Tubulointerstitial Diseases

Braden, Gregory; O'Shea, Michael; Mulhern, Jeffrey G.

doi:10.1053/j.ajkd.2005.03.024

Cited by 33 publications

(18 citation statements)

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“…This may be explained, as for hyperphosphatemia, by higher protein intake among younger patients. 40 As reported by Braden et al, 41 we observed that patients with tubulointerstitial nephritis had a higher odds ratio for metabolic acidosis, but it was not statistically significant. Men were also at higher risk for hyperkalemia.…”

Section: Discussionsupporting

confidence: 61%

Timing of Onset of CKD-Related Metabolic Complications

Moranne

Froissart²,

Rossert³

et al. 2009

Journal of the American Society of Nephrology

411

283

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Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR Ͻ60 ml/min per 1.73 m 2 for complications, but little evidence supports the use of a single GFR threshold for all metabolic disorders. We used data from the NephroTest cohort, including 1038 adult patients who had stages 2 through 5 CKD and were not on dialysis, to study the occurrence of metabolic complications. GFR was measured using renal clearance of 51 Cr-EDTA (mGFR) and estimated using two equations derived from the Modification of Diet in Renal Disease study. As mGFR decreased from 60 to 90 to Ͻ20 ml/min per 1.73 m 2 , the prevalence of hyperparathyroidism increased from 17 to 85%, anemia from 8 to 41%, hyperphosphatemia from 1 to 30%, metabolic acidosis from 2 to 39%, and hyperkalemia from 2 to 42%. Factors most strongly associated with metabolic complications, independent of mGFR, were younger age for acidosis and hyperphosphatemia, presence of diabetes for acidosis, diabetic kidney disease for anemia, and both male gender and the use of inhibitors of the renin-angiotensin system for hyperkalemia. mGFR thresholds for detecting complications with 90% sensitivity were 50, 44, 40, 39, and 37 ml/min per 1.73 m 2 for hyperparathyroidism, anemia, acidosis, hyperkalemia, and hyperphosphatemia, respectively. Analysis using estimated GFR produced similar results. In summary, this study describes the onset of CKD-related complications at different levels of GFR; anemia and hyperparathyroidism occur earlier than acidosis, hyperkalemia, and hyperphosphatemia.

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Section: Discussionsupporting

confidence: 61%

Timing of Onset of CKD-Related Metabolic Complications

Moranne

Froissart²,

Rossert³

et al. 2009

Journal of the American Society of Nephrology

411

283

View full text Add to dashboard Cite

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“…Finally, fibroblasts and, especially under pathological conditions, myofibroblasts form part of the tubular interstitium. Primary tubulointerstitial diseases [41] are idiopathic, genetic or due to (i) the chemical action of toxics and drugs that accumulate in the tubules inducing apoptosis or necrosis of tubular epithelial cells; (ii) infection and inflammation of the tubulointerstitium as a result of reflux/chronic pyelonephritis or other causes; (iii) increased intratubular pressure induced by mechanical stress and related to obstruction of lower urinary tract caused by lithiasis, prostatitis, fibrosis, or retroperitoneal tumors; and (iv) transplant rejection due to immune response. In many cases, the cause of the disease remains unknown.…”

Section: Tubular Diseasesmentioning

confidence: 99%

Etiopathology of chronic tubular, glomerular and renovascular nephropathies: Clinical implications

et al. 2011

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Chronic kidney disease (CKD) comprises a group of pathologies in which the renal excretory function is chronically compromised. Most, but not all, forms of CKD are progressive and irreversible, pathological syndromes that start silently (i.e. no functional alterations are evident), continue through renal dysfunction and ends up in renal failure. At this point, kidney transplant or dialysis (renal replacement therapy, RRT) becomes necessary to prevent death derived from the inability of the kidneys to cleanse the blood and achieve hydroelectrolytic balance. Worldwide, nearly 1.5 million people need RRT, and the incidence of CKD has increased significantly over the last decades. Diabetes and hypertension are among the leading causes of end stage renal disease, although autoimmunity, renal atherosclerosis, certain infections, drugs and toxins, obstruction of the urinary tract, genetic alterations, and other insults may initiate the disease by damaging the glomerular, tubular, vascular or interstitial compartments of the kidneys. In all cases, CKD eventually compromises all these structures and gives rise to a similar phenotype regardless of etiology. This review describes with an integrative approach the pathophysiological process of tubulointerstitial, glomerular and renovascular diseases, and makes emphasis on the key cellular and molecular events involved. It further analyses the key mechanisms leading to a merging phenotype and pathophysiological scenario as etiologically distinct diseases progress. Finally clinical implications and future experimental and therapeutic perspectives are discussed.

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“…It is characterized by infiltration of inflammatory cells, mainly lymphocytes, into the interstitium and tubular wall of the kidney [1,2]. In rare cases, renal changes are accompanied by uveal inflammation; this is referred to as tubulointerstitial nephritis with uveitis (TINU) [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Clinical outcome and occurrence of uveitis in children with idiopathic tubulointerstitial nephritis

et al. 2010

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Acute idiopathic tubulointerstitial nephritis (TIN) is considered a condition with a good long-term prognosis. However, there is evidence that some patients develop permanent renal impairment. The aim of this study was to evaluate the clinical characteristics of TIN at the time of diagnosis in children and determine whether the findings upon presentation predict renal outcome. The clinical data and biopsy findings from 26 children with idiopathic TIN admitted to four Finnish university hospitals were analyzed retrospectively. Twenty-five patients (96%) manifested renal insufficiency. After the mean follow-up time of 2.75 years (SD 2.5; 0.9-13.5), 4 patients (15%) had permanent renal insufficiency and 8 patients (31%) had persistent low-molecular weight proteinuria. Uveitis was found in 12 patients (46%). Four of these patients (33%) developed chronic uveitis. Our analysis showed that none of the laboratory or biopsy findings upon presentation prognosticated renal outcome. No correlation between renal disease and uveitis could be found either. The occurrence of uveitis among TIN patients was higher than previously reported. Uveitis may develop late and without recurrence of renal dysfunction. Therefore, follow-up by a pediatrician and by an ophthalmologist is warranted in children with acute TIN for at least 12 months from diagnosis.

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Tubulointerstitial Diseases

Cited by 33 publications

References 0 publications

Timing of Onset of CKD-Related Metabolic Complications

Timing of Onset of CKD-Related Metabolic Complications

Etiopathology of chronic tubular, glomerular and renovascular nephropathies: Clinical implications

Clinical outcome and occurrence of uveitis in children with idiopathic tubulointerstitial nephritis

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