Proximal tubular damage

Glucosuria (which may be indicative of proximal tubular damage if the serum glucose concentration is within the normal physiological range)... 

Active transport of compounds by the tubular cells. Compounds that are actively transported from the blood into the tubular fluid may accumulate in the proximal tubular cells, especially at concentrations where saturation of the transport system occurs. Again, concentrations to which tubular cells are exposed may be very much higher than in the bloodstream. An example of this is the drug cephaloridine, which causes proximal tubular damage as discussed in more detail in chapter 7. 

Urine Cystatin C as a Marker for Proximal Tubular Damage. 84... 

Comment increasing amounts of either in urine suggest proximal tubular damage, extrarenal effects also possible (e.g., diabetes)... 

Lysozyme or muramidase, is an enzyme that catalyses the hydrolysis of the peptidoglycan layer of bacterial cell walls. The urinary excretion of lysozyme increases during urinary tract infections, proximal tubular damage, and excessive endogenous lysozyme synthesis that overwhelm the absorption capacity of the proximal tubule. 

Backman, L., Appelkvist, E. L., Ringden, O., and Dallner, G., Urinary levels of basic glutathione transferase as an indicator of proximal tubular damage in renal transplant recipients. Transplant. Proc. 21, 1514-1516 (1989). 

Toxicity of streptozocin includes nausea, which is a frequent side effect. Renal or hepatic toxicity occurs in approximately two thirds of cases although usually reversible, renal toxicity may be fatal, and proximal tubular damage is the most important toxic effect. Serial determinations of urinary protein are most valuable in detecting early renal effects. Hematological toxicity — anemia, leukopenia, or thrombocytopenia — occurs in 20% of patients. 

Lead exposure may cause kidney damage (Lim et al. 2001). In acute lead toxicity, there is proximal tubular damage, which may result in a reversible Fanconi syndrome-like condition with aminoaciduria, glucosuria, and hyperphosphaturia. Further, the tubular damage may cause leakage of enzymes (e.g., lysosomal NAG) from the cells into the urine (Skerfving 1993) at B-Pbs in the range 1.5-2.0 pmolL. This effect may be reversible. 

Rats developed proximal tubular damage at lead levels in the kidney of 45 mgkg (Goyer etal. 1989). UK subjects without occupational exposure seem to have lead levels of - 0.8 mgkg in the kidney cortex. 

In most studies, a combination of more than two or three enzymes has provided better information than the measurement of a single enzyme, with measurements based on regional and cellular location. Urinary enzymes have been particularly useful in detection of acute renal damage and, specihcally, proximal tubular damage however, they are correspondingly less valuable in providing information about chronic injury. 

Glucosuria. Normal serum glucose concentration may reveal proximal tubular damage (such as with gentamicin and maleic acid). 

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