D-Penicillamine reduces renal injury in the remnant model of chronic renal failure in the rat

Throssell, David; Brown, Joanna; Furness, Peter; Rutty, G.; Walls, John; Harris, Kevin

doi:10.1093/ndt/12.6.1116

Cited by 3 publications

(3 citation statements)

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“…Early reports of a correlation between urinary hydrogen ion content and protein excretion in human subjects [lo] have been confirmed in rats, which develop proteinuria when made acidotic for short periods by dietary ammonium chloride (NH,Cl) [l 13. It was originally proposed that this proteinuria resulted from increased protein filtration at the glomerulus, but recent data from this laboratory have shown that short-term acidosis causes a significant increase in urinary lysozyme and N-acetylglucosaminidase, while excretion of immunoglobulin G remains relatively unchanged [12]. This profile suggests tubular, rather than glomerular, injury and is consistent with immunohistochemical studies of kidneys from rats given dietary hydrochloric acid supplements for 14 days.…”

Section: Introductionsupporting

confidence: 69%

Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat

et al. 1995

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1. Metabolic acidosis invariably accompanies chronic renal failure, and short periods of metabolic acidosis cause renal growth and proteinuria in normal rats. Rates of ammoniagenesis are increased in chronic renal failure, and it has been suggested that this contributes to disease progression. This study assessed (i) whether prolonged acidosis causes chronic renal injury in the normal kidney and (ii) whether abrogation of acidosis slows disease progression in the remnant kidney. 2. Metabolic acidosis was induced in normal rats by dietary hydrochloric acid. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing after 14 weeks, kidney weights, glomerular filtration rates and serum creatinine were the same in both groups, but kidney/body weight and kidney/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nephrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood pressure, histological injury and time to the development of terminal uraemia were no better in bicarbonate-supplemented animals than in controls. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in patients with chronic renal failure.

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Section: Introductionsupporting

confidence: 69%

Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat

et al. 1995

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“…262 Other studies have used cytokines such as relaxin, 187 hepatocytegrowthfactor, 263,264 and bone morphogenetic protein 7. 202 Antifibrotic agents [265][266][267] have also produced encouraging results. Dietary Modification.…”

Section: Early Nephrology Referralmentioning

confidence: 99%

Progression of Chronic Renal Failure

2003

Arch Intern Med

121

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Chronic renal failure is characterized by a persistently abnormal glomerular filtration rate. The rate of progression varies substantially. Several morphologic features are prominent: fibrosis, loss of native renal cells, and infiltration by monocytes and/or macrophages. Mediators of the process include abnormal glomerular hemodynamics, hypoxia, proteinuria, hypertension, and several vasoactive substances (ie, cytokines and growth factors). Several predisposing host factors may also contribute to the process. Treatments to delay progression are aimed at treating the primary disease and at strictly controlling the systemic blood pressure and proteinuria. The role of antihypertensive agents, statins, and use of other maneuvers such as protein restriction and novel approaches are also discussed herein.

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“…In the commonly used 5/6 nephrectomy model, the remnant kidney usually exhibits early compensatory hypertrophy, glomerular perfusion, a high filtration rate, and hyperpressure; these developments are followed by glomerular sclerosis, capillary loop collapse, progressive mesangial expansion, tubular interstitial damage, and, ultimately, progressive renal failure [22]. Also, rats from which two-thirds of kidney tissue has been removed have been used to investigate residual renal destruction [24]. However, this model is not widely employed.…”

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Applications of Urinary Proteomics in Renal Disease Research Using Animal Models

Cai

Chen

2014

Urine Proteomics in Kidney Disease Biomarker Discovery

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Animal models of renal disease are essential tools in research on kidney disease and have provided valuable insights into pathogenesis. Use of animal models minimises inter-individual differences, allows specific pathological changes to be examined, and facilitates collection of tissue samples. Thus, mechanistic research and identification of biomarkers are possible. Various animal models manifesting specific pathological lesions can be used to investigate acute or chronic kidney disease (CKD). Urine, a terminal metabolic product, is produced via glomerular filtration, reabsorption, and excretion in the tubular and collecting ducts, reflecting the functions of glomeruli or tubular tissue stimulated in various ways or subject to disease. Almost 70 % of urinary proteins originate from the kidney (the other 30 % come from plasma), and urinary sampling is important to noninvasively detect renal disease. Proteomics is powerful when used to screen urine components. Increasingly, urine proteomics is used to explore the pathogenesis of kidney disease in animals and to identify novel biomarkers of renal disease. In this section, we will introduce the field of urinary proteomics as applied in different models of animal renal disease and the valuable role played by proteomics in noninvasive diagnosis and rational treatment of human renal disease.

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D-Penicillamine reduces renal injury in the remnant model of chronic renal failure in the rat

Abstract: These findings demonstrate that DPC reduces renal injury in the remnant kidney, and raise the possibility of a therapeutic role for DPC in the treatment of patients with chronic renal failure.

Cited by 3 publications

References 1 publication

Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat

Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat

Progression of Chronic Renal Failure

Applications of Urinary Proteomics in Renal Disease Research Using Animal Models

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