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Renal Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Axelsson and Piscator10 gave rabbits daily s.c. injections of cadmium chloride, 0.25 mg Cd per kilogram body weight, 5 days/week. After 23 weeks there was considerable proteinuria and excretion of cadmium. In another group of rabbits10 exposure conditions were similar to those stated above, but exposure was discontinued after 24 weeks, after which the animals were followed up for another 30 weeks. Urine investigations showed that protein excretion increased during exposure and was about two to three times higher than the control group at 24 weeks. The excretion reached a maximum about 1 month after exposure had ceased, and was followed by an apparent reduction in protein excretion. At the end of the observation time the protein excretion was the same as that at 24 weeks, but due to individual variation, the difference between exposed animals and controls was not statistically significant. Electrophoretic examination of urinary proteins showed a predominance of proteins with a mobility like α- and β-globulins. It was concluded that this corresponded to the tubular proteinuria found in human beings.38 The renal cortex in the exposed animals contained large amounts of cadmium,10 about 235 mg/kg wet weight, after 11 weeks’ exposure, about 460 mg/kg after 17 weeks, and about 250 mg/kg at the end of exposure (see further data in Section IV.D).
The kidneys
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
There may also be tubular proteinuria, which usually refers to low-molecular-weight proteins that are normally produced in the body, filtered across the glomerular membrane and reabsorbed in the proximal tubule, but appear in the urine as a result of proximal tubular damage, for example α1-microglobulin and retinol binding protein. However, tubular proteinuria also occurs when proximal tubular enzymes and proteins, such as N-acetyl-β-D-glucosaminidase (NAG), are released into the urine due to tubular cell injury. See Chapter 19.
The Nature of Renal Function
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
Several low–molecular weight proteins are present in normal plasma in measurable concentrations. Examples are α-1 microglobulin, β-2 microglobulin, and retinol-binding protein (RBP). Because they are smaller than the size barrier of the glomerular ultrafilter, significant amounts are present in glomerular filtrate and enter the proximal tubule, where they are reabsorbed by pinocytosis into the tubular epithelial cells where they are digested to their component amino acids and returned to the body protein pool. They are therefore virtually absent from normal urine. Proximal tubular dysfunction, however, leads to a urinary leak of these proteins and a characteristic pattern of low–molecular weight proteinuria known as tubular proteinuria. Measurement of urinary excretion of β-2 microglobulin and RBP, usually expressed as fractional excretion rates, is a useful means of distinguishing between proteinuria of glomerular and nonglomerular (tubulo-interstitial) origin (34).
Non-diabetic glycosuria as a diagnostic clue for acute tubulointerstitial nephritis in patients with azotemia
Published in Renal Failure, 2020
In proximal tubular injury, low molecular weight proteins filtered through glomeruli are not reabsorbed and appear in the urine. The tubular proteinuria can be identified in protein electrophoresis by its characteristic pattern [33], and can be a clue for ATIN. In this study, some of the samples had too low protein concentration for electrophoresis, and tubular proteinuria was detected in 8 (40%) of 20 patients who submitted urine for the test. Thus, the sensitivity of urine protein electrophoresis in the detection of ATIN was lower than that of urine glucose test. However, there was a patient who had no glycosuria, but had a positive result of tubular proteinuria. So, urine protein electrophoresis may be used in conjunction with urine glucose to improve the sensitivity in the diagnosis of ATIN.
Hypotonia and delayed motor development as an early presentation of Lowe syndrome: case report and literature review
Published in Acta Clinica Belgica, 2019
Sara David, Kathleen De Waele, Bram De Wilde, Franny Faes, Olivier Vanakker, Sophie Walraedt, Agnieszka Prytuła
In our patient the presence of tubular proteinuria in urine analysis provided an important clue to diagnosis. Affected boys have varying degrees of renal tubular dysfunction. In early life most children do not exhibit specific symptoms of renal dysfunction. During the first months of life children develop failure to thrive caused by renal bicarbonate, salt and water wasting. Urine analysis at birth shows low-molecular weight proteinuria in all LS patients [7]. This is an interesting finding which can be useful for early diagnosis in patients as this case, when the typical clinical presentation of congenital cataract is absent. Equally, early urine testing is useful in children with congenital cataract, because in the majority of cases of LS, this is the first clinical symptom. When tubular dysfunction becomes more profound later in life, urine analysis can show phosphaturia, aminoaciduria, hypercalciuria, potassium wasting and glycosuria [2].
Simplification to dual-therapy containing lamivudine and darunavir/ritonavir or atazanavir/ritonavir in HIV-infected patients on virologically suppressive antiretroviral therapy
Published in Infectious Diseases, 2018
Leonardo Calza, Matteo Cafaggi, Vincenzo Colangeli, Marco Borderi, Enrico Barchi, Massimiliano Lanzafame, Stefano Nicole’, Anna Maria Degli Antoni, Isabella Bon, Maria Carla Re, Pierluigi Viale
The following demographic, clinical and laboratory data were recorded at the start of therapy and at 3-month interval during the 12-month follow-up: sex, age, race, physical examination, body mass index (BMI), arterial pressure, clinical manifestations, current and past medications; spot urinalysis, estimated glomerular filtration rate (eGFR) and serum levels of triglycerides, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, glucose, complete liver and kidney function tests, creatine kinase, CD4 + and CD8 + T lymphocyte count and HIV viral load. Patients with abnormal proteinuria on spot urines (>30 mg/dL) underwent proteinuria and albuminuria (by protein electrophoresis) on 24-h collected urines, and abnormal proteinuria was defined as tubular proteinuria if the albumin excretion was <50% of the total protein excretion. Hypophosphoremia was diagnosed when serum phosphorus concentration was <2.5 mg/dL. The eGFR was calculated using the 2009 CKD-EPI equation formula [15], and reduced eGFR was defined as an eGFR <80 mL/min/1.73 m2 or a reduction in the eGFR ≥10% in the last year.