Renal tubular injury

Chisolm JJ Jr. 1962. Aminoaciduria as a manifestation of renal tubular injury in lead intoxication and a comparison with patterns of aminoaciduria seen in other diseases. J Pediatr 60 1-17. 

Inhalation exposure of mice at 7000ppm 6hrs/day, 5 days week for 14 weeks caused hyperreactivity and diminished response to an auditory alerting stimulus during exposures and significantly increased liver weights at the end of exposures rats similarly exposed also had a significantly increased incidence of hepatic centrilobular hypertrophy. Repeated intraperitoneal administration of 1.5g/kg caused evidence of renal tubular injury in rats effects were attributed to cyclohexanol, the main metabolite of cyclohexane."... 

Renal impairment, including cases of acute renal failure and Fanconi syndrome (renal tubular injury with severe hypophosphatemia), has been reported in association with the use of tenofovir disoproxil fumarate. 

Renal damage is the most significant toxic reaction. Renal impairment occurs in nearly all patients treated with clinically significant doses of amphotericin. The degree of azotemia is variable and often stabilizes during therapy, but can be serious enough to necessitate dialysis. A reversible component is associated with decreased renal perfusion and represents a form of prerenal renal failure. An irreversible component results from renal tubular injury and subsequent dysfunction. 

Urinary enzyme activity provides a means to determine the presence and location of renal tubular injury as opposed to an index to the functional status of the nephron. Urine enzymes provide several advantages over urine protein for the assessment of tubular injury (Stonard et al. 1987 Vanderlinde et al. 1981 Price 1982 Plummer et al. 1986 Clemo 1998 Dubach et al. 1988 Westhuyzen et al. 2003) ... 

Fraser JS, Muller AF, Smith DJ, Newman DJ, Lamb EJ. Renal tubular injury is present in acnte inflammatory bowel disease prior to the introdnction of dmg therapy. Aliment Pharmacol Ther 2001 15(8) 1131-7. 

Transient renal tubular dysfunction has been reported in a patient with asthma requiring mechanical ventilation who received sevoflurane for 9 days (36). Soda hme was not used, and the cumulative dose was 298 MAC-hours. Serum and urinary inorganic fluoride concentrations reached maximum concentrations of 71 and 2047 pmoPl respectively. Markers of renal tubular injury were also greatly raised (urinary A-acetyl-beta-o-glucosaminidase and beta2-microglobulin). However, urine volume, creatinine clearance, and serum creatinine and urea concentrations were unaffected. 

The effect of the uricosuric agent probenecid in prolonged sevoflurane anesthesia has been examined in 64 patients randomized to receive high-flow or low-flow anesthesia with sevoflurane with or without preoperative oral probenecid (61). There were no differences in urea, creatinine, or creatinine clearance among the treatments. However, patients who received low-flow sevoflurane had some evidence of renal tubular injury (raised urinary markers) compared with those who received either high-flow anesthesia or probenecid. 

Kobayashi E, Suwazono Y, Honda R, Dochi M, Nishijo M, KidoT, Nakagawa H. Serial changes in urinary cadmium concentrations and degree of renal tubular injury after soil replacement in cadmium-polluted rice paddies.Toxicol Lett. 2007 Nov 1. 

Another previous report [187] described severe hypocalcemia with tetany in patients with AIDS concomitantly receiving pentamidine and foscarnet. The hypocalcemia, however, was attributed to the administration of foscarnet. Despite magnesium replacement, magnesium wasting may persist up to two months after the discontinuation of pentamidine, suggesting that anatomic renal tubular injury may be responsible [183,185]. Both abnormalities developed within 6 to 10 days of pentamidine administration. Because life-threatening arrhythmias can develop, especially at serum magnesium levels less than 1.6 mg/dl, early replacement therapy is clinically warranted. 

Roels et al. [38] points out that the analytical techniques identified in Table 1 are not easily available and are not well-suited for routine biomonitoring of occupational or environmental exposures. Instead, indirect biomarkers such as urinary enzymes are often used with success to evaluate mercury exposure and injury. Zalups [35] identifies numerous methods used to detect renal tubular injury induced by mercury. These methods monitor the urinary excretion of enzymes that leak from injured and necrotic proximal tubules, including lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and N-acetyl-P-D-glucosaminidase (NAG). Although advocated by Zalups (35) to detect renal tubular injury, Mason et al. (48) questions the practical utility of such biomarkers in occupational surveillance. According to Mason et al., small increases in NAG, leucine... 

Sherman, R. A., Feinfeld, D. A., Ohmi, N., Arias, I. M., and Levine, S. D., A prospective study of urinary ligandin in patients at risk of renal tubular injury. Uremia Invest. 8,111-115 (1985). 

During certain disease states that result in renal tubular injury, NH4 production by renal proximal tubules may increase in order to maintain net acid excretion. However, this may also contribute to further renal damage by modifying the third component of complement and initiating the alternative complement pathway (Clark et al. 1990). Ammonia can chemically interact with an internal thiolester bond of complement 3 (C3), resulting in an amide linkage and a subsequent conformational change of the C3. 

Renal tubular acidosis and chronic alkalosis Renal tubular injury... 

Nephrotoxicity is another problem observed in patients given chemotherapeutic agents. Venkatesan et al. " showed that curcumin prevents adriamycin (ADR)-induced nephrotoxicity in rats. Treatment with curcumin markedly protected against ADR-induced proteinuria, albuminuria, hypoalbuminemia, and hyperhpidemia. Similarly, curcumin inhibited ADR-induced increase in urinary excretion of N-acetyl- )-D-glucosaminidase (a marker of renal tubular injury), fibronectin, glycosaminoglycan, and... 

C. Systemic absorption can produce hepatic and renal tubular injury. Hemolysis has been associated with copper exposure from hemodialysis equipment or absorption through burned skin. 

C. Chronic excessive use of vitamin D is associated with hypercalcemia, producing weakness, altered mental status, gastrointestinal upset, renal tubular injury, and occasionally cardiac arrhythmias. 

Chamberlain, A.C. (1943) Fallout of lead and uptake by crops. Atmos. Environ., 17, 693-706 Chisholm, J.J. and Leahy, N.B. (1962) Aminoaciduria as a manifestation of renal tubular injury in lead intoxication and a comparison with patterns of aminoaciduria seen in other diseases. ]. Pediat., 60, 1-17... 

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