Structural-functional correlations in renal disease

Striker, Gary E.; Schainuck, Lewis I.; Cutler, Ralph E.; Benditt, Earl P.

doi:10.1016/s0046-8177(70)80060-0

Cited by 120 publications

(19 citation statements)

References 4 publications

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“…It is now well accepted that chronic tubulointerstitial injury including interstitial infiltration of mononuclear cells and interstitial fibrosis is the major determinant for the progression of renal disease [47]. Studies in human biopsies have shown that the decline in renal function correlates most closely with changes in the tubules and the interstitium, rather than in the glomeruli [48, 49]. STZ-induced diabetes mellitus, the most widespread animal model for type I diabetes, does not lead to significant changes in the tubulointerstitium and does not progress to renal insufficiency, rendering this model less than satisfactory as an experimental model for human diabetic nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia and Hyperlipidemia Act Synergistically to Induce Renal Disease in LDL Receptor-Deficient BALB Mice

Spencer¹,

Mühlfeld

Segerer

et al. 2004

Am J Nephrol

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Diabetic nephropathy is the leading cause of end-stage renal disease in Western countries, but only a portion of diabetic patients develop diabetic nephropathy. Dyslipidemia represents an important aspect of the metabolic imbalance in diabetic patients. In this study, we addressed the impact of combined hyperlipidemia and hyperglycemia on renal pathology. Kidneys from wild-type (WT) or LDL receptor-deficient BALB/cBy mice (BALB.LDLR–/–) were examined at 22 weeks of age. Diabetes was induced by administration of streptozotocin and mice were randomly assigned to either standard chow or Western diet. Chow fed BALB.LDLR–/– mice did not demonstrate renal abnormalities, whereas BALB. LDLR–/– mice fed a Western diet showed occasional glomerular and tubulointerstitial foam cells. Diabetic WT mice had modestly increased glomerular cellularity and extracellular matrix. Hyperlipidemic and diabetic BALB.LDLR–/– mice exhibited an increase in glomerular cellularity and extracellular matrix, accumulation of glomerular and tubulointerstitial foam cells and mesangial lipid deposits. The tubular epithelium demonstrated pronounced lipid induced tubular degeneration with increased tubular epithelial cell turnover. Hyperlipidemia and hyperglycemia seem to act synergistically in inducing renal injury in the BALB.LDLR–/– mouse. This model of diabetic nephropathy is unique in its development of tubular lesions and may represent a good model for hyperlipidemia-exacerbated diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia and Hyperlipidemia Act Synergistically to Induce Renal Disease in LDL Receptor-Deficient BALB Mice

Spencer¹,

Mühlfeld

Segerer

et al. 2004

Am J Nephrol

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“…Tubulointerstitial fibrosis is the major histopathological change seen in a variety of renal disorders [1]and is closely related to renal dysfunction [2, 3]. Unilateral ureteral obstruction (UUO) is a well-established model of experimental renal disease that results in tubulointerstitial fibrosis [4, 5].…”

Section: Introductionmentioning

confidence: 99%

Mizoribine Ameliorates the Tubulointerstitial Fibrosis of Obstructive Nephropathy

Sato

Shiraiwa²,

Kang³

et al. 2001

Nephron

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Mizoribine has been shown to possess an immunosuppressive action that inhibits the proliferation of lymphocytes selectively by interfering with inosine monophosphate dehydrogenase. Recent studies have demonstrated that mizoribine improves renal tubulointerstitial fibrosis in the rat model of unilateral ureteral obstruction (UUO) by inhibiting the infiltration of macrophages. We, therefore, examined the dose dependency of the suppressive effect of mizoribine on the infiltration of interstitial macrophages and T lymphocytes and the interstitial volume in UUO-treated kidneys. Furthermore, we investigated the expression of osteopontin (OPN), known to be a chemoattractant protein for macrophages, in the renal cortex. In rats with UUO, the interstitial volume was markedly expanded, and macrophage and T lymphocyte infiltration in the interstitium and the expression of OPN in the cortical tubules were greatly increased. Treatment with mizoribine ameliorated the increase in interstitial volume induced by UUO. Interstitial infiltration of macrophages and T lymphocytes was dose dependently suppressed by mizoribine, and the decreased macrophage infiltration was correlated with inhibition of tubular OPN expression. These results suggest that mizoribine has a beneficial effect on several steps contributing to the progression of tubulointerstitial fibrosis caused by obstruction of the ureter.

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“…Three groups of investigators in London [1], Seattle [2, 3]and Tübingen [4, 5]have shown that in glomerular diseases the impairment of the glomerular filtration rate correlated better with the extent of tubulointerstitial damage than with the degree of the glomerular damage and suggested that the major events which determine the outcome of these diseases probably occur in the interstitium. In these last 15 years, the importance of tubulointerstitial involvement for the progression of renal damage in glomerular diseases has been supported by a continuously increasing amount of clinical and experimental data, emerging mainly from two types of studies: (1) studies of natural history of large cohorts of patients, showing correlations between single clinical or histological features and progression, and (2) studies based on molecular biology and immunohistochemistry of biopsy specimens, showing the expression of the mRNA and/or the protein of single cytokines or growth factors in the epithelial tubular cells, in the leukocytes infiltrating the interstitium and in the resident interstitial fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Tubulointerstitium as Predictor of Progression of Glomerular Diseases

D’Amico¹

1999

Nephron

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Structural-functional correlations in renal disease

Cited by 120 publications

References 4 publications

Hyperglycemia and Hyperlipidemia Act Synergistically to Induce Renal Disease in LDL Receptor-Deficient BALB Mice

Hyperglycemia and Hyperlipidemia Act Synergistically to Induce Renal Disease in LDL Receptor-Deficient BALB Mice

Mizoribine Ameliorates the Tubulointerstitial Fibrosis of Obstructive Nephropathy

Tubulointerstitium as Predictor of Progression of Glomerular Diseases

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