropathy compared with those with 0-4 yr of diabetes. Hypertension was associated with a 60% higher likelihood of symptoms. Diabetic individuals whose blood glucose was high all or most of the time or whose urine tests showed glucose all of the time were > 2 times as likely to have symptoms of sensory neuropathy than those who did not report hyperglycemia or glycosuria. Age, sex, ethnicity, cigarette smoking, and height were not determinants of sensory neuropathy. CONCLUSIONS: Symptoms of sensory neuropathy affect 30-40% of diabetic patients in the U.S. Men and women are affected equally. Prevalence of these symptoms increases with longer duration of diabetes; hypertension and hyperglycemia predispose to symptoms of sensory neuropathy.

Adolescent↗
PubMedDate not supplied

Some social factors related to control of diabetes mellitus in adult Jamaican patients.

A population of 103 adult diabetic patients was interviewed at the Outpatient Clinic for diabetic patients of the University Hospital of the West Indies to examine the effects of severity of the illness and social variables, such as facilities at home, education attained, employment status, informal medication, and understanding of the illness in relation to its control. Patients were classified as severe if there were clinical evidence of vascular or neurologic complications of diabetes and as mild if there were no complications. Control of diabetes was regarded as good if the patients were free from or had less than 2+ glycosuria and as poor if they had had 2+ or more glycosuria during the six months before the study. We found that the quality of control was mainly determined by the severity of the disease. In the mild diabetic, proper diabetic control was not influenced by any social variable examined. In the severe diabetic the quality of control was associated with social amenities, educational status, employment status, and understanding of the disease.

Adult↗
PubMed1991

The severity of diabetes is a major determinant of myocardial damage in the rat.

The severity of insulin-dependent diabetes mellitus had a marked effect upon the development of myocardial sequelae in the rat. Even with the same degree of hyperglycemia, glycosuria, polydipsia, and polyuria, moderately diabetic animals did not develop the degenerative ultrastructural changes seen in myocardium from more severely diabetic rats. These included decreased cardiocyte size, loss and disorganization of myofibrils, and loss of sarcoplasmic reticulum and transverse tubules. Since hyperglycemia and glycosuria are frequently used as the primary, and often sole, criteria for identifying diabetes in experimental animals, this study demonstrates the need to more specifically define the severity of the disease in studies of the heart.

Animals↗
PubMedDate not supplied

Transient clinical diabetes mellitus in cats: 10 cases (1989-1991).

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.

Animals↗
PubMed1998

[Gliclazide and metformin combination in patients with type 2 diabetes. Preliminary data].

BACKGROUND: This preliminary study is aimed at the evaluation of the efficacy and tolerability of combined therapy with gliclazide and metformin in the treatment of patients with type 2 diabetes mellitus inadequately controlled with maximal doses of gliclazide. METHODS: A prospective, uncontrolled study, with a follow-up of 3 months, was performed in two Outpatient Diabetes Care Units. Fifty-seven patients affected by type 2 diabetes for at least 5 years, aged 61.0 +/- 3.4 years, with a duration of diabetes of 9.2 +/- 3.9 years, Body Mass Index (BMI) 30.5 +/- 3.7 kg/m2, previously treated with gliclazide 240 mg/day, and with HbA1c > 8.5%, were studied. The patients were treated with gliclazide 120 mg/day and metformin 1500 mg/day for 3 months; HbA1c, 24-hour glycosuria, and fasting and post-prandial glycaemia, were determined at the beginning and at the end of the study. RESULTS: After a 3-month treatment, a reduction of fasting and post-prandial glycaemia, glycosuria (15.0 +/- 5.3 versus 5.7 +/- 4.0 g/l, p < 0.01), and HbA1c (9.9 +/- 1.1 versus 8.4 +/- 1.0%, p < 0.01) was observed, while no significant changes occurred in body weight. The treatment was generally well tolerated. CONCLUSIONS: In conclusion, the combination of gliclazide and metformin, which could theoretically show some advantages over the association of glibenclamide and metformin with regards to lipid and haemorheologic profiles, resulted to be effective and well tolerated in patients with type 2 diabetes inadequately controlled with sulphonylurea monotherapy.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

[The metabolic effects of the angiotensin converting enzyme inhibitors in experimental diabetes mellitus].

We have studied the effects exerted by the angiotensin converting enzyme inhibitor (ACEI) Enalapril upon the glycemic profile in diabetic rats. With respect to the subacute character of our experiment (15 days), the following parameters have been recorded: diuresis, glycosuria, ketonuria and glycemia. In the diabetic rats treated with ACEI we haven noted slight, statistically insignificant improvements in glycosuria and glycemia, compared to the untreated diabetic subjects. Conversely, a statistically significant improvement of ketonuria has been noted in the diabetic rats receiving ACEI compared to the untreated ones. The short-term administration of ACEI in experimental diabetes mellitus acutely improves the glycemic profile, probably by the amelioration of the tissular sensitivity to insulin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Insulin: discovery and controversy.

During the first two decades of the 20th century, several investigators prepared extracts of pancreas that were often successful in lowering blood sugar and reducing glycosuria in test animals. However, they were unable to remove impurities, and toxic reactions prevented its use in humans with diabetes. In the spring of 1921, Frederick G. Banting, a young Ontario orthopedic surgeon, was given laboratory space by J.J.R. Macleod, the head of physiology at the University of Toronto, to investigate the function of the pancreatic islets. A student assistant, Charles Best, and an allotment of dogs were provided to test Banting's hypothesis that ligation of the pancreatic ducts before extraction of the pancreas, destroys the enzyme-secreting parts, whereas the islets of Langerhans, which were believed to produce an internal secretion regulating sugar metabolism, remained intact. He believed that earlier failures were attributable to the destructive action of trypsin. The name "insuline" had been introduced in 1909 for this hypothetic substance. Their experiments produced an extract of pancreas that reduced the hyperglycemia and glycosuria in dogs made diabetic by the removal of their pancreases. They next developed a procedure for extraction from the entire pancreas without the need for duct ligation. This extract, now made from whole beef pancreas, was successful for treating humans with diabetes. Facilitating their success was a development in clinical chemistry that allowed blood sugar to be frequently and accurately determined in small volumes of blood. Success with purification was largely the work of J.B. Collip. Yield and standardization were improved by cooperation with Eli Lilly and Company. When the Nobel Prize was awarded to Banting and Macleod for the discovery of insulin, it aggravated the contentious relationship that had developed between them during the course of the investigation. Banting was outraged that Macleod and not Best had been selected, and he briefly threatened to refuse the award. He immediately announced that he was giving one-half of his share of the prize money to Best and publicly acknowledged Best's contribution to the discovery of insulin. Macleod followed suit and gave one-half of his money award to Collip. Years later, the official history of the Nobel Committee admitted that Best should have been awarded a share of the prize.

Animals↗
PubMed2002

Control of hyperglycemia and retardation of cataract by mulberry (Morus indica L.) leaves in streptozotocin diabetic rats.

Dried leaf powder of mulberry (M. indica L.) when given along with the diet at 25% level to streptozotocin induced diabetic male Wistar albino rats for 8 weeks, controlled hyperglycemia, glycosuria, albuminuria and retarded onset of retinopathy. Untreated diabetic rats showed hyperglycemia, glycosuria, albuminuria and developed lenticular opacity after 8 weeks of experimental period.

Animals↗
PubMed2002

[Transcapillary filtration of plasma proteins in patients with diabetes type II microangiopathy complications].

UNLABELLED: This study presents the results of the research on transcapillary filtration of plasma proteins in patients with non-insulin dependent diabetes mellitus (NIDDM). The aims of the study were as follows: (a) Examination of transcapillary filtration of plasma proteins in patients with NIDDM; (b) Search for correlations between metabolic status of diabetes, severity of diabetic microangiopathy and penetration of individual protein fractions into the blister fluid; (c) Examination of the influence of nonenzymatic glycation on albumin fragmentation and its transcapillary filtration. It was also decided to check whether changes in the blister fluid would appear earlier than fundal fluorescein angiography or microalbuminuria, two markers of diabetic microangiopathy. The study enrolled 34 patients with type II diabetes mellitus, aged 35-78 years, with a mean disease duration of 12.5 years (SD = 7.8). The control group included 10 non-diabetic volunteers aged 31-76 years. The mean age in both groups did not differ significantly. The cantharidin blister method was used to study the permeability of capillary vessels. The following laboratory tests were done: concentrations of serum urea, creatinine, glucose, fructosamine, glycated hemoglobin, cholesterol, and triglycerides. Electrophoretic separation of proteins in plasma and blister fluid was performed and the concentration of fructosamine in fluid was measured. Routine urinalysis was supplemented with microalbuminuria. The eye fundus was inspected and fundal fluorescein angiography was done. The influence of nonenzymatic glycation on protein fragmentation and its possible impact on the permeability of capillary vessels was determined with in vitro glycation of human serum albumin. In patients without diabetic retinopathy the Cb:Cs ratio for beta-globulin turned out to be significantly lower than in patients with proliferative retinopathy. Patients with normoalbuminuria had the Cb:Cs ratio for alpha 2-globulin significantly lower than patients with urinary albumin concentrations > or = 165 mg/L. When the group was divided with regard to serum fructosamine concentrations, the subgroup with fructosamine concentrations lower than 3 mmol/L revealed a significantly higher Cb:Cs ratio for fructosamine than the subgroup with fructosamine > or = 3 mmol/L. Concentrations of total protein, albumin, beta-globulin and gamma-globulin in blister fluid correlated positively with glycemia in the control group. Blister fluid concentration of beta-globulin correlated positively with HbAIC concentration. In the study group, total protein content in blister fluid correlated negatively with duration of diabetes and level of glycosuria. Concentrations of blister fluid alpha 1-globulin and gamma-globulin correlated negatively with glycosuria. Concentrations of blister fluid beta-globulin correlated negatively with duration of diabetes. Electrophoretic separation of in vitro SDS glycosylated human serum revealed no additional fraction in the incubated samples. Electrophoretic separation of in vitro glycosylated albumin disclosed co-migration of albumin monomers incubated for varying times with glucose. CONCLUSIONS: 1. Glycation of human serum and albumin does not cause fragmentation of the proteins, but decreases transcapillary filtration of albumin due to change of molecular electric charge. 2. Patients with non-insulin dependent diabetes and microangiopathic complications reveal increased transcapillary transport of alpha 2- and beta-globulin in skin. 3. Increased permeability of skin capillary vessels for alpha 2- and beta-globulin in diabetic microangiopathy reflects an advanced stage of the disease and may facilitate progression.

Adult↗
PubMedDate not supplied

[Acute tubulointerstitial nephritis in children].

UNLABELLED: Acute tubulointerstitial nephritis (ATIN) is a rare renal disorder in children. Patients usually present non-specific symptoms and signs so that the diagnosis of ATIN is often delayed. The disease may be infection- or drug-induced or it may occur without a known cause. Early recognition and appropriated therapy usually lead to an excellent prognosis. The aim of the study was to describe clinical and laboratory findings and the course of ATIN in 21 patients, that are typical enough to enable early recognition of the disease as it is potentially reversible. METHODS: Between 1986 and 1997 we observed 21 patients, aged 7-16 years (mean, 12.8), with acute tubulointerstitial nephritis, including eight with tubulointerstitial nephritis and uveitis (TINU syndrome). Laboratory studies included urinalysis, complete blood count, erytrocyte sedimentation rate (ESR), plasma creatinine, glomerular filtration rate (GFR), electrolytes, proteins, IgG, C3, C4 antinuclear-antibodies (ANA), antistreptolysin-O and antibodies to hantaviruses. Renal ultrasound was done in all patients. Renal biopsy was performed in 5 children. RESULTS: All children had previously been healthy. The symptoms of ATIN developed within a few days (Table 1). The most common initial symptoms were fatigue, fever, gastrointestinal disturbances, anorexia and weight loss. Less common complaints included headache, arthralgias and maculopapular rash. On addmition no patient had hypertension, oedema or evidence of acute infection. ESR, plasma urea and creatinine concentrations were increased in all, plasma proteins and IgG levels in the majority of patients. ANA were negative in 15 pts in whom this analysis was performed; C3 and C4 levels were normal. In two children recent strepococcal and in the other 6 hantavirus infection was serologicaly proved. All patients had non-oliguric acute renal failure (ARF): GFR was 21.7 +/- 8 9 in 14 pts and 67 +/- 9.7 in 7 pts. Low urine specific gravity (1003-1014), mild proteinuria (0.3-0.4 g/24 h), leukocyturia and/or haematuria were found in all patients; glycosuria, aminoaciduria and decreased tubular reaposrption of phosphate (TRP) were found in 12/21, 9/21 and 9/14 patients, respectively. Urine cultures were negative in all children. Renal US demonstrated enlarged hyperechoic kidneys in 11 pts, in remaining 10 pts no abnormalities were found. Renal biopsy, performed in 5 children, confirmed the diagnosis of ATIN. Eight patients subsequently developed anterior uveitis as part of TINU syndrome. Treatment included supportive therapy in all and six patients received prednisolone for 4-8 weeks (40-60 mg/m2/24 h for 10-14 days with subsequent reduction of dose over several weeks). Anterior uveitis was successfully treated with topical steroids. Renal function completely recovered in all patients: GFR (109 +/- 22.6 ml/min) within a mean interval of 47 +/- 33 days, concentration ability within 2-12 (mean 4.5) months. DISCUSSION: Common clinical features of ATIN are non-oliguric acute renal failure of various degrees, signs of tubular dysfunction, proteinuria, haematuria, leukocyturia and absence of hypertension. All our patients had normal blood pressure, non-oliguric renal failure, proteinuria, hypostenuria and abnormal urinary sediment; about half of them had glycosuria and/or other signs of proximal tubular dysfunction. The most important causes of ATIN in children reported in literature are systemic infections and drugs. However, the cause of ATIN in our patients was assessed as being related to infection only in 8 patients and to diclofenac in one. No infection, drug, toxin or other cause could be identified in 4, as well as in 8 pts with TINU syndrome. The prognosis of ATIN in children is considered to be favourable, but some patients may develop chronic renal failure. Renal function completely recovered in all our patients; that is consistent with outcome data from the most reports. CONCLUSION: Acute tubulointerstitial nephritis is an important cause of ARF in children, its aetiology may be different and it carries an excellent prognosis. ATIN should be suspected in a child who presents typical, although non-specific symptoms and signs, associated with lukocyturia and/or microhaematuria, signs of tubular dysfunction and unexplained renal failure. The diagnosis can be verified at renal biopsy. Early recognition of the disease is important to remove possible aetiologic agents and to treat them before chronic lesions are present to avoid long-term renal damage.

Acute Disease↗
PubMed1992

Familial progressive renal tubulopathy.

We report herein data on 6 male patients with progressive tubulopathy. These patients belonged to two families: the propositus, his father, a paternal first cousin, two paternal uncles, and a maternal uncle. A 7-year-old proband had mild proteinuria (1 g/day), consisting of beta 2-microglobulin, alpha 1-microglobulin and lysozyme, and aminoaciduria. Glycosuria and acidosis were absent. A 38-year-old father had mild proteinuria (2 g/day), including low-molecular-weight protein. Hypokalemia, hypophosphatemia, glucosuria, phosphaturia, aminoaciduria, and reduced urinary concentrating ability were also present. The other 4 affected family members also had low-molecular-weight proteinuria, detected by screening for beta 2-microglobulin. In addition, there were several abnormalities; aminoaciduria in all 6, phosphaturia in 4 of 6, hypercalciuria in all 6 and glycosuria in 2 of 6 patients. Tubular dysfunction was more severe in the older subjects, hence, the disease seems to progress with age. Familial low-molecular-weight proteinuria is apparently a progressive disease linked to a X-linked or to an autosomal dominant inheritance.

Adolescent↗
PubMedDate not supplied

An interim report of an intervention strategy for diabetes care in Jamaica.

The high prevalence (17.9%) of diabetes mellitus and its attendant costs have been recognized for some time. The diabetic public has hitherto been too oriented to seeking health care at the secondary and tertiary health care centres; a much too costly approach. As a part of a wellness promotion thrust as well as an awareness and intervention strategy, a number of health care agencies have collaborated in a training programme of lay diabetes facilitators. This was intended to allow a domino effect of "each one teach one" within the community. This intervention programme was undertaken over an 18-month period. No significant changes were achieved in glycaemia levels. The impact on hospital admissions and community awareness is yet to be assessed. Laboratory results indicated good correlation between glycosuria and hyperglycaemia. This could influence the thrust in maintaining glycosuria assessment alongside blood glucose monitoring. This approach would have a cost benefit for government clinics islandwide. Whilst it may be difficult to identify any one parameter that may be responsible for change, it will be possible to assume that this intervention strategy, the only innovation in the health care delivery modalities, may have contributed.

Aged↗
PubMedDate not supplied

[Abdominal pain in diabetic ketoacidosis: report of four cases].

Four cases of diabetic ketoacidosis presenting with abdominal pain are reported. Case 1: a 14-year-old boy suffered from sudden onset of mid-abdominal pain, then migrating to the right lower quadrant. Nausea and vomiting occurred subsequently. Appendectomy was performed under the impression of acute appendicitis in an outside surgical clinic. The patient became comatose the next day and then was transferred to our hospital. Diabetic ketoacidosis was diagnosed after the detection of hyperglycemia, glycosuria, and ketonuria on the day of admission. Unfortunately, he expired on the same day in spite of vigorous resuscitation. Case 2: a 9-year-old boy complained of abdominal pain for 10 days. There was no specific finding in the physical examination. Diabetic ketoacidosis was confirmed four days later when conscious disturbance, dehydration, and tachypnea were noticed. Case 3: a 10-year-old girl presented with a history of intermittent abdominal pain for one month. The character of the abdominal pain was nonspecific. Glycosuria was detected in a pediatric clinic. Diabetic ketoacidosis was confirmed after her referral to our hospital. Case 4: a 5-year-old girl suffered from acute abdominal pain for four hours. She was found to have tachypnea, lethargy, and ill-looking. Diabetic ketoacidosis was diagnosed after serial examinations. The abdominal pain in diabetic ketoacidosis may lead the pediatrician into diagnostic error. Therefore, when a child presented with non-specific abdominal pain, a routine urine sugar should be checked in order not to miss the possibility of diabetic ketoacidosis.

Abdominal Pain↗
PubMedDate not supplied

Focal glomerulosclerosis manifested with nephrotic syndrome.

To assess the long-term outcome for nephrotic children with focal glomerulosclerosis, 23 patients were studied. Twenty were male and three female; the mean age at onset was 7.2 +/- 4.0 years. Twenty of the 23 children had focal segmental glomerulosclerosis, and the other 3 showed focal global sclerosis in renal biopsy specimens. Hypertension (11/23) and hematuria (9/23) were frequent clinical features. Glycosuria (4/23) was occasionally noted. Of the patients studied 13 were initial steroid responders and 10, steroid nonresponders. The mean duration of follow-up for the entire group was 4.7 +/- 4.0 years (ranging from 1 to 13.5 years). From the total study group, 13% had renal deaths; 13% had decreased creatinine clearance, but not end-stage renal disease; 35% had persistent proteinuria; and 39% were in remission. None of the three patients with focal global sclerosis developed chronic renal failure. The data suggest that for children with focal glomerulosclerosis, clinical outcome is not too pessimistic. Except for glycosuria, no clinical or morphologic features were predictive of the development of chronic renal failure, in this study.

Adolescent↗
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↗
PubMedDate not supplied

Proteinuria and statural growth.

In order to assess the possible effects of proteinuria on statural growth, we studied 14 children with various glomerulopathies and proteinuria persistently above 30 mg/kg/day which were followed-up for 1.5-4.3 years. They had received only short-term steroid therapy or no steroids at all. During the follow-up, 3 patients lost 1-2.1 height standard deviation scores. These patients had proteinuria above 100 mg/kg/day with associated glycosuria, and they went into chronic renal failure. The other patients had minor variations of the growth curve. In our experience heavy proteinuria represents a risk factor for growth delay when it is associated with glycosuria and chronic renal failure.

Body Height↗
PubMedDate not supplied

Cardiac ultrastructural changes in streptozotocin-induced diabetic rats: effects of insulin treatment.

The effect of insulin treatment on myocardial ultrastructure was studied in experimentally induced diabetic male rats. Rats received an intravenous injection of 60 mg/kg streptozotocin and were tested for glycosuria 3 days later. Half of these animals were then given 3.0 U of protamine zinc insulin daily subcutaneously and again tested for glycosuria. The significant loss in weight observed in the untreated diabetics was prevented in the insulin-treated diabetics. Electron microscopic observation of the left ventricular myocardium from 3 month untreated diabetics revealed mild edema adjacent to the sarcoplasmic reticulum. A more severe form of edema, focal in nature, was also observed. Some distended mitochondria and disrupted banding were associated with these focal areas of edema. Increased lipid levels and intramitochondrial dense staining particles were found in the untreated diabetics. On the other hand, hearts from insulin-treated diabetics did not exhibit these alterations. They did, however, exhibit mitochondrial clumping which was also seen in the untreated diabetics and the same capillary changes. The latter involved a thickening of the lamina densa, loss of the lamina lucida and an increased number of micropinocytotic vesicles in the capillary walls. These results suggest that insulin treatment is capable of preventing only some of the ultrastructural changes induced by streptozotocin-diabetes in rat hearts.

Animals↗