The predictive value of enzymuria in cyclosporin ainduced renal toxicity in the rat

McAuley, F. T.; Simpson, John G.; Thomson, A. W.; Whiting, P. H.

doi:10.1016/0378-4274(86)90063-9

Cited by 12 publications

(5 citation statements)

References 9 publications

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“…Such results confirm the early increases in urinary levels of this parameter described elsewhere in the literature. [15,16] Here, the trauma itself plays a major role with fluid losses and hypotonic phases. The raised excretion rates following on from the 5th to 7th days of treatment must have been due to intensive care measures such as controlled ventilation with PEEP, fluid substitution, or the administration of blood derivatives, colloids or potentially toxic medications.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

Dehne¹,

Sablotzki²,

Mühling³

et al. 2002

Renal Failure

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During treatment in the ICU, all examined patients showed at times pathological excretion rates of specialized kidney function parameters. Such transient damage was only apparent in a few of the patients when the standard parameters serum creatinine and serum urea were employed. In 90% of the surviving patients the kidney parameters had normalized until the time they were transferred, indicating that such parameters reflected the general state of health of these patients.

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Section: Discussionmentioning

confidence: 99%

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

Dehne¹,

Sablotzki²,

Mühling³

et al. 2002

Renal Failure

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“…These findings demonstrate that in creased urinary excretion of N-acetyl-|3-Dglucosaminidase directly follows affection of proximal tubular cells, resulting in an imbal ance between the release and supply of active enzyme. In cyclosporine-A-induced nephro toxicity, it precedes functional and morpho logical alterations [24] and then parallels the other signs of renal dysfunction [3,6]. How ever, the effects of this drug on renal cell struc ture apparently do not correspond to those on renal function.…”

Section: Discussionmentioning

confidence: 99%

Nephrotoxicity of Cyclosporine A in the Rat

Schmid¹,

Lindmeier²,

Schmitt³

et al. 1993

Kidney Blood Press Res

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Cyclosporine A (15,30 or 50 mg/kg day) or olive oil (30 mg/kg day) were administered orally to 32 male Sprague-Dawley rats for 12 or 24 days, or withdrawn for 24 days following 24 days of treatment. The specific activity of a lysosomal marker enzyme N-acetyl-β-D-glucosaminidase was determined fluorometrically in single nephron segments microdissected from lyophilized kidney sections of these animals and of an additional 2 normal rats. The segments were classified according to their normal or reduced succinate dehydrogenase activity as detected in stained adjacent sections. In addition, urine specimens collected after 12, 24, 36, and 48 days of the experiment were tested for N-acetyl-β-D-glucosaminidase activity. After treatment with cyclosporine A, changes in the activities of N-acetyl-β-D-glucosaminidase were found only in the proximal tubules. In the convoluted segments with normal succinate dehydrogenase activity, the activity of N-acetyl-β-D-glucosaminidase was 138-163%, and in those with reduced succinate dehydrogenase activity, it was unchanged or 66-83% of the control values. In the straight segments with reduced succinate dehydrogenase activity, the activity of N-acetyl-β-D-glucosaminidase increased gradually along the medullary rays (122-214%) to the outer stripe of the outer medulla (178-263%) in comparison to the control values. In the urine specimens, the activity of N-acetyl-β-D-glucosaminidase was increased to 148-152%. These tubular and urinary changes were similar for each dosage and treatment period. After withdrawal of cyclosporine A they were not present. The variety of alterations occurring within the lysosomes along the proximal tubules of cyclosporine-A-treated rats implies the convoluted part as the site of increased release of N-acetyl-β-D-glucosaminidase into the urine.

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“…Such results confirm the early increases in urinary levels of this parameter described elsewhere in the literature. [20,21] Here, the trauma itself plays a major role with fluid losses and hypotonic phases. The raised excretion rates following from the fifth to seventh days of treatment must have been due to intensive care measures such as controlled ventilation with PEEP, fluid substitution, or the administration of blood derivatives, colloids, or potentially toxic medications.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of sE-Selectin and sICAM-1 as Parameters for Renal Function

Dehne¹,

Sablotzki

Mühling

et al. 2008

Renal Failure

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Introduction. In order to monitor acute renal failure, intensive care patients were examined, and routine as well as specialized parameters were compared. Materials and Methods. Thirty-three patients at the Surgical Intensive Care Unit (ICU) were examined daily over the entire period for which they stayed in the ICU. The patients were retrospectively classified as being either with or without acute renal failure. Group 1 consisted of 22 patients who resided in the ICU for 11-15 (median 14) days without ARF. Group 2 consisted of 11 patients who developed an ARF during their stay of 13-18 (median 16) days in the ICU. In addition to the routine parameters of diuresis, serum creatinine/urea, and clearance of creatinine, specialized parameters for kidney function, including the excretion rates of α1-microglobulin, Nacetyl-β-D-glucosaminidase, and total protein, were compared with the excretion rate of soluble ICAM-1 and sESelectin. Results. Diuresis, serum creatinine, urea, and enzyme elimination were pathological among patients with ARF. Already on the day of admission, raised elimination rates of sICAM-1 were found in the urine of patients who had developed an ARF. While high values were still shown upon discharge, levels kept falling among patients without ARF. Clearly raised values were also shown for sE-Selectin compared to patients without ARF. Conclusions. sICAM-1 and sE-Selectin as supplementary parameters indicating renal function revealed early signs of kidney damage. These parameters may play a major role in the development of novel therapeutic approaches for ARF (antibodies against ICAM-1 or sE-Selectin).

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The predictive value of enzymuria in cyclosporin ainduced renal toxicity in the rat

Cited by 12 publications

References 9 publications

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

Nephrotoxicity of Cyclosporine A in the Rat

Evaluation of sE-Selectin and sICAM-1 as Parameters for Renal Function

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