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 1,027 records · Page 57Linked to original sources

PubMed2002

Partial rescue of insulin receptor-deficient mice by transgenic complementation with an activated insulin receptor in the liver.

Insulin receptor (IR)-deficient mice develop severe diabetes mellitus, diabetic ketoacidosis (DKA) and liver steatosis and die within 1 week after birth. We examined in this work whether the metabolic phenotype of IR(-/-) mutants could be improved by transgenic complementation with IR selectively in the liver. We first generated transgenic mice expressing a human DNA complementary to RNA encoding a truncated constitutively activated form of IR (IRdelta) under the control of liver-specific phenylalanine hydroxylase (PAH) gene promoter. These mice presented more pronounced fasting hypoglycemia and showed slightly improved glucose tolerance as compared to controls. The transgenic mice were crossed with IR(+/-) mutants to generate IR(-/-) mice carrying the PAH-IRDelta transgene. Although such mutants developed glycosuria, DKA was delayed by more than 1 week and survival was prolonged to 8-20 days in approximately 10% of mice. In these partially rescued pups, serum glucose and triglyceride levels were lowered, hepatic glycogen stores were reconstituted and liver steatosis was absent as compared with pups which developed strong DKA and died earlier. Thus, lack of insulin action in the liver is responsible in large part for the metabolic disorders seen in IR(+/-) mice. This study should stimulate interest in therapeutic strategies aimed at improving hepatic function in diabetes.

Animals↗

PubMed2002

Tubulo-interstitial nephritis caused by sodium valproate.

A severely handicapped 14-year-old Japanese girl had epilepsy and was treated with sodium valproate (SV) from the age of 7 years. Although the epileptic seizures were well controlled, she sometimes had a fever and hypokalemia from the age of 13 years. Laboratory examinations revealed metabolic acidosis, hypouricemia, hypophosphatemia, glycosuria, proteinuria and aminoaciduria, thus suggesting Fanconi syndrome. Gallium scanning showed marked renal uptake. A renal biopsy revealed interstitial nephritis without immuno-deposition. SV was replaced since it was considered to be the most probable cause of the renal involvement. Thereafter, she showed marked improvement of the clinical symptoms and the laboratory data gradually, and she never had a fever. Although SV is an effective anti-epileptic drug, we have to pay attention to adverse renal effects such as Fanconi syndrome and interstitial nephritis.

Adolescent↗

PubMed1991

[Acidoketosis in a chronic alcoholic woman].

A 37-year-old chronic alcoholic female was admitted with epigastric pain, complete anorexia, vomiting and diarrhoea. She was dehydrated, and had polypnoea. Laboratory investigations revealed severe metabolic acidosis (pH 7.14) with a major anion gap (37.4 mmol.l-1), and ketone bodies in blood and urine. Blood glucose concentration was 6.1 mmol.l-1, there was no glycosuria. Rehydration (2 l.day-1 of 5% glucose) together with sodium bicarbonate (500 ml of 1.4% sodium bicarbonate over the first four hours) normalized the pH (7.37). The ketone bodies disappeared on the following day. During the acute illness, were found high blood levels of glucagon and low levels of insulin. The diagnosis of alcoholic ketoacidosis, the pathogenesis of which remains unknown, is discussed.

Acid-Base Equilibrium↗

PubMed1999

Acquired Fanconi's syndrome associated with monoclonal gammopathies.

Franconi's syndrome is a rare complication of the monoclonal gammopathies characterized by diffuse failure in reabsorption at the level of the proximal renal tubule resulting in glycosuria, generalized aminoaciduria, and hypophosphatemia. Current evidence suggests monoclonal light chains that are incompletely digested in renal tubule lysosomes cause renal injury. The light-chain fragments serve as a nidus for crystal formation, and the crystals interfere with a broad range of apical membrane transporters. Franconi's syndrome is predominantly associated with monoclonal kappa in the urine, but rare instances of FS caused by lambda light chains have been described. Overt hematologic malignancies such as multiple myeloma, Waldenström's macroglobulinemia, or other lymphoproliferative disorders occur in one third of patients. Clinical manifestations include slowly progressive renal failure and bone pain caused by osteomalacia. The osteomalacia is caused by chronic hypophosphatemia and may be exacerbated by secondary hyperparathyroidism and renal tubular acidosis. Treatment consists of supplementation with phosphorus, calcium, and vitamin D. The osteomalacia is often completely reversible with mineral supplementation. Patients with an associated symptomatic malignancy or rapidly progressive renal failure may also benefit from chemotherapy. The prognosis is good in the absence of overt malignant disease.

Fanconi Syndrome↗

PubMed1992

Diabetes and adrenal disease.

Disorders of the adrenal cortex and medulla can result in glucose intolerance or overt diabetes mellitus. Cushing's syndrome, characterized by excessive secretion of glucocorticoids, impairs glucose tolerance primarily by causing insulin resistance at the post-receptor level. On the other hand, phaeochromocytoma and hyperaldosteronism, via the respective actions of catecholamines and hypokalaemia on the pancreatic beta-cell, impair glucose tolerance primarily by inhibiting insulin release. The glucose intolerance associated with these adrenal disorders is usually only mild to moderate in severity. Marked hyperglycaemia, glycosuria, and polyuria are uncommon and ketosis is rare. Moreover, the late complications of diabetes mellitus are distinctly uncommon in patients with these disorders, and the prognosis for morbidity and death is usually that of the underlying disease and not that of diabetes mellitus. The impaired glucose tolerance induced by all three of these adrenal disorders usually returns to normal once the underlying aetiology has been cured. These factors must guide the clinician in treatment of these secondary forms of diabetes, and suggest that tight (near normal) blood glucose control may not be an appropriate goal in patients with these disorders. The relationship between adrenal androgens and glucose tolerance is more uncertain. Several studies in humans have demonstrated an acute decline in serum concentrations of the adrenal steroids DHEA and DHEA-sulfate in response to experimentally-induced hyperinsulinaemia, but the regulatory role of insulin on adrenal androgen metabolism in normal physiology or disease remains speculative. In several animal models DHEA appears to exert potent anti-obesity and anti-diabetogenic actions, but such effects have yet to be demonstrated in humans. Human studies of DHEA are limited, and more research needs to be conducted to determine whether the observations made in animal models will prove applicable to man.

Adrenal Gland Diseases↗

PubMed1991

Steroid trials in the assessment of reversibility of air flow limitation: a survey of current clinical practice of chest physicians.

To evaluate how steroid trials are currently used in the assessment of reversibility of air flow limitation, a postal questionnaire was sent to 355 consultant members of the British Thoracic Society working in England and Wales; 253 questionnaires were returned (71% response rate). Two respondents did not undertake steroid trials; of the remaining 251, 75% prescribed 30-40 mg oral prednisolone, with the commonest treatment period being 2 weeks. A high dose steroid inhaler was sometimes used as an alternative by 31% of respondents. Although 71% of respondents made lung function measurements on several occasions before starting steroids and 76% made measurements during treatment, 78% assessed patients on only one occasion at the end of the trials to ascertain its outcome. Weight, blood pressure and glycosuria were measured less frequently after the steroid treatment compared to the pre-trial period. Blood glucose and serum electrolytes were infrequently measured both before and after treatment. Wide variations exist in steroid trial regimens and current practice may neither provide definitive evidence of treatment benefit nor an adequate safeguard for patients against potential side-effects.

Chronic Disease↗

PubMed2001

Glycemic control in the prevention of diabetic complications.

The relationship between abnormal circulating glucose levels and the development of long-term diabetic complications became apparent soon after the introduction of insulin 70 years ago and the avoidance of early death due to ketoacidosis. Classic observational studies by Pirart described the relationship between increased glycosuria and the ultimate development of diabetic retinopathy, nephropathy, and neuropathy. Nonetheless, it required the findings of randomized, controlled clinical trials to finally and definitively establish the relationship between glucose control and microvascular diabetic complications. With the publication of the Diabetes Control and Complications Trial, the Kumomoto Trial, and the United Kingdom Prospective Diabetes Study, the impact of glycemic control in the development of microvascular complications was confirmed. Our understanding of the pathophysiology of diabetes--particularly, the dysmetabolic changes seen in type 2 diabetes--includes abnormalities in lipid metabolism, fuel flux, and endothelial function. Diabetes control, therefore, can no longer be viewed exclusively as glucose management. Rather, a more global approach is necessary to minimize risks of both microvascular and macrovascular complications. This article explores data supporting a variety of interventions that have been shown to reduce morbidity and mortality associated with long-standing diabetes mellitus. In addition to acknowledging the relationship between complications and diabetic metabolic abnormalities, this article presents a health economics perspective by examining the cost-effectiveness and health utility of these interventions.

Cost-Benefit Analysis↗

PubMed2006

C-peptide replacement improves weight gain and renal function in diabetic rats.

AIM: Recent experimental and clinical data suggest that C-peptide replacement during type 1 diabetes exerts beneficial effects on diabetic nephropathy. The aim of this study was to determine if physiological C-peptide administration in replacement dose during 28 days had beneficial effects on metabolic status and renal functions in type-1 diabetic rats. METHODS: Four groups of rats were investigated: a non diabetic group treated with buffer (C group, n=6), three streptozotocin diabetic-induced groups treated with either buffer (D group, n=6), insulin (D-I group, n=6) or rat homologous C-peptide (D-C group, n=6). Weight gain was measured every week. All animals were housed in metabolic cages on day 28 for assessment of metabolic data. Blood and urine samples were collected to allow measurement of plasmatic osmolality, C-peptide concentration, sodium, and glucose losses and proteinuria. Glomerular filtration rate (GFR) was determined by creatinine clearance. RESULTS: All streptozotocin-treated animals were diabetic. Glycaemic control (mg/dl), was markedly improved in D-I (133+/-65) when compared with either D (547+/-49, P<0.05) or D-C (520+/-48, P<0.05) groups. Conversely, weight gain during the study, was improved in D-I and D-C as compared with D animals (135+/-13 and 41+/-18 vs 18+/-21 respectively), despite different glycaemic control. Diabetes-induced glomerular hyperfiltration (ml/min/kg), urinary protein leakage (g/kg/day), and Na urinary losses (mmol/100 g/day) respectively, were significantly (P<0.05) reduced in D-C (3.95+/-0.6; 0.08+/-0.06; 1.5+/-0.9) in comparison with D (4.95+/-0.8; 0.18+/-0.16; 3.7+/-2.1) and D-I (5+/-0.9; 0.19+/-0.11; 2.7+/-0.8) animals. Plasmatic osmolality was significantly increased in D group whereas there were no differences between C group and D-C group. Food and water intakes, urinary volume as well as urinary glucose losses were not significantly different between D-C and D groups. CONCLUSIONS: C-peptide administration in replacement dose to streptozotocin diabetic rats induces weight gain regardless hyperglycaemia or glycosuria. Diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with reduction of the diabetes-induced glomerular hyperfiltration.

Animals↗

PubMed1998

Child death related to insulin omission by mother.

A 4-year-old child was found dead in her house. She had been suffering from insulin-dependent diabetes mellitus (IDDM) for 3 years. She had been admitted to hospital three times, and attended the hospital once a month. Her glycaemic control remained poor. Autopsy findings revealed a remarkably fatty liver and lack of beta cells in the pancreatic islets of Langerhans. The laboratory reported ketoacidosis, ketonuria, glycosuria, and high levels of vitreous glucose and ketones. Her father had been absent for the 3 days before her death, and the mother should have fed her. Her mother was found drunk on the floor. No detailed history was available because of the mother's death, but the probability of the mother's omission of the insulin injection was suggested. Poor control of IDDM might have also been closely connected to general neglect by the mother. This case was considered child abuse.

Journal Article↗

PubMed2003

Cellobiose and lactulose coupled with mannitol and determined using ion-exchange chromatography with pulsed amperometric detection, are reliable probes for investigation of intestinal permeability.

Lactulose/mannitol and cellobiose/mannitol tests are currently used in the investigation of intestinal permeability (IP) in many gastrointestinal diseases. The aim of this study was to produce a good technique for the determination and comparison of the above-mentioned sugar probes to overcome the problem caused by the presence of significant glycosuria in patients affected by particular metabolic disorders such as diabetes mellitus. Tests were performed in 25 healthy volunteers, using either cellobiose (Ce) (5 g) and mannitol (Ma) (2 g), or lactulose (La) (5 g) and mannitol (2 g), given as oral isosmolar loads. Sugars were recovered in urine collected for 5 h. Analysis was carried out by using anion-exchange chromatography (AEC) with pulsed amperometric detection (PAD). Baseline separation of the above carbohydrates was achieved within 13 min by using a Carbopac PA-100 column and linear gradient elution. Carbohydrate quantification was performed by an internal standard method. The calibration curve for each sugar is linear to 40 mM. The limit of sugar detection is 0.01 mM. Recovery of sugar probes is between 98.2 and 100%. The %La, %Ce, %Ma in urine were evaluated and their ratios (Ce/Ma and La/Ma) were calculated. No significant difference in IP parameters were shown (La/Ma to Ce/Ma 0.018+/-0.014 vs. 0.012+/-0.007; the attendant probability of the null hypothesis being P=0.0714). Ce/Ma and/or La/Ma tests result similarly reliable in the clinical investigation of IP and the described new method is also helpful in urine even with high glucose concentration, without any interference.

Adolescent↗

PubMed1992

Factors influencing oral carriage of yeasts among individuals with diabetes mellitus.

A total of 439 individuals with diabetes mellitus were examined for carriage of yeasts by the oral rinse and palatal swab techniques. Eighteen genetic or environment variables were assessed for their contribution to carriage of yeasts. The factor contributing to palatal and oral carriage of yeasts among individuals with insulin dependent diabetes mellitus (IDDM) was age (P < 0.01). The factor contributing to palatal carriage of yeasts among individuals with non-insulin dependent diabetes mellitus (NIDDM) was poor glycaemic control (glycosuria P < 0.01); carriage in the oral cavity as a whole was influenced additionally by non-secretion of ABH blood group antigens (P < 0.05). Introduction of a denture altered the above risk factors. For individuals with IDDM, oral carriage was associated with the presence of retinopathy (P < 0.05); palatal carriage was influenced by poor glycaemic control (HbA1P < 0.01, plasma glucose levels P < 0.05) and age (P < 0.05). For those with NIDDM, palatal carriage was associated with continuous presence of the denture in the mouth (P < 0.01); oral carriage was associated with plasma glucose levels (P < 0.05).

Adult↗

PubMed2001

NMR and pattern recognition studies on the time-related metabolic effects of alpha-naphthylisothiocyanate on liver, urine, and plasma in the rat: an integrative metabonomic approach.

We present here a novel integrative metabonomic approach to probe toxic effects of drugs in experimental animals using alpha-naphthylisothiocyanate (ANIT) as a model hepatotoxicant. Male Han-Wistar rats were dosed with ANIT (150 mg/kg, n = 25), and plasma and liver samples were collected for NMR and magic-angle spinning (MAS) NMR spectroscopy at 3, 7, 24, 31, and 168 h postdosing. Urine was collected continuously for 3 days prior to dosing and up to 168 h postdose. Histopathology and plasma clinical chemistry was also performed at all time points. Liver samples were analyzed either intact by 600 MHz 1H MAS NMR techniques or using high resolution (liquid state) 1H NMR of water-acetonitrile extracts. These data were related to sequential 1H NMR measurements in urine and plasma using pattern recognition methods. 1D 1H NMR spectra were data-reduced and analyzed using principal components analysis (PCA) to show the time-dependent biochemical variations induced by ANIT toxicity. From the eigenvector loadings of the PCA, those regions of the 1H NMR spectra and hence the combinations of endogenous metabolites marking the main phase of the toxic episode were identified. The ANIT-induced biochemical manifestations included a hepatic lipidosis associated with hyperlipidaemia; hyperglycaemia and glycosuria; increased urinary excretion of taurine and creatine; a shift in energy metabolism characterized by increased plasma ketone bodies with reduced urinary excretion of tricarboxylic acid cycle intermediates and raised hepatic bile acids leading to bile aciduria. The integration of metabolic data derived from several sources gives a holistic approach to the study of time-related toxic effects in the intact system and enables the characterization of key metabolic effects during the development and recovery from a toxic lesion.

1-Naphthylisothiocyanate↗

PubMed1998

Nuclear magnetic resonance spectroscopic and principal components analysis investigations into biochemical effects of three model hepatotoxins.

1H NMR spectroscopy of urine combined with pattern recognition (PR) methods of data analysis has been used to investigate the time-related biochemical changes induced in Sprague-Dawley rats by three model hepatotoxins: alpha-naphthyl isothiocyanate (ANIT), d-(+)-galactosamine (GalN), and butylated hydroxytoluene (BHT). The development of hepatic lesions was monitored by conventional plasma analysis and liver histopathology. Urine was collected continuously postdosing up to 144 h and analyzed by 600-MHz 1H NMR spectroscopy. NMR spectra of the urine samples showed a number of time-dependent perturbations of endogenous metabolite levels that were characteristic for each hepatotoxin. Biochemical changes common to all three hepatotoxins included a reduction in the urinary excretion of citrate and 2-oxoglutarate and an increased excretion of taurine and creatine. Increased urinary excretion of betaine, urocanic acid, tyrosine, threonine, and glutamate was characteristic of GalN toxicity. Both GalN and ANIT caused increased urinary excretion of bile acids, while glycosuria was evident in BHT- and ANIT-treated rats. Data reduction of the NMR spectra into 256 integrated regions was used to further analyze the data. Mean values of each integrated region were analyzed by principal components analysis (PCA). Each toxin gave a unique time-related metabolic trajectory that could be visualized in two-dimensional PCA maps and in which the maximum distance from the control point corresponded to the time of greatest cellular injury (confirmed by conventional toxicological tests). Thereafter, the metabolic trajectories changed direction and moved back toward the control region of the PR map during the postdose recovery phase. The combination of urinary metabolites which were significantly altered at various time points allowed for differentiation between biliary and parenchymal injury. This NMR-PR approach to the noninvasive detection of liver lesions will be of value in furthering the understanding of hepatotoxic mechanisms and assisting in the discovery of novel biomarkers of hepatotoxicity.

1-Naphthylisothiocyanate↗

PubMed1999

The historical discovery of macular edema.

The occurrence of macular edema, or of intraretinal fluid in general, was largely unknown prior to the invention of the ophthalmoscope. One of the first reports on 'Retinitis in Glycosuria', a disease complex, which today would partly be described as diabetic maculopathy, was published in 1856 by Jaeger. His observations were confirmed less than twenty years later by Nettleship in London, and in 1875 Appolinaire Bouchardat from Paris described fluid and lipid accumulation in the macula which led--in his words--to a glucose induced amblyopia. The first pathophysiological hypotheses of fluid accumulation in the posterior pole were then put forward in 1882 by Tartuferi, who thought the edema represented swelling of photoreceptor sheaths. In 1896, the Frenchman Nuel coined the term 'oedème maculaire' which he had observed in a retinitis pigmentosa patient. However, it was not until the end of the first World War, that the Swiss ophthalmologist Alfred Vogt observed macular edema in a variety of other ocular conditions such as iridocyclitiOFF macular edema to a macular hole. A quarter of a century later Bangerter coined the German term 'Zystoides Makulaödem', and in 1950, Hruby was the first to draw attention to the development of macular edema after cataract extraction. Three years later this was followed by Irvine's classical paper on cystoid macular edema after intra- and extracapsular cataract extraction which had been complicated by incarceration of the vitreous in the anterior segment with consecutive tugging on the macula. A decade later, the phenomenon of cystic fluid accumulation in the macula after cataract extraction was further characterised by Gass and Norton using fluorescein angiography. The ensuing years saw the emergence of new concepts regarding the blood-retinal barrier and the paramount role of its dysfunction in the development of macular edema.

Fluorescein Angiography↗

PubMed2000

Glucose transporters: structure, function and consequences of deficiency.

There are two mechanisms for glucose transport across cell membranes. In the intestine and renal proximal tubule, glucose is transported against a concentration gradient by a secondary active transport mechanism in which glucose is cotransported with sodium ions. In all other cells, glucose transport is mediated by one or more of the members of the closely related GLUT family of glucose transporters. The pattern of expression of the GLUT transporters in different tissues is related to the different roles of glucose metabolism in different tissues. Primary defects in glucose transport all appear to be extremely rare and not all possible deficiencies have been identified. Deficiency of the secondary active sodium/glucose transporters result in glucose/galactose malabsorption or congenital renal glycosuria. GLUT1 deficiency produces a seizure disorder with low glucose concentration in cerebrospinal fluid and GLUT2 deficiency is the basis of the Fanconi-Bickel syndrome, which resembles type I glycogen storage disease.

Animals↗

PubMed2004

Hyperinsulinaemia and increased risk of breast cancer: findings from the British Women's Heart and Health Study.

OBJECTIVE: To assess the association between fasting insulin levels and breast cancer. DESIGN: Cross sectional study. PARTICIPANTS: 3868 women aged 60-79 years. MAIN OUTCOME MEASURE: Prevalent breast cancer (151 cases). RESULTS: Insulin levels were positively associated with breast cancer. The age adjusted odds ratio (95% confidence interval) for a one unit increase in log(e) insulin levels among women without diabetes was 1.34 (1.02, 1.77). This association was not substantively altered by adjustment for potential confounding factors (age of menopause, hysterectomy/oophorectomy, hormone replacement use, oral contraceptive use, parity, adult social class and smoking) or potential mediating factors (body mass index, waist to hip ratio, leg length, age at menarche and childhood social class). Women with both long legs and higher insulin levels were at particularly increased risk, with breast cancer prevalence being 5.7% among women in the highest thirds of both insulin levels and leg-length compared to 1.8% among those in the lowest thirds of both. Positive associations between insulin levels and breast cancer were found for both pre- and post-menopausal breast cancers. Fasting glucose levels, HOMA score, diabetes and a history of gestational glycosuria or diabetes were also positively associated with breast cancer CONCLUSIONS: Hyperinsulinaemia is positively associated with breast cancer in this cohort of older women. This effect may be mediated via a number of hormonal pathways acting at different stages of the life course.

Aged↗

PubMed1993

Lack of nephrotoxicity of oral ammine/amine platinum (IV) dicarboxylate complexes in rodents.

The comparative nephrotoxicity of i.v. cisplatin, i.v. carboplatin and six p.o. ammine/amine Pt(IV) dicarboxylates was studied in rodents following single MTD treatments. In mice, i.v. cisplatin caused proteinuria (1 g l-1), glycosuria (16.7 mM) and decreased GFR at 4 days, and histological kidney damage with onset at 6 days. In contrast, mice treated with i.v. carboplatin or p.o. ammine/amine Pt(IV) dicarboxylates had urinary glucose, urinary protein, GFR and kidney histology within the control range. In rats, i.v. cisplatin caused 5-fold elevations in plasma creatinine (188 +/- 33 microM) and urea (30.4 +/- 8.9 mM), a 10-fold fall in creatinine clearance (0.54 +/- 0.31 ml min-1 kg-1), a 25-fold elevation in urine/plasma glucose concentration ratio (3.28 +/- 0.17), a 20% increase in kidney weight (7.9 +/- 0.56 mg gm-1 body weight) and extensive histological damage 4 days after treatment. In contrast, i.v. carboplatin and p.o. JM216 (the lead compound of this series) caused neither abnormalities in renal function nor histological damage in rats. The nephrotoxicity of single MTD treatments of p.o. ammine/amine Pt(IV) dicarboxylate complexes appears less than i.v. cisplatin and comparable to i.v. carboplatin.

Administration, Oral↗

PubMed1980

Renal tubular function in glycerol-induced acute renal failure.

The purpose of this study was to examine proximal and distal tubular function in rats with nonoliguric, myohemoglobinuric acute renal failure (ARF). ARF was induced with glycerol (50%, 10 ml/kg of body wt, i.m.), and renal function was studied 24 hours after glycerol or saline (controls) injection. Glycerol injection caused a 50 to 90% depression in GFR and a significant rise in blood urea nitrogen concentration. Animals with ARF exhibited glycosuria with normal blood sugar levels and a striking depression in tubular glucose reabsorption per milliliter of GFR. The capacity to reabsorb (mEq/liter GFR) was intact at normal blood bicarbonate levels, but was markedly depressed when blood bicarbonate was raised. The tubular maximum for para-aminohippurate (PAH) secretion and the renal extraction fraction of PAH were strikingly depressed in rats with ARF. Distal acidification as assessed by the urine-to-blood gradient of PCO2 (UB PCO2) was normal both during maximal alkalinization of the urine with bicarbonate (urine pH, approximately 7.8) or during neural phosphate infusion (urine pH, approximately 7.0). Net acid excretion per milliliter GFR and minimal urine pH (less than 5.5) following 3 days of ammonium chloride ingestion was similar in control and ARF animals. Potassium excretion was intact in maximal urinary osmolality were significantly altered in animals with ARF. Cortical and outer medullary Na-K-ATPase specific activities were significantly depressed in ARF rats. This occurred as a consequence of enzyme loss and not secondary to alterations in enzyme kinetics of absolute tubular sodium reabsorption. Light and electron microscopy showed diffuse proximal tubular damage, whereas glomeruli and distal tubules were intact. These data demonstrate that glycerol injection produces a diffuse proximal tubular transport defect associated with histologic and enzymatic alterations.

Acute Kidney Injury↗